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Accurate Diagnosis in Lesions of the Shoulder and Knee Joint
Accurate Diagnosis in Lesions of the Shoulder and Knee Joint ANTHONY F. DEPALMA, M.D.*
LESIONS OF THE SHOULDER
ALTHOUGH one must admit that all causative factors of a "painful-stiff" shoulder have not been uncovered, considerable progress has been made in this direction within the past two decades. Since the masterful work of Codmanl on lesions of the musculotendinous cuff published in 1934, many observers have taken a keen interest in disorders affecting the shoulder. As a result of this scrutiny, several distinct clinical entities have been brought to light. Comprehension of the pathogenesis of these lesions is responsible for the effective methods of treatment involved. An intelligent approach to any shoulder problem necessitates an understanding of the functional anatomy of the shoulder joint and an appreciation of what constitutes a normal shoulder in each successive decade. FunCtional Mechanism of Shoulder Joint It is generally conceded that the shoulder joint is not adequately adapted from a functional viewpoint to meet the functional demands made upon it by a prehensile extremity. This is reflected in the extensive degenerative alterations that occur in each successive decade in the biceps tendon, the ligaments and rotator cuff, and in the articular surfaces of the humeral head and glenoid cavity. In a previous publication4 • 5 the author described these alterations in detail; they make their appearance as early as the second decade. Also, it was recorded that many of these degenerative abnormalities are compatible with normal function. A study of the role of the biceps tendon in shoulder disorders reveals that this structure functions at a great mechanical disadvantage. This is the result of certain morphologic changes that have occurred in the scapula and humerus. These factors render this tendon vulnerable to repeated trauma during normal joint function. Moreover, critical analysis of sevFrom the Department of Orthopedic Surgery, Jefferson Medical College Hospital, Philadelphia.
* James Edwards Professor of Orthopedic Surgery, and Head of Department, Jefferson Medical College; Attending Orthopedic Surgeon, Jefferson Medical College Hospital and Methodist Episcopal Hospital,' Rotating Orthopedic Surgeon, Philadalphia General Hospital. 1761
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eral hundred cases of painful shoulders leads the author to believe that implication of the biceps tendon is the most common cause of a painful stiff shoulder. This concept has met with great resistance; however, it is pleasing to record that more and more observers are becoming aware of the entity, bicipital tenosynovitis; In 1896 Duplay 6 coined the term "scapulohumeral periarthritis." He was of the opinion that inflammation of the subacromial bursa was the responsible pathologic lesion for pain and limitation of motion in the scapulohumeral joint. Soon this designation came to embrace a large and heterogeneous group of cases whose only common denominators were pain and stiffness in the region of the shoulder joint. Later, the term "subacromial bursitis" became even more popular and is still in common use today. In contradiction to this premise, the author is of the opinion that primary subacromial bursitis per se does not exist, but that, when this structure is implicated, it is a sequel of some other lesion, especially calcareous tendinitis . .. The lesions most frequently responsible for pain and stiff shoulders are oicipital tenosynovitis, calcareous tendinitis, frozen shoulder and partial or complete rupture of the rotator cuff. Each of these clinical entities is characterized by distinctive clinical features which are readily demonst'rable and, if recognized, facilitate a correct diagnosis. BICIPITAL TENOSYNOVITIS
Many workers have regarded implication of the long head of the biceps tendon .as a possible cause of shoulder disorders. Notable among them are Meyer, Pasteur, Schrager, Lippmann, Hitchcock and Bechtol, and the author. In spite of the comprehensive articles that have appeared in the literature, many physicians, particularly those not specializing in orthopedic surgery, are not aware of its clinical manifestations. It is the author's opinion that this lesion IS, by far, one of the most common causes of shoulder dysfunction and that it is the most frequent lesion parading under the erroneous diagnosis of subacromial bursitis. In addition, when it occurs in patients over forty years of age, it may initiate pathologic processes in the soft tissues of the shoulder joint which terminate in frozen shoulder. This phase of the disorder will be discussed subsequently. l'athogenesis
Essentially, bicipital tenosynovitis comprises an inflammatory process involving the synovial sheath of the tendon (Fig. 553). Gross examination of the tendon-tendon sheath gliding mechanism reveals varying degrees of thickening and edema of the tendon sheaths; also the sheaths are invariably injected. Numerous veil-like, red filmy adhesions are demonstrable between the tendon and the tendon sheath and the roof and floor of the bicipital groove. Frequently, and especially in old cases, the process extends into the joint cavity, involving the distal end of the • intracapsular portion of the biceps tendon and the adjacent surface of the capsul~. The severity of the process parallels the duration of the disease and, as a rule, is more intense in the older age group in which de-
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generative changes are more advanced. In advanced cases the biceps tendon is firmly anchored to the floor of the groove by stout adhesions, and the tendon-tendon sheath gliding mechanism may be no longer discernible. Clinical Features
This clinical entity is encountered in both the young and older age groups. In most instances the onset is insidious; in a smaller number of cases the disorder is initiated by an injury or dislocation or fracture of
Fig. 553. Microphotograph of a specimen obtained from a case with bicipital tenosynovitis. Note the extensive inflammatory process implicating the tendinous fibers and the synovial sheath.
the humerus, or by simple overexertion. In the former group one must assume that physiologic use of the shoulder produces frictional stresses between the biceps tendon and its sheath, and the floor of the bicipital groove. The intensity of these stresses is accentuated by the mechanical disadvantages at which the tendon functions in the groove. With the formation of adhesions in the gliding mechanism, a mechanical barrier is produced which tends to impede the normal arcs of excursion. of the humeral head on the biceps tendon. This explains the phenomenon of intense pain experienced by the patient when the arm is carried through those movements which require a greater excursion of the head of the humerus on the tendon. Severe trauma or repeated minor traumas may precipitate the same clinical syndrome. The author has observed a number of young athletes mild subluxation of the biceps tendon which
in
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was responsible for the disorder (one patient was a baseball pitcher and another a tennis player). In the mild forms the first clinical manifestation may be some discomfort in the outer and lateral aspects of the arm and twinges of pain at the limits of the normal arcs of motion. Not infrequently the pain is projected to the anterolateral aspect of the arm and to the insertion of the deltoid muscle. Pain is accentuated by activity and relieved by rest. Increased pain at night is a common complaint. The arcs of abduction and external rotation and backward flexion and external rotation may be decreased. The most significant physical finding is tenderness revealed on pressure over the bicipital groove and on rolling the tendon of the long head of the biceps muscle under the examiner's thumb. Roentgenographic examination fails to provide any significant information except in cases of fracture of the upper end of the humerus which involves the bicipital groove, or in rare instances in which bony excrescences or spurs may be demonstrable in the floor of the groove. The clinical course of the illness is unpredictable; it may remain in a static state, neither progressing nor retrogressing for many months; on the other hand, it may disappear completely for varying periods of time, only to reappear again. In one patient the duration of symptoms was eleven years. It is interesting to note that in patients over the age of forty years, bicipital tenosynovitis may be the initiating factor responsible for frozen shoulder, which is a common sequel in patients in this age group. This is in contradistinction to patients under thirty years in whom this disabling complication never develops. The presence of degenerative alterations in the biceps tendon and rotator cuff in the older age group with bicipital tenosynovitis is a factor essential to the development of pathologic processes which terminate in frozen shoulders. The frequency of this clinical entity and the unfavorable complications that may occur in patients past the third decade of life make it imperative that the disorder be recognized readily by all physicians. Although treatment of shoulder lesions is not within the scope of this presentation, it is not amiss to point out at this time that the great majority of these cases respond to simple conservative measures. In those that do not, the syndrome can be eradicated only by obliteration of the tendon-tendon sheath gliding mechanism. This is achieved by transplantation of the tendon to the coracoid process or to the shaft of the humerus. The author prefers the former procedure. CALCAREOUS TENDINITIS
This clinical entity, like bicipital tenosynovitis, is responsible for pain and stiffness in the shoulder in a high percentage of the cases; it is even more common than bicipital tenosynovitis. In most instances the diagnosis is made readily because the calcareous deposits are demonstrable in roentgenograms. Its pathogenesis, however, is still not clear in the minds of many workers. For this reason the disorder is often erroneously interpreted as "subdeltoid" or "subacromial bursitis with calcification" or "calcified deposits in the supraspinatus tendon."
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Pathogenesis
In a previous investigation4 • 6 it was reported that degenerative changes occur early in the rotator cuff. These alterations increase progressively from decade to decade; they comprise shredding and tearing of the tendon fibers. During normal function of the shoulder girdle, the greatest strain is in the region of the supraspinatus tendon; hence degenerative lesions are encountered more frequently in this area than elsewhere in the cuff. It is generally conceded that these degenerative abnormalities are essential before calcareous, material is deposited in the affected area. The process begins with degeneration of the central tendon fibers, usually just proximal to the insertion of the tendons of the musculotendinous cuff (rotator cuff, comprising the supraspinatus, infraspinatus, teres minor and subscapularis tendons). There is still considerable controversy relative to the actual mechanism of calcium deposition in degenerated tissue. According to Howland and Wells, calcium and inorganic phosphorus are held in solution in the blood serum in much higher concentration than would be possible in water because of the high carbon dioxide tension and colloids in the blood serum. Cellular activity tends to maintain a high carbon dioxide tension and prevents precipitation of salts from intercellular fluids. In the presence of dead or degenerated tissue, carbon dioxide tension is lowered (producing a relative state of alkalinity). This favors precipitation of calcium carbonate or calcium phosphate, or both, in a molecular combination. This is a local physiochemical proceSs. Calcareous deposits are most frequently encountered in the supraspinatus portion of the cuff, but they may occur in the tendons of other rotator muscles. The size of the deposit varies from a few millimeters to 5 or 6 cm. They may be discrete, localized lesions deep within the substance of the affected tendons, or they may be in a tluid or semifluid state composed of calcareous material and serum, and lying in close proximity tq the floor of the subacromial bursa. Varying degrees of inflammation may surround the latter group of lesions. In the more acute form the deposit may actually break through the floor of the bursa ll:nd escape into the bursal sac. In the light of these observations, it becomes obvious that implication of the subacromial bursa is a secondary and not a primary feature. Furthermore, this has the following important clinical significance: Rapid and severe distention of the floor of the bursa by an underlying calcareous deposit is responsible for the intense pain experienced by the patients. However, as soon as the deposit ruptures into the bursa, all tension is relieved and the pain is reduced in severity or even disappears. Clinical Features
The lesion may occur in one or multiple areas of the cuff, the supraspinatus tendon being the most frequently involved region (Fig. 554). It affects males more commonly than females and generally occurs in the fourth and fifth decades; the average age is forty-five years. It is primarily a disease of persons employed in occupations; often sedentary;
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involving the use of the arms in slight abduction for hours at a time. Clerks, typists and surgeons may be victims. Excessive use of the arm which inflicts undue strain on the cuff may be considered a form of trauma, and the cumulative effect may be responsible for the degenerative changes in the involved tissues. Infection has never been proved to be an etiologic factor. Pain, muscle spasm, restriction of motion, and muscle atrophy are the pertinent clinical features of calcareous tendinitis. These symptoms differ greatly in intensity and severity. It must be emphasized at this point
Fig. 554. Note the dense, discrete calcareous mass in the supraspinatus region of the cuff. This lesion gave rise only to mechanical impingement of the cuff against the acromion upon elevation of the arlll .
that deeply seated, discrete lesions may give rise to no symptoms and are often uncovered accidentally by roentgenograms. Occasionally this type of lesion may cause a "catch" or slight twinge of pain on internal rotation or elevation of the arm. The symptom is the result of mechanical impingement Of the calcareous mass against the coracoacromial arch. Such a syndrome may persist for years without much apparent disability. At any time, however (especially if the factor of trauma or excessive use is added), the lesions may pursue a more acute course. Most cases of calcareous tendinitis pursue a subacute course. The onset is insidious, characterized by a twinge of pain when the arm is brought to the elevated position. Gradually the pain becomes more severe and the patient instinctively avoids motions which produce pain, using the arm only i~ ~he. painless arcs. Such a syndrome may remain static for many
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months, and then it may disappear. On the other hand, pain may become excruciating at the level of impingement, and it may be proje('ted to the insertion of the deltoid muscle, the inferior angle of the scapula or to the suboccipital region. In severe forms the pain may be referred to the forearm and fingers, particularly the thumb and index finger. Generally, the pain is more severe at night; the patient has great difficulty in finding a comfortable position for the arm; he is unable to lie on the affected side. Pressure over the greater tuberosity of the humerus
Fig. 555. Large defect in the rotator cuff implicating the supraspinatus and infraspinatus regions. This specimen was obtained from a patient who exhibited no shoulder dysfunction, making it apparent that such lesions do not preclude strong abduction of the arm. (Modified from Anthony F.PePalma, M.D.: Surgery of the Shoulder. Philadelphia, J. B. Lippincott.)
elicits pronounced tenderness; at times pain is produced when pressure is made over the deltoid tubercle. Occasionally a small tender· mass which rotates with the humerus can be palpated over the greater tuberos~ ity. In long-standing cases, atrophy of the spinatus muscle is discernible, also varying degrees of loss of scapulohumeral motion. The latter finding may be so severe that the patient now presents a typical clinical picture of a frozen shoulder. A subacute or chronic lesion may give rise, without warning, to an acute syndrome. The acute syndrome runs a relatively short fulminating course. As a rule, the onset is sudden, at times following overuse of the arm. In some instances there may be no clinical evidence of any pathologic dis-
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order in the shoulder region. The cardinal clinical features are sudden, intense pain on any attempts at motion, with localized tenderness and severe spasm of the rotator muscles. Pain is most severe at night; it is projected to the insertion of the deltoid muscle and even to the fingers; it fails to respond to the usual sedatives. In untreated cases the symptoms may persist for a week or two, and then subside. Spasm becomes less, and restoration of function is achieved gradually. The cause of alleviation of pain is rupture of the calcareous mass into the subacromial bursa, thereby relieving all tension on the sensitive bursal floor. It becomes apparent that the goal in the treatment of all acute lesions is to relieve tension; this may be attained by surgical intervention or needling of the calcareous mass; irradiation has no place in the treatment of this disorder. FROZEN SHOULDER
This entity, although its pathogenesis is controversial, exhibits certain distinctive clinical features. The disorder primarily is characterized by a gradual loss of scapulohumeral motion. It occurs in persons after forty years of age, the greatest number between fifty ~and sixty years. Any factor which restricts normal glenohumeral motion may initiate the syndrome. The common precipitating factor (and one. which is not generally recognized) is bicipital tenosynovitis. It .was:definitely shown in a previous publicationS that in the presence of degenerative changes in the cuff, restriction of scapulohumeral motion, regardless of the cause, initiates a diffuse inflammatory process implicating all the soft tissue elements of the joint. The biceps tendon and its sheath are invariably involved in the process. It has also been demonstrated that the bicipital involvement is responsible for the pain in this disorder. Hence bicipital tenosynovitis may be a primary feature of the disease or a secondary manifestation. It becomes apparent that correct management of this disorder must take into consideration eradication of the agent responsible for loss of scapulohumeral motion and deletion of the pain factor which is due to the associated bicipital tenosynovitis. ACUTE INJURIES OF THE SHOULDER JOINT
Severe acute injuries of the shoulder joint are characterized by severe pain in the anterior and lateral aspects of the shoulder, muscle spasm and marked limitation of motion. It is the author's opinion that during the acute stage it is impossible to ascertain by any clinical methods whether or not the patient has a complete tear of the rotator cuff of sufficient degree to interfere with abduction of the arm. Loss of abduction in these cases may be the result of pain and muscle spasm, or of pain, muscle spasm and a torn cuff. The author has shown on many occasions by exploration of the shoulder joint that minor or even moderate cuff tears do not preclude powerful and complete elevation of the arm; This also has been demonstrated on cadaver specimens which disclosed varying
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degrees of cuff tears, but the subjects from whom these specimens were removed were unaware of any disability in the shoulder girdle prior to death. On the other hand, it has also been demonstrated that severe cuff tears which interrupt the stabilizing mechanism of the humeral head in the glenoid cavity during abduction result in weak abduction or no abduction of the arm. However, this distinctive feature cannot be determined in acute stages until sufficient time has elapsed. In the presence of minor or moderate tears of the cuff, abduction in the shoulder will be initiated after the acute symptoms subside (ten days to two weeks), and within a period of six to eight weeks restoration of function approaching normality is achieved. This is in contradiction to ·severely torn cuffs with a disrupted stabilizing rotator mechanism which, after all acute symptoms have subsided and a period of at least four to six weeks has elapsed, exhibit weak or no abduction of the arm. It becomes apparent that accurate diagnosis can be made only after sufficient time has elapsed and after it becomes obvious that in spite of the recession of all acute symptoms, the patient fails to attain strong and powerful abduction of the arm. LESIONS OF THE KNEE JOINT
Lack of comprehension and appreciation of the delicate, intrinsic functional mechanism of the knee joint is responsible for many erroneous diagnoses and mismanagement of some of the more common affections of this articulation, particularly those resulting from trauma. On the other hand, adequate understanding of the mechanical features of the knee joint not, only facilitates early recognition of the causative agents producing the disorder, but also allows intelligent institution of a plan of treatment based on sound mechanical principles. Such management will reduce the incidence of unfavorable sequelae which result in protracted and, in many instances, permanent dysfunction of the joint. Functional Mechanism of the Knee Joint
The knee joint is the largest articuiation in the human skeletal system; also, it is the most superficial and the most vulnerable. Nature has endowed this articulation with distinctive anatomic features which adapt it to meet the varied static and dynamic functional demands made upon it by man. To meet the constantly changing stresses on the joint during weight bearing, and to fulfill adequately the mechanism of propulsion of the body in locomotion, the articulating bones comprising the joint are unusually massive, and yet their configuration is such that free and easy motion is executed. The joint is situated at the ends of the longest bones in the body, predisposing it to great stresses in all planes; these stresses are neutralized by a network of stout ligamentous supports. Finally, and most important, the requisites of the acts of balance and propulsion have been responsible for the evolvement of-'a muscular apparatus motorizing this articulation, which is'"'powerfuf{on the one hand and, on the other, complicated and delicate. This intricate muscu-
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lar development allows both coarse and refined movements at the knee joint in the sagittal plane and in a rotary direction. The quadriceps group, comprising the rectus femoris and the three vasti muscles, is the most important component of the muscular apparatus of the knee joint. Analysis of the role the quadriceps assumes in the stability of the knee brings forcefully to light the importance of this muscle mass in the maintenance of the erect posture in man. This is achieved by the ability to produce powerful extension of the knee, to stabilize the joint and to maintain its equilibrium. In addition, it counterbalances the action of the flexor muscles, gravity and body weight. Its mechanical efficiency is enhanced by the presence of the patella (a fact which is being disregarded by many surgeons, as is evidenced by the number of patellectomies performed for varied reasons). The patella increases the strength of the quadriceps by improving leverage. These functional demands made on the quadriceps explain its great muscle volume and great force of action. Under normal conditions this muscle has considerable reserve force which is readily demonstrated when one stands on one extremity; the muscle will shorten and become tense. At this point, the part played by the extensors as stabilizers of the knee joint must be re-emphasized. Loss of volume and power of contractionof the quadriceps reduces its stabilizing influence and predisposes the ligamentous apparatus and the synovial lining of the joint to repeated trauma. This in turn, if not controlled adequately, initiates a sequence of events characterized by progressive weakness of the quadriceps, repeated episodes of effusion into the knee joint, permanent thickening and hypertrophy of the synovialis and, finally, osteoarthritis of the knee joint. The ability to extend fully the knee and to stabilize the joint in varying positions of flexion to complete extension are late acquisitions in the functional evolution of the quadriceps. This is substantiated by the clinical observation that the intrinsic quadriceps mechanism, being unstable, is readily unbalanced by even trivial injuries which interfere with normal joint function. This disorder is reflected in the loss of muscle volume, diminished power of contraction and disorientation of the muscle mass. Varying degrees of severity are encountered; the more severe derangements present features not unlike those of flaccid paralysis. Of the four components of the quadriceps group, the vastus internus (medialis) exhibits the most profound alterations. Since this muscle is concerned primarily with balancing movements, especially in varying degrees of flexion of the knee joint, any insufficiency of the quadriceps is characterized by "giving way" of the knee when in different phases of flexion. QUADRICEPS INSUFFICIENCY
As previously recorded, this is a clinical manifestation of the quadriceps apparatus comprising three elements: loss of muscle volume (atrophy), diminished power of contraction, and disorientation of the muscle mass. This manifestation in varying degrees is a concomittant
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finding of all affections implicating the knee joint. In traumatic lesions the more obvious derangements may obscure this condition, so that it progresses in intensity unnoticed until the patient attempts to use the extremity. It then becomes apparent that in spite of adequate repair of the injured structures, the patient is unable to use the extremity without "giving way" of the knee joint. The abnormal stresses placed on the ligaments and capsule are followed by an effusion into the joint which tends to increase the laxity of the ligamentous apparatus. In order to allow the effusion to be absorbed, the limb is put to rest; this in turn results in a further decrease in the volume and power of contraction of the muscle. Once such a cycle is established, every effort must be expended to interrupt it. This can be done only by nonweight-bearing active exercises, progressively increasing in intensity until sufficient volume, tone and control have been restored in the quadriceps muscle to prevent aggravation of an existing injury and to protect the joint from new traumas. Failure to overcome quadriceps insufficiency may result in permanent dysfunction of the knee joint. A case in point is the following history. CASE REPORT. E. F., a man 52 years of age, struck the anterior aspect of the knee again!'t an opened door. The next day the knee was swollen and painful, and the patient sought medical aid. The attending physician ordered the patient to bed and applied ice bags to the knee. After 10 days the swelling had disappeared and the patient was allowed to bear weight on the affected limb. About one month later he was seen in the out-patient department; his chief complaints were "buckling of the knee" and constant swelling. Examination of the extremity at this time disclosed marked atrophy and poor power of contraction of the quadriceps muscle. In addition, a moderate effusion was demonstrable in the knee joint. Roentgenographic examination failed to reveal any evidence of bone pathology (Fig. 556, a). A diagnosis of quadriceps insufficiency was made, and admission to the hospital was advised. It was hoped that under a closely supervised regimen of exercises the affected quadriceps would be restored to sufficient power to stabilize the knee and protect it from further injury. He refused admission. The patient was again seen in the out-patient department eight months later. During the interval between the first and second visits he was treated I;>y numerous physkians, one of whom made a diagnosis of a torn internal meniscus and recommended its removal; the patient had been subjected to this surgical procedure. However, he was not relieved of the pain, swelling and instability of the knee joint which had become progressively worse. Examination at this time revealed a boggy, swollen knee with advanced thickening of the capsular tissues. The quadriceps muscle mass was barely perceptible when the patient attempted to contract the muscle; atrophy of the muscle was profound. Roentgenogrltphic examination disclosed advanced osteoarthritic changes comprising thinning of the joint spaces and marked marginal lipping of the femoral and tibial articular surfaces (Fig. 556, b). These changes were not present in the roentgenograms taken at the first examination. It became apparent the the condition had progressed to an irreversible point, and radical measures were indicated. It was decided to perform a synovectomy, provided the patient would first cooperate in restoring some power and volume to the quadriceps before operation was undertaken. To this he promised, but he refused to put any real effort in the program outlined for him. After six weeks
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it became apparent that our efforts were in vain, the patient being most uncooperative. An arthrodesis of the knee was then performed. At operation it was interesting to note the advanced degenerative alterations that had occurred within a
Fig. 556. a, Radiograms of patient E. F. taken at the first admission to the outpatient department. Note the absence of any degenerative changes in the knee joint. b, Radiograms of the same knee taken approximately eight months after roentgenograms shown in a. Note the severe degenerative changes that have taken place, particularly in the medial joint compartment and the articular surface of the patella. This is an excellent demonstration of the secondary changes that may occur following chronic synovitis of the knee joint resulting from quadriceps insufficiency. period of less than one year. The synovialis was thickened and studded with numerous villus formations. The articular surface of the femur exhibited areas of erosion and chondromalacia; the same findings, but of less severity, were noted in the articular surfaces of the tibia.
1
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This case illustrates emphatically the pitfalls that may be encountered after a simple contusion of the knee joint. I am certain that all the unfortunate sequelae noted in this instance could have been prevented if the presence of quadriceps insufficiency had been recognized and treated correctly at the time of the initial injury. SWELLING OF THE KNEE JOINT FOLLOWING INJURY
This clinical manifestation is frequently encountered after direct or indirect injuries to the knee joint. Swelling is not a clinical entity; it is a concomitant feature of injury to the elements of the articulation. In general, two varieties occur: traumatic synovial effusion and hemarthrosis. Traumatic Synovial Effusion
Although it is common knowledge that all acute injuries of the knee joint are followed by a synovial effusion, many physicians are content to make a diagnosis of traumatic synovitis without attempting to uncover the more serious associated lesions. It cannot be emphasized too strongly that effusion resulting from traumatic synovitis without the presence of other pathology is indeed a rare clinical entity. On the other hand, as noted before, all acute injuries of the knee are invariably accompanied by an effusion. The clinical features of an effusion distinguish it from hemarthrosis. The importance of arriving at a correct diagnosis is essential in order to institute correct treatment. As a rule, synovial effusions per se are demonstrable after a relatively long period of time, usually six to eight hours after the injury. This differs .from a hemarthrosis, in which the swelling appears shortly after the injury, within one half to one hour. It becomes apparent that if hemorrhage and effusion occur concurrently, the interval is greatly shortened. A constant and pertinent symptom in effusion is the absence of intense pain. The patient is aware of a sense of fullness in the knee, and distention will elicit varying degrees of discom~ fort, but not acute pain. In massive effusions the knee is maintained in a position 'of slight flexion, the outlines of the suprapatellar pouch encircling the periphery of the patella are discernible, and palpation discloses ballottement of the patella. Also gentle palpation (with the fingers of both hands placed on the medial and lateral surfaces of the knee on a level with the center of the patella) reveals that the tissues are stretched but not boggy, nor do they convey the sense of resistance and tumefaction so characteristic of a massive hemarthrosis. It becomes apparent that in the advent of a synovial effusion, the prime concern of the physician is to determine first the presence or absence of other lesions such as a torn meniscus. If such a lesion is demonstrable, the choice of treatment must take into consideration the injury as a whole and must 'not be directed solely to the management of the effusion. Failure to adhere to this precaution will result in delay of adequate management for traumatic lesions which, if not promptly recognized and treated correctly, may give rise to unfavorable sequelae resulting in permanent dysfunction of the knee joint.
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The accumulation of blood in the articular cavity of the knee joint is always indicative of injury to some other structure or structures. Realization of this fact should always incite further investigation of the injury when the presence of a hemarthrosis is established. As Smillie12 pointed out, there are two varieties of hemarthrosis: one in which there is little or no tendency for the blood to coagulate, and the other in which coagulation of blood is a prominent feature. This variation depends upon the amount of synovial effusion found in association with the blood. It is generally known that synovial fluid has anticoagulant properties. If it is present in sufficient quantities, the blood remains fluid; if it is overwhelmed by a large volume of blood, coagulation is not precluded. It is interesting to note that the conditions in which the blood fails to coagulate are usually of minor severity and have a favorable outlook. They include tears of the synovial lining associated with sprains of the collateral ligaments, varying degrees of tears of the anterior cruciate ligament, or fractures of the tibial spine. Massive hemorrhage with coagulation of blood is usually encountered in severe injuries to the quadriceps apparatus as fracture of the patella, complete tears of the quadriceps tendon or patellar tendon and complete tears of the collateral ligaments. A massive hemarthrosis is seldom a concomitant feature of a torn meniscus except in rare instances when t1;le meniscus is torn from its peripheral attachment. In the light of these observations, it ,becomes obvious that correct evaluation of the type of hemarthrosis present in a given case provides a clue to:the seriousness and the prognosis of the injury. As in traumatic effusion, correct and prompt management of the etiologic factors responsible for the hemorrhage prevents unfavorable complications and decreases the degree of permanent impairment of function in many cases. THE "BUCKLING KNEE"
This complaint is associated with severe forms of disorders of the knee joint. Notable among these are tears of the posterior portion of the meniscus, quadriceps insufficiency and rupture of the anterior cruciate ligament. It becomes apparent that an accurate diagnosis can be made only by a careful examination of the part and consideration of the most likely' etiologic factors. Tears of the Posterior Segment of the Internal Meniscus
It is erroneous to believe that locking of a knee joint is the most important symptom of tears of the internal meniscus. This clinical feature OC,curs orily when the longitudinal tear implicates the anterior segment of the meniscus. More important, but less recognized, is the sense of insecurity of, the joint when the patient walks on uneven ground, or "buckling" when certain unguarded movements are performed as'turning suddenly or stepping off a curb. Moreover, the patient often offers the -information, that he feels a "click" in the joint as if some loose body were
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moving about the joint. These features are characteristic of a tear of the posterior segment of the meniscus (Fig. 557). As a rule the lesion isa longitudinal tear, but it may be shredding, with maceration of the posterior segment without a complete longitudinal split. In addition, firm pressure over the inner joint line immediately behind the collateral liganient invariably elicits exquisite tenderness.
Fig. 557. a, Tear of posterior portion of internal meniscus, giving rise to a sense of instability and buckling of the knee joint, but no locking. b, Extensive longitudinal tear extending into the anterior portion of the meniscus. This type of lesion causes locking of the joint.
Quadriceps Insufficiency
Although quadriceps insufficiency is a concomitant feature of all disorders of the knee joint, on occasion it is encountered singly following a period of functional inactivity unrelated to the knee joint or following such minor injuries as sprains and contusions of the joint. Loss of volume and tone of the quadriceps mass, especially the vastus medialis, may be so profound and rapid that severe dysfunction results. The clinical features of this disorder have been discussed previously~ I wish to emphasize at this point that "buckling" or "giving way" of the knee is a constant feature of quadriceps insufficiency which may be the only remaining clinical manifestation of some previous disorder. It becomes obvious that all other causative agents which may be responsible for
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the symptom and which may be still active must be eliminated before quadriceps insufficiency per se is credited for the disability. Rupture of the Anterior Cruciate Ligament
It is essential to be cognizant of the observation that not all patients with rupture of the anterior cruciate ligament complain of "giving way" or "buckling" of the knee joint. This is explained by the knowledge that a strong quadriceps muscle and intact collateral ligaments are capable of compensating sufficiently for the torn ligament so that no dysfunction ensues. In the presence, however, of quadriceps insufficiency and laxity of the collateral ligaments, chiefly the tibial collateral ligament, this symptom may be a pertinent and disabling manifestation. In such cases clinical examination reveals varying degrees of quadriceps atrophy and a positive drawer sign (abnormal forward displacement of the tibia on the fixed femur). Occasionally this sign may be actively produced by the patient by contraction of the gastrocnemius muscle.
SUMMARY In this brief presentation the more common lesions of the shoulder and knee joint have been discussed and the pertinent distinctive features of each entity have been considered so that an accurate diagnosis can be made. The necessity of an accurate diagnosis is essential in order that correct and adequate management may be instituted.
REFERENCES 1. Codman, E. A.: The Shoulder. Boston, Thomas Todd, 1934. 2. DePalma, A. F.: Surgery of the Shoulder. Philadephia, J. B. Lippincott Company, 1950. 3. DePalma, A. F.: Loss of Scapulohumeral Motion (Frozen Shoulder). Ann. Surg., February 1952. 4.DePalma, A. F., Callery, G. E., and Bennett, G. A.: Variational Anatomy and Degenerative Lesions of the Shoulder Joint. Am. Acad. Orthopedic Surgeons Instructional Course Lectures, 1949. 5. DePalma, A. F., White, J. B., and Callery, G. E.: Degenerative Lesions of the Shoulder Joint at Various Age Groups Which Are Compatible with Good Function. Am. Acad. Orthopedic Surgeons Instructional Course Lectures, 1950. 6. Duplay, S.: De la periarthrite scapulo-humerale. Rev. frat. d. trav. de med., 53: 226, 1896 (Tr. M. Week, 4: 253, 1896; M. Press, 59: 571-573, 1900). 7. Hitchcock, H. H., and Bechtol, C. 0.: Painful Shoulder; Observations of the Role of the Tendon of the Long Head of the Biceps Brachii in Its Causation. J. Bone & Joint Surg., 30-A: 263, 1948. 8. Hueter, C.: Arch. f. klin. chir., 5: 321-323, 1864. 9. Lippmann, R. K.: Frozen Shoulder; Periarthritis and Bicipital Tenosynovitis. Arch. Surg., 47: 283-296, 1943. 10. Pasteur, F.: La teno-bursite bicepitale. J. de radiol. et d'electrol., 16: 419426, 1932. 11. Schrager, V. L.: Tenosynovitis of the Long Head of the Biceps Humeri. Surg., Gynec. & Obst., 66: 785-790,1938. 12. Smillie, I. S.: Injuries of the Knee Joint. Baltimore, Williams & Wilkins Company, 1951.
LESIONS OF THE SHOULDER
ALTHOUGH one must admit that all causative factors of a "painful-stiff" shoulder have not been uncovered, considerable progress has been made in this direction within the past two decades. Since the masterful work of Codmanl on lesions of the musculotendinous cuff published in 1934, many observers have taken a keen interest in disorders affecting the shoulder. As a result of this scrutiny, several distinct clinical entities have been brought to light. Comprehension of the pathogenesis of these lesions is responsible for the effective methods of treatment involved. An intelligent approach to any shoulder problem necessitates an understanding of the functional anatomy of the shoulder joint and an appreciation of what constitutes a normal shoulder in each successive decade. FunCtional Mechanism of Shoulder Joint It is generally conceded that the shoulder joint is not adequately adapted from a functional viewpoint to meet the functional demands made upon it by a prehensile extremity. This is reflected in the extensive degenerative alterations that occur in each successive decade in the biceps tendon, the ligaments and rotator cuff, and in the articular surfaces of the humeral head and glenoid cavity. In a previous publication4 • 5 the author described these alterations in detail; they make their appearance as early as the second decade. Also, it was recorded that many of these degenerative abnormalities are compatible with normal function. A study of the role of the biceps tendon in shoulder disorders reveals that this structure functions at a great mechanical disadvantage. This is the result of certain morphologic changes that have occurred in the scapula and humerus. These factors render this tendon vulnerable to repeated trauma during normal joint function. Moreover, critical analysis of sevFrom the Department of Orthopedic Surgery, Jefferson Medical College Hospital, Philadelphia.
* James Edwards Professor of Orthopedic Surgery, and Head of Department, Jefferson Medical College; Attending Orthopedic Surgeon, Jefferson Medical College Hospital and Methodist Episcopal Hospital,' Rotating Orthopedic Surgeon, Philadalphia General Hospital. 1761
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Anthony F. DePalma
eral hundred cases of painful shoulders leads the author to believe that implication of the biceps tendon is the most common cause of a painful stiff shoulder. This concept has met with great resistance; however, it is pleasing to record that more and more observers are becoming aware of the entity, bicipital tenosynovitis; In 1896 Duplay 6 coined the term "scapulohumeral periarthritis." He was of the opinion that inflammation of the subacromial bursa was the responsible pathologic lesion for pain and limitation of motion in the scapulohumeral joint. Soon this designation came to embrace a large and heterogeneous group of cases whose only common denominators were pain and stiffness in the region of the shoulder joint. Later, the term "subacromial bursitis" became even more popular and is still in common use today. In contradiction to this premise, the author is of the opinion that primary subacromial bursitis per se does not exist, but that, when this structure is implicated, it is a sequel of some other lesion, especially calcareous tendinitis . .. The lesions most frequently responsible for pain and stiff shoulders are oicipital tenosynovitis, calcareous tendinitis, frozen shoulder and partial or complete rupture of the rotator cuff. Each of these clinical entities is characterized by distinctive clinical features which are readily demonst'rable and, if recognized, facilitate a correct diagnosis. BICIPITAL TENOSYNOVITIS
Many workers have regarded implication of the long head of the biceps tendon .as a possible cause of shoulder disorders. Notable among them are Meyer, Pasteur, Schrager, Lippmann, Hitchcock and Bechtol, and the author. In spite of the comprehensive articles that have appeared in the literature, many physicians, particularly those not specializing in orthopedic surgery, are not aware of its clinical manifestations. It is the author's opinion that this lesion IS, by far, one of the most common causes of shoulder dysfunction and that it is the most frequent lesion parading under the erroneous diagnosis of subacromial bursitis. In addition, when it occurs in patients over forty years of age, it may initiate pathologic processes in the soft tissues of the shoulder joint which terminate in frozen shoulder. This phase of the disorder will be discussed subsequently. l'athogenesis
Essentially, bicipital tenosynovitis comprises an inflammatory process involving the synovial sheath of the tendon (Fig. 553). Gross examination of the tendon-tendon sheath gliding mechanism reveals varying degrees of thickening and edema of the tendon sheaths; also the sheaths are invariably injected. Numerous veil-like, red filmy adhesions are demonstrable between the tendon and the tendon sheath and the roof and floor of the bicipital groove. Frequently, and especially in old cases, the process extends into the joint cavity, involving the distal end of the • intracapsular portion of the biceps tendon and the adjacent surface of the capsul~. The severity of the process parallels the duration of the disease and, as a rule, is more intense in the older age group in which de-
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generative changes are more advanced. In advanced cases the biceps tendon is firmly anchored to the floor of the groove by stout adhesions, and the tendon-tendon sheath gliding mechanism may be no longer discernible. Clinical Features
This clinical entity is encountered in both the young and older age groups. In most instances the onset is insidious; in a smaller number of cases the disorder is initiated by an injury or dislocation or fracture of
Fig. 553. Microphotograph of a specimen obtained from a case with bicipital tenosynovitis. Note the extensive inflammatory process implicating the tendinous fibers and the synovial sheath.
the humerus, or by simple overexertion. In the former group one must assume that physiologic use of the shoulder produces frictional stresses between the biceps tendon and its sheath, and the floor of the bicipital groove. The intensity of these stresses is accentuated by the mechanical disadvantages at which the tendon functions in the groove. With the formation of adhesions in the gliding mechanism, a mechanical barrier is produced which tends to impede the normal arcs of excursion. of the humeral head on the biceps tendon. This explains the phenomenon of intense pain experienced by the patient when the arm is carried through those movements which require a greater excursion of the head of the humerus on the tendon. Severe trauma or repeated minor traumas may precipitate the same clinical syndrome. The author has observed a number of young athletes mild subluxation of the biceps tendon which
in
Anthony F. DePalma
1764
was responsible for the disorder (one patient was a baseball pitcher and another a tennis player). In the mild forms the first clinical manifestation may be some discomfort in the outer and lateral aspects of the arm and twinges of pain at the limits of the normal arcs of motion. Not infrequently the pain is projected to the anterolateral aspect of the arm and to the insertion of the deltoid muscle. Pain is accentuated by activity and relieved by rest. Increased pain at night is a common complaint. The arcs of abduction and external rotation and backward flexion and external rotation may be decreased. The most significant physical finding is tenderness revealed on pressure over the bicipital groove and on rolling the tendon of the long head of the biceps muscle under the examiner's thumb. Roentgenographic examination fails to provide any significant information except in cases of fracture of the upper end of the humerus which involves the bicipital groove, or in rare instances in which bony excrescences or spurs may be demonstrable in the floor of the groove. The clinical course of the illness is unpredictable; it may remain in a static state, neither progressing nor retrogressing for many months; on the other hand, it may disappear completely for varying periods of time, only to reappear again. In one patient the duration of symptoms was eleven years. It is interesting to note that in patients over the age of forty years, bicipital tenosynovitis may be the initiating factor responsible for frozen shoulder, which is a common sequel in patients in this age group. This is in contradistinction to patients under thirty years in whom this disabling complication never develops. The presence of degenerative alterations in the biceps tendon and rotator cuff in the older age group with bicipital tenosynovitis is a factor essential to the development of pathologic processes which terminate in frozen shoulders. The frequency of this clinical entity and the unfavorable complications that may occur in patients past the third decade of life make it imperative that the disorder be recognized readily by all physicians. Although treatment of shoulder lesions is not within the scope of this presentation, it is not amiss to point out at this time that the great majority of these cases respond to simple conservative measures. In those that do not, the syndrome can be eradicated only by obliteration of the tendon-tendon sheath gliding mechanism. This is achieved by transplantation of the tendon to the coracoid process or to the shaft of the humerus. The author prefers the former procedure. CALCAREOUS TENDINITIS
This clinical entity, like bicipital tenosynovitis, is responsible for pain and stiffness in the shoulder in a high percentage of the cases; it is even more common than bicipital tenosynovitis. In most instances the diagnosis is made readily because the calcareous deposits are demonstrable in roentgenograms. Its pathogenesis, however, is still not clear in the minds of many workers. For this reason the disorder is often erroneously interpreted as "subdeltoid" or "subacromial bursitis with calcification" or "calcified deposits in the supraspinatus tendon."
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Pathogenesis
In a previous investigation4 • 6 it was reported that degenerative changes occur early in the rotator cuff. These alterations increase progressively from decade to decade; they comprise shredding and tearing of the tendon fibers. During normal function of the shoulder girdle, the greatest strain is in the region of the supraspinatus tendon; hence degenerative lesions are encountered more frequently in this area than elsewhere in the cuff. It is generally conceded that these degenerative abnormalities are essential before calcareous, material is deposited in the affected area. The process begins with degeneration of the central tendon fibers, usually just proximal to the insertion of the tendons of the musculotendinous cuff (rotator cuff, comprising the supraspinatus, infraspinatus, teres minor and subscapularis tendons). There is still considerable controversy relative to the actual mechanism of calcium deposition in degenerated tissue. According to Howland and Wells, calcium and inorganic phosphorus are held in solution in the blood serum in much higher concentration than would be possible in water because of the high carbon dioxide tension and colloids in the blood serum. Cellular activity tends to maintain a high carbon dioxide tension and prevents precipitation of salts from intercellular fluids. In the presence of dead or degenerated tissue, carbon dioxide tension is lowered (producing a relative state of alkalinity). This favors precipitation of calcium carbonate or calcium phosphate, or both, in a molecular combination. This is a local physiochemical proceSs. Calcareous deposits are most frequently encountered in the supraspinatus portion of the cuff, but they may occur in the tendons of other rotator muscles. The size of the deposit varies from a few millimeters to 5 or 6 cm. They may be discrete, localized lesions deep within the substance of the affected tendons, or they may be in a tluid or semifluid state composed of calcareous material and serum, and lying in close proximity tq the floor of the subacromial bursa. Varying degrees of inflammation may surround the latter group of lesions. In the more acute form the deposit may actually break through the floor of the bursa ll:nd escape into the bursal sac. In the light of these observations, it becomes obvious that implication of the subacromial bursa is a secondary and not a primary feature. Furthermore, this has the following important clinical significance: Rapid and severe distention of the floor of the bursa by an underlying calcareous deposit is responsible for the intense pain experienced by the patients. However, as soon as the deposit ruptures into the bursa, all tension is relieved and the pain is reduced in severity or even disappears. Clinical Features
The lesion may occur in one or multiple areas of the cuff, the supraspinatus tendon being the most frequently involved region (Fig. 554). It affects males more commonly than females and generally occurs in the fourth and fifth decades; the average age is forty-five years. It is primarily a disease of persons employed in occupations; often sedentary;
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Anthony F. DePalma
involving the use of the arms in slight abduction for hours at a time. Clerks, typists and surgeons may be victims. Excessive use of the arm which inflicts undue strain on the cuff may be considered a form of trauma, and the cumulative effect may be responsible for the degenerative changes in the involved tissues. Infection has never been proved to be an etiologic factor. Pain, muscle spasm, restriction of motion, and muscle atrophy are the pertinent clinical features of calcareous tendinitis. These symptoms differ greatly in intensity and severity. It must be emphasized at this point
Fig. 554. Note the dense, discrete calcareous mass in the supraspinatus region of the cuff. This lesion gave rise only to mechanical impingement of the cuff against the acromion upon elevation of the arlll .
that deeply seated, discrete lesions may give rise to no symptoms and are often uncovered accidentally by roentgenograms. Occasionally this type of lesion may cause a "catch" or slight twinge of pain on internal rotation or elevation of the arm. The symptom is the result of mechanical impingement Of the calcareous mass against the coracoacromial arch. Such a syndrome may persist for years without much apparent disability. At any time, however (especially if the factor of trauma or excessive use is added), the lesions may pursue a more acute course. Most cases of calcareous tendinitis pursue a subacute course. The onset is insidious, characterized by a twinge of pain when the arm is brought to the elevated position. Gradually the pain becomes more severe and the patient instinctively avoids motions which produce pain, using the arm only i~ ~he. painless arcs. Such a syndrome may remain static for many
T Lesions of Shoulder and Knee Joint
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months, and then it may disappear. On the other hand, pain may become excruciating at the level of impingement, and it may be proje('ted to the insertion of the deltoid muscle, the inferior angle of the scapula or to the suboccipital region. In severe forms the pain may be referred to the forearm and fingers, particularly the thumb and index finger. Generally, the pain is more severe at night; the patient has great difficulty in finding a comfortable position for the arm; he is unable to lie on the affected side. Pressure over the greater tuberosity of the humerus
Fig. 555. Large defect in the rotator cuff implicating the supraspinatus and infraspinatus regions. This specimen was obtained from a patient who exhibited no shoulder dysfunction, making it apparent that such lesions do not preclude strong abduction of the arm. (Modified from Anthony F.PePalma, M.D.: Surgery of the Shoulder. Philadelphia, J. B. Lippincott.)
elicits pronounced tenderness; at times pain is produced when pressure is made over the deltoid tubercle. Occasionally a small tender· mass which rotates with the humerus can be palpated over the greater tuberos~ ity. In long-standing cases, atrophy of the spinatus muscle is discernible, also varying degrees of loss of scapulohumeral motion. The latter finding may be so severe that the patient now presents a typical clinical picture of a frozen shoulder. A subacute or chronic lesion may give rise, without warning, to an acute syndrome. The acute syndrome runs a relatively short fulminating course. As a rule, the onset is sudden, at times following overuse of the arm. In some instances there may be no clinical evidence of any pathologic dis-
Anthony:F. DePalma
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order in the shoulder region. The cardinal clinical features are sudden, intense pain on any attempts at motion, with localized tenderness and severe spasm of the rotator muscles. Pain is most severe at night; it is projected to the insertion of the deltoid muscle and even to the fingers; it fails to respond to the usual sedatives. In untreated cases the symptoms may persist for a week or two, and then subside. Spasm becomes less, and restoration of function is achieved gradually. The cause of alleviation of pain is rupture of the calcareous mass into the subacromial bursa, thereby relieving all tension on the sensitive bursal floor. It becomes apparent that the goal in the treatment of all acute lesions is to relieve tension; this may be attained by surgical intervention or needling of the calcareous mass; irradiation has no place in the treatment of this disorder. FROZEN SHOULDER
This entity, although its pathogenesis is controversial, exhibits certain distinctive clinical features. The disorder primarily is characterized by a gradual loss of scapulohumeral motion. It occurs in persons after forty years of age, the greatest number between fifty ~and sixty years. Any factor which restricts normal glenohumeral motion may initiate the syndrome. The common precipitating factor (and one. which is not generally recognized) is bicipital tenosynovitis. It .was:definitely shown in a previous publicationS that in the presence of degenerative changes in the cuff, restriction of scapulohumeral motion, regardless of the cause, initiates a diffuse inflammatory process implicating all the soft tissue elements of the joint. The biceps tendon and its sheath are invariably involved in the process. It has also been demonstrated that the bicipital involvement is responsible for the pain in this disorder. Hence bicipital tenosynovitis may be a primary feature of the disease or a secondary manifestation. It becomes apparent that correct management of this disorder must take into consideration eradication of the agent responsible for loss of scapulohumeral motion and deletion of the pain factor which is due to the associated bicipital tenosynovitis. ACUTE INJURIES OF THE SHOULDER JOINT
Severe acute injuries of the shoulder joint are characterized by severe pain in the anterior and lateral aspects of the shoulder, muscle spasm and marked limitation of motion. It is the author's opinion that during the acute stage it is impossible to ascertain by any clinical methods whether or not the patient has a complete tear of the rotator cuff of sufficient degree to interfere with abduction of the arm. Loss of abduction in these cases may be the result of pain and muscle spasm, or of pain, muscle spasm and a torn cuff. The author has shown on many occasions by exploration of the shoulder joint that minor or even moderate cuff tears do not preclude powerful and complete elevation of the arm; This also has been demonstrated on cadaver specimens which disclosed varying
r Lesions of Shoulder and Knee Joint
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degrees of cuff tears, but the subjects from whom these specimens were removed were unaware of any disability in the shoulder girdle prior to death. On the other hand, it has also been demonstrated that severe cuff tears which interrupt the stabilizing mechanism of the humeral head in the glenoid cavity during abduction result in weak abduction or no abduction of the arm. However, this distinctive feature cannot be determined in acute stages until sufficient time has elapsed. In the presence of minor or moderate tears of the cuff, abduction in the shoulder will be initiated after the acute symptoms subside (ten days to two weeks), and within a period of six to eight weeks restoration of function approaching normality is achieved. This is in contradiction to ·severely torn cuffs with a disrupted stabilizing rotator mechanism which, after all acute symptoms have subsided and a period of at least four to six weeks has elapsed, exhibit weak or no abduction of the arm. It becomes apparent that accurate diagnosis can be made only after sufficient time has elapsed and after it becomes obvious that in spite of the recession of all acute symptoms, the patient fails to attain strong and powerful abduction of the arm. LESIONS OF THE KNEE JOINT
Lack of comprehension and appreciation of the delicate, intrinsic functional mechanism of the knee joint is responsible for many erroneous diagnoses and mismanagement of some of the more common affections of this articulation, particularly those resulting from trauma. On the other hand, adequate understanding of the mechanical features of the knee joint not, only facilitates early recognition of the causative agents producing the disorder, but also allows intelligent institution of a plan of treatment based on sound mechanical principles. Such management will reduce the incidence of unfavorable sequelae which result in protracted and, in many instances, permanent dysfunction of the joint. Functional Mechanism of the Knee Joint
The knee joint is the largest articuiation in the human skeletal system; also, it is the most superficial and the most vulnerable. Nature has endowed this articulation with distinctive anatomic features which adapt it to meet the varied static and dynamic functional demands made upon it by man. To meet the constantly changing stresses on the joint during weight bearing, and to fulfill adequately the mechanism of propulsion of the body in locomotion, the articulating bones comprising the joint are unusually massive, and yet their configuration is such that free and easy motion is executed. The joint is situated at the ends of the longest bones in the body, predisposing it to great stresses in all planes; these stresses are neutralized by a network of stout ligamentous supports. Finally, and most important, the requisites of the acts of balance and propulsion have been responsible for the evolvement of-'a muscular apparatus motorizing this articulation, which is'"'powerfuf{on the one hand and, on the other, complicated and delicate. This intricate muscu-
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Anthony F. DePalma
lar development allows both coarse and refined movements at the knee joint in the sagittal plane and in a rotary direction. The quadriceps group, comprising the rectus femoris and the three vasti muscles, is the most important component of the muscular apparatus of the knee joint. Analysis of the role the quadriceps assumes in the stability of the knee brings forcefully to light the importance of this muscle mass in the maintenance of the erect posture in man. This is achieved by the ability to produce powerful extension of the knee, to stabilize the joint and to maintain its equilibrium. In addition, it counterbalances the action of the flexor muscles, gravity and body weight. Its mechanical efficiency is enhanced by the presence of the patella (a fact which is being disregarded by many surgeons, as is evidenced by the number of patellectomies performed for varied reasons). The patella increases the strength of the quadriceps by improving leverage. These functional demands made on the quadriceps explain its great muscle volume and great force of action. Under normal conditions this muscle has considerable reserve force which is readily demonstrated when one stands on one extremity; the muscle will shorten and become tense. At this point, the part played by the extensors as stabilizers of the knee joint must be re-emphasized. Loss of volume and power of contractionof the quadriceps reduces its stabilizing influence and predisposes the ligamentous apparatus and the synovial lining of the joint to repeated trauma. This in turn, if not controlled adequately, initiates a sequence of events characterized by progressive weakness of the quadriceps, repeated episodes of effusion into the knee joint, permanent thickening and hypertrophy of the synovialis and, finally, osteoarthritis of the knee joint. The ability to extend fully the knee and to stabilize the joint in varying positions of flexion to complete extension are late acquisitions in the functional evolution of the quadriceps. This is substantiated by the clinical observation that the intrinsic quadriceps mechanism, being unstable, is readily unbalanced by even trivial injuries which interfere with normal joint function. This disorder is reflected in the loss of muscle volume, diminished power of contraction and disorientation of the muscle mass. Varying degrees of severity are encountered; the more severe derangements present features not unlike those of flaccid paralysis. Of the four components of the quadriceps group, the vastus internus (medialis) exhibits the most profound alterations. Since this muscle is concerned primarily with balancing movements, especially in varying degrees of flexion of the knee joint, any insufficiency of the quadriceps is characterized by "giving way" of the knee when in different phases of flexion. QUADRICEPS INSUFFICIENCY
As previously recorded, this is a clinical manifestation of the quadriceps apparatus comprising three elements: loss of muscle volume (atrophy), diminished power of contraction, and disorientation of the muscle mass. This manifestation in varying degrees is a concomittant
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finding of all affections implicating the knee joint. In traumatic lesions the more obvious derangements may obscure this condition, so that it progresses in intensity unnoticed until the patient attempts to use the extremity. It then becomes apparent that in spite of adequate repair of the injured structures, the patient is unable to use the extremity without "giving way" of the knee joint. The abnormal stresses placed on the ligaments and capsule are followed by an effusion into the joint which tends to increase the laxity of the ligamentous apparatus. In order to allow the effusion to be absorbed, the limb is put to rest; this in turn results in a further decrease in the volume and power of contraction of the muscle. Once such a cycle is established, every effort must be expended to interrupt it. This can be done only by nonweight-bearing active exercises, progressively increasing in intensity until sufficient volume, tone and control have been restored in the quadriceps muscle to prevent aggravation of an existing injury and to protect the joint from new traumas. Failure to overcome quadriceps insufficiency may result in permanent dysfunction of the knee joint. A case in point is the following history. CASE REPORT. E. F., a man 52 years of age, struck the anterior aspect of the knee again!'t an opened door. The next day the knee was swollen and painful, and the patient sought medical aid. The attending physician ordered the patient to bed and applied ice bags to the knee. After 10 days the swelling had disappeared and the patient was allowed to bear weight on the affected limb. About one month later he was seen in the out-patient department; his chief complaints were "buckling of the knee" and constant swelling. Examination of the extremity at this time disclosed marked atrophy and poor power of contraction of the quadriceps muscle. In addition, a moderate effusion was demonstrable in the knee joint. Roentgenographic examination failed to reveal any evidence of bone pathology (Fig. 556, a). A diagnosis of quadriceps insufficiency was made, and admission to the hospital was advised. It was hoped that under a closely supervised regimen of exercises the affected quadriceps would be restored to sufficient power to stabilize the knee and protect it from further injury. He refused admission. The patient was again seen in the out-patient department eight months later. During the interval between the first and second visits he was treated I;>y numerous physkians, one of whom made a diagnosis of a torn internal meniscus and recommended its removal; the patient had been subjected to this surgical procedure. However, he was not relieved of the pain, swelling and instability of the knee joint which had become progressively worse. Examination at this time revealed a boggy, swollen knee with advanced thickening of the capsular tissues. The quadriceps muscle mass was barely perceptible when the patient attempted to contract the muscle; atrophy of the muscle was profound. Roentgenogrltphic examination disclosed advanced osteoarthritic changes comprising thinning of the joint spaces and marked marginal lipping of the femoral and tibial articular surfaces (Fig. 556, b). These changes were not present in the roentgenograms taken at the first examination. It became apparent the the condition had progressed to an irreversible point, and radical measures were indicated. It was decided to perform a synovectomy, provided the patient would first cooperate in restoring some power and volume to the quadriceps before operation was undertaken. To this he promised, but he refused to put any real effort in the program outlined for him. After six weeks
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Anthony F. DePalma
it became apparent that our efforts were in vain, the patient being most uncooperative. An arthrodesis of the knee was then performed. At operation it was interesting to note the advanced degenerative alterations that had occurred within a
Fig. 556. a, Radiograms of patient E. F. taken at the first admission to the outpatient department. Note the absence of any degenerative changes in the knee joint. b, Radiograms of the same knee taken approximately eight months after roentgenograms shown in a. Note the severe degenerative changes that have taken place, particularly in the medial joint compartment and the articular surface of the patella. This is an excellent demonstration of the secondary changes that may occur following chronic synovitis of the knee joint resulting from quadriceps insufficiency. period of less than one year. The synovialis was thickened and studded with numerous villus formations. The articular surface of the femur exhibited areas of erosion and chondromalacia; the same findings, but of less severity, were noted in the articular surfaces of the tibia.
1
i
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1773
This case illustrates emphatically the pitfalls that may be encountered after a simple contusion of the knee joint. I am certain that all the unfortunate sequelae noted in this instance could have been prevented if the presence of quadriceps insufficiency had been recognized and treated correctly at the time of the initial injury. SWELLING OF THE KNEE JOINT FOLLOWING INJURY
This clinical manifestation is frequently encountered after direct or indirect injuries to the knee joint. Swelling is not a clinical entity; it is a concomitant feature of injury to the elements of the articulation. In general, two varieties occur: traumatic synovial effusion and hemarthrosis. Traumatic Synovial Effusion
Although it is common knowledge that all acute injuries of the knee joint are followed by a synovial effusion, many physicians are content to make a diagnosis of traumatic synovitis without attempting to uncover the more serious associated lesions. It cannot be emphasized too strongly that effusion resulting from traumatic synovitis without the presence of other pathology is indeed a rare clinical entity. On the other hand, as noted before, all acute injuries of the knee are invariably accompanied by an effusion. The clinical features of an effusion distinguish it from hemarthrosis. The importance of arriving at a correct diagnosis is essential in order to institute correct treatment. As a rule, synovial effusions per se are demonstrable after a relatively long period of time, usually six to eight hours after the injury. This differs .from a hemarthrosis, in which the swelling appears shortly after the injury, within one half to one hour. It becomes apparent that if hemorrhage and effusion occur concurrently, the interval is greatly shortened. A constant and pertinent symptom in effusion is the absence of intense pain. The patient is aware of a sense of fullness in the knee, and distention will elicit varying degrees of discom~ fort, but not acute pain. In massive effusions the knee is maintained in a position 'of slight flexion, the outlines of the suprapatellar pouch encircling the periphery of the patella are discernible, and palpation discloses ballottement of the patella. Also gentle palpation (with the fingers of both hands placed on the medial and lateral surfaces of the knee on a level with the center of the patella) reveals that the tissues are stretched but not boggy, nor do they convey the sense of resistance and tumefaction so characteristic of a massive hemarthrosis. It becomes apparent that in the advent of a synovial effusion, the prime concern of the physician is to determine first the presence or absence of other lesions such as a torn meniscus. If such a lesion is demonstrable, the choice of treatment must take into consideration the injury as a whole and must 'not be directed solely to the management of the effusion. Failure to adhere to this precaution will result in delay of adequate management for traumatic lesions which, if not promptly recognized and treated correctly, may give rise to unfavorable sequelae resulting in permanent dysfunction of the knee joint.
Anthony F. DePalma
1774 Traumatic Hemarthrosis
The accumulation of blood in the articular cavity of the knee joint is always indicative of injury to some other structure or structures. Realization of this fact should always incite further investigation of the injury when the presence of a hemarthrosis is established. As Smillie12 pointed out, there are two varieties of hemarthrosis: one in which there is little or no tendency for the blood to coagulate, and the other in which coagulation of blood is a prominent feature. This variation depends upon the amount of synovial effusion found in association with the blood. It is generally known that synovial fluid has anticoagulant properties. If it is present in sufficient quantities, the blood remains fluid; if it is overwhelmed by a large volume of blood, coagulation is not precluded. It is interesting to note that the conditions in which the blood fails to coagulate are usually of minor severity and have a favorable outlook. They include tears of the synovial lining associated with sprains of the collateral ligaments, varying degrees of tears of the anterior cruciate ligament, or fractures of the tibial spine. Massive hemorrhage with coagulation of blood is usually encountered in severe injuries to the quadriceps apparatus as fracture of the patella, complete tears of the quadriceps tendon or patellar tendon and complete tears of the collateral ligaments. A massive hemarthrosis is seldom a concomitant feature of a torn meniscus except in rare instances when t1;le meniscus is torn from its peripheral attachment. In the light of these observations, it ,becomes obvious that correct evaluation of the type of hemarthrosis present in a given case provides a clue to:the seriousness and the prognosis of the injury. As in traumatic effusion, correct and prompt management of the etiologic factors responsible for the hemorrhage prevents unfavorable complications and decreases the degree of permanent impairment of function in many cases. THE "BUCKLING KNEE"
This complaint is associated with severe forms of disorders of the knee joint. Notable among these are tears of the posterior portion of the meniscus, quadriceps insufficiency and rupture of the anterior cruciate ligament. It becomes apparent that an accurate diagnosis can be made only by a careful examination of the part and consideration of the most likely' etiologic factors. Tears of the Posterior Segment of the Internal Meniscus
It is erroneous to believe that locking of a knee joint is the most important symptom of tears of the internal meniscus. This clinical feature OC,curs orily when the longitudinal tear implicates the anterior segment of the meniscus. More important, but less recognized, is the sense of insecurity of, the joint when the patient walks on uneven ground, or "buckling" when certain unguarded movements are performed as'turning suddenly or stepping off a curb. Moreover, the patient often offers the -information, that he feels a "click" in the joint as if some loose body were
Lesions of Shoulder and Knee Joint
1775
moving about the joint. These features are characteristic of a tear of the posterior segment of the meniscus (Fig. 557). As a rule the lesion isa longitudinal tear, but it may be shredding, with maceration of the posterior segment without a complete longitudinal split. In addition, firm pressure over the inner joint line immediately behind the collateral liganient invariably elicits exquisite tenderness.
Fig. 557. a, Tear of posterior portion of internal meniscus, giving rise to a sense of instability and buckling of the knee joint, but no locking. b, Extensive longitudinal tear extending into the anterior portion of the meniscus. This type of lesion causes locking of the joint.
Quadriceps Insufficiency
Although quadriceps insufficiency is a concomitant feature of all disorders of the knee joint, on occasion it is encountered singly following a period of functional inactivity unrelated to the knee joint or following such minor injuries as sprains and contusions of the joint. Loss of volume and tone of the quadriceps mass, especially the vastus medialis, may be so profound and rapid that severe dysfunction results. The clinical features of this disorder have been discussed previously~ I wish to emphasize at this point that "buckling" or "giving way" of the knee is a constant feature of quadriceps insufficiency which may be the only remaining clinical manifestation of some previous disorder. It becomes obvious that all other causative agents which may be responsible for
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the symptom and which may be still active must be eliminated before quadriceps insufficiency per se is credited for the disability. Rupture of the Anterior Cruciate Ligament
It is essential to be cognizant of the observation that not all patients with rupture of the anterior cruciate ligament complain of "giving way" or "buckling" of the knee joint. This is explained by the knowledge that a strong quadriceps muscle and intact collateral ligaments are capable of compensating sufficiently for the torn ligament so that no dysfunction ensues. In the presence, however, of quadriceps insufficiency and laxity of the collateral ligaments, chiefly the tibial collateral ligament, this symptom may be a pertinent and disabling manifestation. In such cases clinical examination reveals varying degrees of quadriceps atrophy and a positive drawer sign (abnormal forward displacement of the tibia on the fixed femur). Occasionally this sign may be actively produced by the patient by contraction of the gastrocnemius muscle.
SUMMARY In this brief presentation the more common lesions of the shoulder and knee joint have been discussed and the pertinent distinctive features of each entity have been considered so that an accurate diagnosis can be made. The necessity of an accurate diagnosis is essential in order that correct and adequate management may be instituted.
REFERENCES 1. Codman, E. A.: The Shoulder. Boston, Thomas Todd, 1934. 2. DePalma, A. F.: Surgery of the Shoulder. Philadephia, J. B. Lippincott Company, 1950. 3. DePalma, A. F.: Loss of Scapulohumeral Motion (Frozen Shoulder). Ann. Surg., February 1952. 4.DePalma, A. F., Callery, G. E., and Bennett, G. A.: Variational Anatomy and Degenerative Lesions of the Shoulder Joint. Am. Acad. Orthopedic Surgeons Instructional Course Lectures, 1949. 5. DePalma, A. F., White, J. B., and Callery, G. E.: Degenerative Lesions of the Shoulder Joint at Various Age Groups Which Are Compatible with Good Function. Am. Acad. Orthopedic Surgeons Instructional Course Lectures, 1950. 6. Duplay, S.: De la periarthrite scapulo-humerale. Rev. frat. d. trav. de med., 53: 226, 1896 (Tr. M. Week, 4: 253, 1896; M. Press, 59: 571-573, 1900). 7. Hitchcock, H. H., and Bechtol, C. 0.: Painful Shoulder; Observations of the Role of the Tendon of the Long Head of the Biceps Brachii in Its Causation. J. Bone & Joint Surg., 30-A: 263, 1948. 8. Hueter, C.: Arch. f. klin. chir., 5: 321-323, 1864. 9. Lippmann, R. K.: Frozen Shoulder; Periarthritis and Bicipital Tenosynovitis. Arch. Surg., 47: 283-296, 1943. 10. Pasteur, F.: La teno-bursite bicepitale. J. de radiol. et d'electrol., 16: 419426, 1932. 11. Schrager, V. L.: Tenosynovitis of the Long Head of the Biceps Humeri. Surg., Gynec. & Obst., 66: 785-790,1938. 12. Smillie, I. S.: Injuries of the Knee Joint. Baltimore, Williams & Wilkins Company, 1951.