JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 8, NUMBER 4
JULY 1992
CLINCAL REVIEW
PATHOLOGY OF THE SHOULDER AS IT RELATES TO THE DIFFERENTIAL DIAGNOSIS
Downloaded by: NYU. Copyrighted material.
OF THORACIC OUTLET COMPRESSION L. Scott Levin and A. Lee Dellon
ABSTRACT Shoulder pathology and its diagnosis must be considered in evaluation of the patient suspected of having thoracic outlet syndrome (TOS). Overlooking usually treatable conditions in the shoulder may lead to unfavorable results, if treatment is directed, instead, to neurolysis of the brachial plexus or first rib resection.
One of the most overlooked conditions that involves upper extremity pain is pathology as it relates to the mechanical function of the shoulder girdle, the glenohumeral joint, and the surrounding musculature. These conditions are often misdiagnosed as, or coexist with, "thoracic outlet syndrome." While there is no doubt that thoracic outlet syndrome (TOS)1 exists, there is still debate over whether the origin of its symptoms is vascular, neurologic, or a combination of both. The term "TOS" is a misnomer, and the condition would more appropriately be termed "thoracic inlet" or "brachial plexus compression," based on the actual anatomy.2 The purpose of this article is to outline shoulder anatomy, the history and physical examination as they relate to shoulder pain, the use of diagnostic local injections, and to describe the various shoulder syndromes that may cause pain similar to that caused by TOS. It is only after these causes of shoulder pain have been eliminated, as well as other sources of similar pain such as peripheral compression neuropathy and cervical disease, that the diagnose of TOS should be considered. Furthermore, these conditions may co-
exist as a "double crush" or "multiple crush syndrome,"3 so that appropriate preoperative evaluation is critical. History Taking. The history is very important in making the diagnosis of pathology about the shoulder.4 The patient's age often helps to identify the type of pathology involved. For example, patients over the age of 50 years may present with shoulder pain as a result of rotator-cuff tears that occur frequently in this patient population. Similarly, the glenohumeral instabilities that often result from shoulder dislocation may become chronic problems, particularly in patients in the second or third decade of life. Taking a careful history will help in determining the origin of shoulder pathology. Provocative maneuvers by the patient that cause pain should be noted. For example, if a patient is unable to sleep on one side or the other, or the patient must change his sleeping habits, this may relate to the so called "impingement syndrome." Inquire into the patients' occupational histories. Do they experience repetitive job stress such as do painters or mechanics, that cause arms to be overhead for prolonged periods of time?5 While these provoca-
Divisions of Orthopaedic, Plastic and Reconstructive Surgery, Duke University, Durham, NC and Department of Plastic and Neurologic Surgery, lohns Hopkins University, Baltimore, MD Reprint requests-. Dr. Levin, Duke University Medical Center, Box 3945, Durham, NC 27710 Accepted for publication February 24, 1992 Copyright © 1992 by Thieme Medical Publishers, Inc., 381 Park Avenue South, New York, NY 10016. All rights reserved.
313
314
tive maneuvers can contribute to TOS, they also may create some of the conditions that relate to biomechanical causes of shoulder pain. Activities involving repetitive use of the arms above the horizontal plane may be more likely to produce a painful shoulder due to "impingement syndrome." Occupations such as painting, wall papering, and carpentry put excess stress on the rotator-cuff mechanism. In young patients, activities such as baseball, tennis, and swimming, may create tendinitis in the shoulder girdle. Neer6 has demonstrated that the functional arc of elevation of the shoulder is forward and not lateral. Subsequently, impingement occurs when the anterior edge of the acromion makes contact with the rotator cuff against the humeral head in abduction. ROTATOR CUFF SYNDROME. The rotator cuff is made up of tendinous insertions of the subscapularis, the infraspinatus, supraspinatus and, to a lesser extent, the teres minor long head of the biceps muscles. These insertions blend with each other and form part of the capsule of the shoulder. Vascular studies by MacNab7 have demonstrated that there are "avascular" zones of the biceps tendon and supraspinatus tendon (part of the rotator cuff) that may contribute to the impingement syndrome. Chronic irritation of the "avascular" zone of these tendons leads to an initial inflammatory response that is reflected in tendinitis. Over time, an infarct occurs and subsequently, older patients may develop rotator-cuff or biceps-tendon ruptures. As the chronic inflammation of the supraspinatus tendon and biceps tendon progresses, involvement may include the acromioclavicular joint, with formation of osteophytes and degenerative changes seen on x-ray. Neer6 has classified the progressive pathology of rotator-cuff and biceps tendinitis into three stages. They include: 1) edema, hemorrhage (this can occur at any age); 2) fibrosis, tendinitis (usually over the age of 25 years); 3) tendon degeneration, bony changes, and tendon ruptures in patients usually over the age of 40 years. The processes of rotator-cuff and bicipital tendinitis involve the biceps tendon, the supraspinatus tendon, subacromial bursa, and eventually, the acromioclavicular joint.8-10 Each one of these anatomic points can contribute to pain and could be confused with TOS. Radiographic evaluation should include an arthrogram of the shoulder in the older patient, to look for evidence of rotator-cuff tears. An MRI may be required to define the pathology precisely. X-rays of the shoulder may demonstrate a high-riding humerus, which results from the over-pull by the deltoid on the humeral head, as the rotator cuff thins because of tearing or infarction. Stage 1 can be treated conservatively, and the diagnosis made on the basis of aching discomfort, usually after activity. If the supraspinatus tendon is involved, the positive clinical signs are: a) point tenderness over the greater tuberosity of the humerus and anterior acromion; b) a painful arc of
JULY 1992
abduction that increases when the humerus is internally rotated at 90° of flexion, a so-called positive impingement sign; and c) the positive straight-armraising test, which consists of resisted forward flexion of the humerus with forearm supinated and elbow extended (Fig. 1). One of the most helpful diagnostic tests is the injection of 10 cc of 1 percent lidocaine beneath the anterior acromion. If pain is relieved, the diagnosis of impingement syndrome can be made with more confidence. In stage 1, the biceps tendon is involved and frequently, there is tenderness over the biceps tendon. The bicipital groove can be injected with lidocaine, and if pain is relieved this suggests bicipital tendinitis (see Fig. 1). Another test for bicipital tendinitis, Yergason's sign, is elicited by resisted supination of the forearm, with the elbow flexed 90° and the humerus adducted (Figs. 2, 3). In stage 2 of rotator-cuff syndrome, structures become more fibrotic and thickened and the painful shoulder becomes more difficult to treat. Stage 2 impingement occurs frequently in the 25- to 40-year-old group. The shoulder joint is stiffer and there may be early arthritic changes in the acromioclavicular joint.
Figure 1. Test for cuff tendinitis. Injection sites 1. Supraspinatus tendon 2. Biceps tendon 3. Glenohumeral joint 4. Subacromial bursa 5. Acromioclavicular joint
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JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 8, NUMBER 4
PATHOLOGY OF THE SHOULDER/LEVIN, DELLON
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Figure 2. A, Pain over supraspinatus insertion with resisted humeral elevation; elbow extended. B, Yergason's test. Patient is asked to supinate forearm held at 90° of flexion. Pain is produced at the level of the intertubercular groove from bicipital tendinitis.
In stage 3 of rotator-cuff syndrome, there is a long history of shoulder pain. Symptoms include aching at night. Patients will have a positive impingement sign and have pain-related weakness. It is not unusual for the patient to have a complete thickness tear of the rotator cuff, diminished range of motion of the shoulder, and inability to actively elevate the arm. Again, performing a subacromial injection of 10 cc of lidocaine may relieve the pain and allow the patient to elevate the arm, demonstrating integrity of the rotator cuff. However, if there is a large tear of the rotator cuff then, despite obliteration of the pain, the patient cannot actively abduct the arm. On physical examination, there will be infraspinatus and supraspinatus muscle wasting, tenderness over the acromioclavicular joint, more limited motion, and possible biceps rupture. Electrodiagnostic testing is valuable to detect neurologic problems that might affect the muscles, such as root lesions of C5 and C6, upper trunk plexus, suprascapular or axillary nerve pathology. An acute tear into the rotator cuff may occur from a direct blow. This usually occurs in young people with sports activities such as football. These patients may go on to have a chronic impingement syndrome. Patients should be tried on a conservative program that includes rest, analgesics, anti-inflammatories, and physical therapy. Current management of impingement includes arthroscopic acromial decompression with synovectomy, and debridement of the rotator cuff, with or without open repair.
Acromioclavicular joint Acromioclavicular joint
Tendon, supraspinatus m
Intertubercular groove
Coracoacromial ligament
Coracoid process Subdeltoid bursae Subscapularis m Biceps tendon
Figure 3. Bony anatomy of the shoulder. Sites for diagnostic or therapeutic blocks of the shoulder region.
315
JULY 1992
shoulder, such as posterior dislocation, may have SHOULDER INSTABILITY. Patients who have had prior shoulder dislocation may have the so-called "ap- weakness of the supraspinatus and infraspinatus musprehensions sign."11 The patient is examined supine cles. This weakness may present as shoulder pain, and the humeral head is forced out of the glenoid. If the which also may be related to an injury of the suprapatient feels as though his shoulder is about to dislo- scapular nerve. An EMG may be helpful in the differencate on provocative testing, then some degree of tial diagnosis. anterior/posterior or global instability exists that will In older patients, the long head of the biceps require reconstruction. Patients who have primary ac- tendon may rupture. This can be treated expectantly. romioclavicular (A-C) pathology may have a history of However, in a young individual, acromion decompresacromioclavicular joint separation and may, on exam- sion and tenodesis of the tendon to the bicipital ination, have deformity in the A-C joint, with a bump or groove is probably indicated. palpable step-off that may be tender. A-C joint arthritis GLENOHUMERAL INSTABILITY. Patients who have can exist as a separate entity or as part of stage 3 had shoulder dislocations may have had injury to the rotator-cuff disease. Joint injection here is diagnostic axillary nerve. This association increases with the inand will eliminate pain in the A-C joint, indicating a creasing age of the patient, the direction of the dislocaprimary A-C joint problem (see Fig. 3). tion (anterior more than posterior), and the amount of trauma involved in the dislocation. Electromyographic CERVICAL SPINE PATHOLOGY. Another differential diagnosis of the impingement syndrome and TOS is evaluation three weeks after dislocation is helpful in cervical spondylosis and degenerative disc disease at documenting this injury, and serial EMGs can docuC5/C6 (Table 1). Correlating motor and sensory findings, ment recovery of function. Most of these peripheral as well as x-rays and EMGs, may be helpful in making nerve injuries recover within six months. Failure to the diagnosis of cervical disc disease. Just as "double document recovery suggests the need to evaluate the crush" can exists with cervical disc disease and carpal axillary nerve surgically, remembering that the quadritunnel syndrome, cervical spine and shoulder prob- lateral space is a potential entrapment site for the 13 lems may occur concomitantly, particularly in the older axillary nerve and may require decompression. Patients who have recurrent glenohumeral instability patient. may be confused with patients who have impingement OTHER CAUSES OF SHOULDER PAIN. In the older patient, arthritis or arthrosis of the glenohumeral joint syndrome, rotator-cuff tears, acromion clavicular joint may cause limitation of shoulder motion, pain, and disease, snapping scapula or intra-articular loose weakness with abduction. Diagnosis can be confirmed bodies, degenerative joint disease, and subluxation of on x-ray. Calcific tendinitis is another entity that is a the long head of the biceps tendon. Examination of the separate pathologic process.12 This can be seen radio- patient includes assessment of the deltoid strength graphically with calcium deposits along the biceps and rotator-cuff muscles, as well as a stress test to tendon. Although present, this calcific deposit may not determine in which direction the glenohumeral joint is relate to the cause of the patient's pain. Here again, unstable. Pain may be produced by provocative madiagnostic xylocaine injections are helpful (see Fig. 3). neuvers for anterior, inferior, posterior, or posteriorPatients who have had a posterior trauma to the inferior instability. Radiographic evaluation should in-
Table 1. D)D
316
Shoulder Pain
Rotator Cuff Tear
Impingement Syndrome
Cuff lateral, anterior deltoid Abduct against resistance
Supraspinatus, anterior acromion Impingement test: abduct; int rotate humerus > 90°
AC ]oint
Arthritis
Bicipital
C-Spine
Tendinitis
A-C joint
Base of neck, radicular
A-C joint palpate
Spurling's test rotation, lateral bending of head Abnormal Abnormal Numbness, dropping objects, weakness
Bicipital groove of humerus Yergason's test
Pain location
Glenohumeral joint
Provocative test
Axial Load/grind Humerus/ glenoid
Motor Sensory History
Normal Normal Slow onset
Abnormal Normal Acute or chronic occupational?
Normal Normal Difficulty sleeping on affected side, occupational?
Normal Normal Injury
Shoulder passive ROM
Possibly limited
Limited abduction
Limited due to pain
Limited due to pain
Normal
Abnormal Abnormal Elbow flexion painful, sudden onset if biceps ruptures Normal
Thoracic Outlet Neck, shoulder, arm, hand Tinel sign Roos' sign
Abnormal Abnormal Injury, occupational?
Normal
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JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 8, NUMBER 4
PATHOLOGY OF THE SHOULDER/LEVIN, DELLON
elude the scapular AP, lateral, and axillary views, as they may reveal old fractures, osteophytes, or incongruities in the glenoid or humeral head. ACROMIOCLAVICULAR JOINT. Perhaps the most overlooked cause of shoulder pain is the acromioclavicular joint. The acromioclavicular joint is a diarthrodial joint averaging 81 mm2 in size. In 10 percent of patients there is a small meniscus. The disease usually presents as an isolated arthritis in the sixth or seventh decade of life and may be a component of the impingement syndrome. Osteolysis of the outer clavicle may be due to trauma, Gorham's disease, or be secondary to hyperparathyroidism. In young patients, pain may be due to inflammations from sports or repetitive work activities, or A-C joint separation from sports injury. FROZEN SHOULDER. While the frozen shoulder may be a result of chronic impingement syndrome, it can occur after upper extremity injuries such as fractures of the hand, forearm, or elbow, and in patients who have had myocardial infarction or breast surgery. It is usually rotator-cuff tendinitis that results in secondary limitation of movement of the glenohumeral joint in all planes. Frozen shoulder occurs in patients over 50 years of age and may present as a dull, aching pain of the shoulder, usually over the deltoid. It occurs more commonly in women. Initially, the patients have a normal range of motion but, as time progresses, an inflammatory stage of the disease leads to limitation of motion due to protective muscle spasm. This tightness may be a cause of brachial plexus compression (TOS). The pain is worse at night and markedly interferes with the patient's ability to sleep. The most notable clinical feature of this presentation is the inability of the patient to abduct the arm. With lack of antagonistic motion, the deltoid firmly pulls the humerus against the glenoid. Contracture of the tendon of the subscapularis 7 and the coracohumeral ligament results in even further restriction of external rotation.
der pain. On subsequent exam, one may notice atrophy of the supraspinatus and infraspinatus muscles. EMG evaluation is again indicated. X-rays may demonstrate osteoporosis resulting from disuse and some superior migration of the humeral head. Arthrography shows obliteration of synovial pouches. In almost every patient, the lesion resolves spontaneously with restoration of movement within 18 months. Therapy should be conservative, and may involve steroids, rest, and general physical therapy. Physical therapy in the acute stages can be aided by suprascapular nerve blocks and side arm traction. Manipulation, particularly under anesthesia, is to be avoided. Rarely, surgery is necessary to release the frozen shoulder.
Often, the patient will compensate for frozen shoulder with scapulothoracic movement. However, this may put traction on the suprascapular nerve in the suprascapular notch, further accentuating the shoul-
12.
1. Campbell JN, Dellon AL, Naff N: Thoracic outlet syndrome. Neurosurg Clin N Am 2:227, 1991 2. Dellon AL: Brachial plexus compression (not thoracic outlet syndrome): Treatment by supraclavicular plexus neurolysis. Presented at the Annual Meeting, Northeastern Society of Plastic Surgery, September, 1990 3. Mackinnon SE, Dellon AL: Multiple crush syndromes. In Surgery of the Peripheral Nerve, New York: Thieme 1988, chap 14 4. Cailliet R: Shoulder pain. In Reconstructive Microsurgery, 2nd ed. Philadelphia: FA. Davis, 1981, pp. 1-89 5. Herbert P, Kadefors R, Hogfors C, Sigholm G: Shoulder pain and heavy manual labor Clin Orthop 191:166, 1984 6. Neer CS, II: Impingement lesions. Clin Orthop 173:70, 1983 7. MacNab I: Rotator cuff tendinitis: "The frozen shoulder." In Everts, CM (ed): Surgery of the Musculoskeletal System, vol. 3.
8. 9.
NY: Churchill Livingstone, 1983, pp 35-47 Cofield RH: Tears of the rotator cuff. In AAOS Instructional Course Lectures, XXX. St. Louis: CV Mosby, 1981, pp 258-273 Neviaser RJ, Neviaser TJ: Lesions of the musculotendinous cuff of the shoulder: Diagnosis and management. Part A: Tears of the rotator cuff. In AAOS Instructional Course Lectures, XXX.
10. 11.
13.
St. Louis: CV Mosby, 1981, pp 239-250 Bonica JJ: The Management of Pain, vol 1, Philadelphia: Lea & Febiger, 1990, pp 906-923 Rowe CR, Zarins BP: Recurrent transient subluxation of the shoulder. I Bone Joint Surg 63A:863, 1981 Uhthoff HK, Sarkar K, Maynard JA: Calcific tendinitis: A new concept of its pathogenesis. Clin Orthop 118:164, 1976 Francel TJ, Dellon AL, Campbell IN: Quadrilateral space syndrome: Diagnosis and operative decompression techniques. Plast Reconstr Surg 87:911, 1991
317
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REFERENCES
JULY 1992
CLINCAL REVIEW
PATHOLOGY OF THE SHOULDER AS IT RELATES TO THE DIFFERENTIAL DIAGNOSIS
Downloaded by: NYU. Copyrighted material.
OF THORACIC OUTLET COMPRESSION L. Scott Levin and A. Lee Dellon
ABSTRACT Shoulder pathology and its diagnosis must be considered in evaluation of the patient suspected of having thoracic outlet syndrome (TOS). Overlooking usually treatable conditions in the shoulder may lead to unfavorable results, if treatment is directed, instead, to neurolysis of the brachial plexus or first rib resection.
One of the most overlooked conditions that involves upper extremity pain is pathology as it relates to the mechanical function of the shoulder girdle, the glenohumeral joint, and the surrounding musculature. These conditions are often misdiagnosed as, or coexist with, "thoracic outlet syndrome." While there is no doubt that thoracic outlet syndrome (TOS)1 exists, there is still debate over whether the origin of its symptoms is vascular, neurologic, or a combination of both. The term "TOS" is a misnomer, and the condition would more appropriately be termed "thoracic inlet" or "brachial plexus compression," based on the actual anatomy.2 The purpose of this article is to outline shoulder anatomy, the history and physical examination as they relate to shoulder pain, the use of diagnostic local injections, and to describe the various shoulder syndromes that may cause pain similar to that caused by TOS. It is only after these causes of shoulder pain have been eliminated, as well as other sources of similar pain such as peripheral compression neuropathy and cervical disease, that the diagnose of TOS should be considered. Furthermore, these conditions may co-
exist as a "double crush" or "multiple crush syndrome,"3 so that appropriate preoperative evaluation is critical. History Taking. The history is very important in making the diagnosis of pathology about the shoulder.4 The patient's age often helps to identify the type of pathology involved. For example, patients over the age of 50 years may present with shoulder pain as a result of rotator-cuff tears that occur frequently in this patient population. Similarly, the glenohumeral instabilities that often result from shoulder dislocation may become chronic problems, particularly in patients in the second or third decade of life. Taking a careful history will help in determining the origin of shoulder pathology. Provocative maneuvers by the patient that cause pain should be noted. For example, if a patient is unable to sleep on one side or the other, or the patient must change his sleeping habits, this may relate to the so called "impingement syndrome." Inquire into the patients' occupational histories. Do they experience repetitive job stress such as do painters or mechanics, that cause arms to be overhead for prolonged periods of time?5 While these provoca-
Divisions of Orthopaedic, Plastic and Reconstructive Surgery, Duke University, Durham, NC and Department of Plastic and Neurologic Surgery, lohns Hopkins University, Baltimore, MD Reprint requests-. Dr. Levin, Duke University Medical Center, Box 3945, Durham, NC 27710 Accepted for publication February 24, 1992 Copyright © 1992 by Thieme Medical Publishers, Inc., 381 Park Avenue South, New York, NY 10016. All rights reserved.
313
314
tive maneuvers can contribute to TOS, they also may create some of the conditions that relate to biomechanical causes of shoulder pain. Activities involving repetitive use of the arms above the horizontal plane may be more likely to produce a painful shoulder due to "impingement syndrome." Occupations such as painting, wall papering, and carpentry put excess stress on the rotator-cuff mechanism. In young patients, activities such as baseball, tennis, and swimming, may create tendinitis in the shoulder girdle. Neer6 has demonstrated that the functional arc of elevation of the shoulder is forward and not lateral. Subsequently, impingement occurs when the anterior edge of the acromion makes contact with the rotator cuff against the humeral head in abduction. ROTATOR CUFF SYNDROME. The rotator cuff is made up of tendinous insertions of the subscapularis, the infraspinatus, supraspinatus and, to a lesser extent, the teres minor long head of the biceps muscles. These insertions blend with each other and form part of the capsule of the shoulder. Vascular studies by MacNab7 have demonstrated that there are "avascular" zones of the biceps tendon and supraspinatus tendon (part of the rotator cuff) that may contribute to the impingement syndrome. Chronic irritation of the "avascular" zone of these tendons leads to an initial inflammatory response that is reflected in tendinitis. Over time, an infarct occurs and subsequently, older patients may develop rotator-cuff or biceps-tendon ruptures. As the chronic inflammation of the supraspinatus tendon and biceps tendon progresses, involvement may include the acromioclavicular joint, with formation of osteophytes and degenerative changes seen on x-ray. Neer6 has classified the progressive pathology of rotator-cuff and biceps tendinitis into three stages. They include: 1) edema, hemorrhage (this can occur at any age); 2) fibrosis, tendinitis (usually over the age of 25 years); 3) tendon degeneration, bony changes, and tendon ruptures in patients usually over the age of 40 years. The processes of rotator-cuff and bicipital tendinitis involve the biceps tendon, the supraspinatus tendon, subacromial bursa, and eventually, the acromioclavicular joint.8-10 Each one of these anatomic points can contribute to pain and could be confused with TOS. Radiographic evaluation should include an arthrogram of the shoulder in the older patient, to look for evidence of rotator-cuff tears. An MRI may be required to define the pathology precisely. X-rays of the shoulder may demonstrate a high-riding humerus, which results from the over-pull by the deltoid on the humeral head, as the rotator cuff thins because of tearing or infarction. Stage 1 can be treated conservatively, and the diagnosis made on the basis of aching discomfort, usually after activity. If the supraspinatus tendon is involved, the positive clinical signs are: a) point tenderness over the greater tuberosity of the humerus and anterior acromion; b) a painful arc of
JULY 1992
abduction that increases when the humerus is internally rotated at 90° of flexion, a so-called positive impingement sign; and c) the positive straight-armraising test, which consists of resisted forward flexion of the humerus with forearm supinated and elbow extended (Fig. 1). One of the most helpful diagnostic tests is the injection of 10 cc of 1 percent lidocaine beneath the anterior acromion. If pain is relieved, the diagnosis of impingement syndrome can be made with more confidence. In stage 1, the biceps tendon is involved and frequently, there is tenderness over the biceps tendon. The bicipital groove can be injected with lidocaine, and if pain is relieved this suggests bicipital tendinitis (see Fig. 1). Another test for bicipital tendinitis, Yergason's sign, is elicited by resisted supination of the forearm, with the elbow flexed 90° and the humerus adducted (Figs. 2, 3). In stage 2 of rotator-cuff syndrome, structures become more fibrotic and thickened and the painful shoulder becomes more difficult to treat. Stage 2 impingement occurs frequently in the 25- to 40-year-old group. The shoulder joint is stiffer and there may be early arthritic changes in the acromioclavicular joint.
Figure 1. Test for cuff tendinitis. Injection sites 1. Supraspinatus tendon 2. Biceps tendon 3. Glenohumeral joint 4. Subacromial bursa 5. Acromioclavicular joint
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JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 8, NUMBER 4
PATHOLOGY OF THE SHOULDER/LEVIN, DELLON
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Figure 2. A, Pain over supraspinatus insertion with resisted humeral elevation; elbow extended. B, Yergason's test. Patient is asked to supinate forearm held at 90° of flexion. Pain is produced at the level of the intertubercular groove from bicipital tendinitis.
In stage 3 of rotator-cuff syndrome, there is a long history of shoulder pain. Symptoms include aching at night. Patients will have a positive impingement sign and have pain-related weakness. It is not unusual for the patient to have a complete thickness tear of the rotator cuff, diminished range of motion of the shoulder, and inability to actively elevate the arm. Again, performing a subacromial injection of 10 cc of lidocaine may relieve the pain and allow the patient to elevate the arm, demonstrating integrity of the rotator cuff. However, if there is a large tear of the rotator cuff then, despite obliteration of the pain, the patient cannot actively abduct the arm. On physical examination, there will be infraspinatus and supraspinatus muscle wasting, tenderness over the acromioclavicular joint, more limited motion, and possible biceps rupture. Electrodiagnostic testing is valuable to detect neurologic problems that might affect the muscles, such as root lesions of C5 and C6, upper trunk plexus, suprascapular or axillary nerve pathology. An acute tear into the rotator cuff may occur from a direct blow. This usually occurs in young people with sports activities such as football. These patients may go on to have a chronic impingement syndrome. Patients should be tried on a conservative program that includes rest, analgesics, anti-inflammatories, and physical therapy. Current management of impingement includes arthroscopic acromial decompression with synovectomy, and debridement of the rotator cuff, with or without open repair.
Acromioclavicular joint Acromioclavicular joint
Tendon, supraspinatus m
Intertubercular groove
Coracoacromial ligament
Coracoid process Subdeltoid bursae Subscapularis m Biceps tendon
Figure 3. Bony anatomy of the shoulder. Sites for diagnostic or therapeutic blocks of the shoulder region.
315
JULY 1992
shoulder, such as posterior dislocation, may have SHOULDER INSTABILITY. Patients who have had prior shoulder dislocation may have the so-called "ap- weakness of the supraspinatus and infraspinatus musprehensions sign."11 The patient is examined supine cles. This weakness may present as shoulder pain, and the humeral head is forced out of the glenoid. If the which also may be related to an injury of the suprapatient feels as though his shoulder is about to dislo- scapular nerve. An EMG may be helpful in the differencate on provocative testing, then some degree of tial diagnosis. anterior/posterior or global instability exists that will In older patients, the long head of the biceps require reconstruction. Patients who have primary ac- tendon may rupture. This can be treated expectantly. romioclavicular (A-C) pathology may have a history of However, in a young individual, acromion decompresacromioclavicular joint separation and may, on exam- sion and tenodesis of the tendon to the bicipital ination, have deformity in the A-C joint, with a bump or groove is probably indicated. palpable step-off that may be tender. A-C joint arthritis GLENOHUMERAL INSTABILITY. Patients who have can exist as a separate entity or as part of stage 3 had shoulder dislocations may have had injury to the rotator-cuff disease. Joint injection here is diagnostic axillary nerve. This association increases with the inand will eliminate pain in the A-C joint, indicating a creasing age of the patient, the direction of the dislocaprimary A-C joint problem (see Fig. 3). tion (anterior more than posterior), and the amount of trauma involved in the dislocation. Electromyographic CERVICAL SPINE PATHOLOGY. Another differential diagnosis of the impingement syndrome and TOS is evaluation three weeks after dislocation is helpful in cervical spondylosis and degenerative disc disease at documenting this injury, and serial EMGs can docuC5/C6 (Table 1). Correlating motor and sensory findings, ment recovery of function. Most of these peripheral as well as x-rays and EMGs, may be helpful in making nerve injuries recover within six months. Failure to the diagnosis of cervical disc disease. Just as "double document recovery suggests the need to evaluate the crush" can exists with cervical disc disease and carpal axillary nerve surgically, remembering that the quadritunnel syndrome, cervical spine and shoulder prob- lateral space is a potential entrapment site for the 13 lems may occur concomitantly, particularly in the older axillary nerve and may require decompression. Patients who have recurrent glenohumeral instability patient. may be confused with patients who have impingement OTHER CAUSES OF SHOULDER PAIN. In the older patient, arthritis or arthrosis of the glenohumeral joint syndrome, rotator-cuff tears, acromion clavicular joint may cause limitation of shoulder motion, pain, and disease, snapping scapula or intra-articular loose weakness with abduction. Diagnosis can be confirmed bodies, degenerative joint disease, and subluxation of on x-ray. Calcific tendinitis is another entity that is a the long head of the biceps tendon. Examination of the separate pathologic process.12 This can be seen radio- patient includes assessment of the deltoid strength graphically with calcium deposits along the biceps and rotator-cuff muscles, as well as a stress test to tendon. Although present, this calcific deposit may not determine in which direction the glenohumeral joint is relate to the cause of the patient's pain. Here again, unstable. Pain may be produced by provocative madiagnostic xylocaine injections are helpful (see Fig. 3). neuvers for anterior, inferior, posterior, or posteriorPatients who have had a posterior trauma to the inferior instability. Radiographic evaluation should in-
Table 1. D)D
316
Shoulder Pain
Rotator Cuff Tear
Impingement Syndrome
Cuff lateral, anterior deltoid Abduct against resistance
Supraspinatus, anterior acromion Impingement test: abduct; int rotate humerus > 90°
AC ]oint
Arthritis
Bicipital
C-Spine
Tendinitis
A-C joint
Base of neck, radicular
A-C joint palpate
Spurling's test rotation, lateral bending of head Abnormal Abnormal Numbness, dropping objects, weakness
Bicipital groove of humerus Yergason's test
Pain location
Glenohumeral joint
Provocative test
Axial Load/grind Humerus/ glenoid
Motor Sensory History
Normal Normal Slow onset
Abnormal Normal Acute or chronic occupational?
Normal Normal Difficulty sleeping on affected side, occupational?
Normal Normal Injury
Shoulder passive ROM
Possibly limited
Limited abduction
Limited due to pain
Limited due to pain
Normal
Abnormal Abnormal Elbow flexion painful, sudden onset if biceps ruptures Normal
Thoracic Outlet Neck, shoulder, arm, hand Tinel sign Roos' sign
Abnormal Abnormal Injury, occupational?
Normal
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JOURNAL OF RECONSTRUCTIVE MICROSURGERY/VOLUME 8, NUMBER 4
PATHOLOGY OF THE SHOULDER/LEVIN, DELLON
elude the scapular AP, lateral, and axillary views, as they may reveal old fractures, osteophytes, or incongruities in the glenoid or humeral head. ACROMIOCLAVICULAR JOINT. Perhaps the most overlooked cause of shoulder pain is the acromioclavicular joint. The acromioclavicular joint is a diarthrodial joint averaging 81 mm2 in size. In 10 percent of patients there is a small meniscus. The disease usually presents as an isolated arthritis in the sixth or seventh decade of life and may be a component of the impingement syndrome. Osteolysis of the outer clavicle may be due to trauma, Gorham's disease, or be secondary to hyperparathyroidism. In young patients, pain may be due to inflammations from sports or repetitive work activities, or A-C joint separation from sports injury. FROZEN SHOULDER. While the frozen shoulder may be a result of chronic impingement syndrome, it can occur after upper extremity injuries such as fractures of the hand, forearm, or elbow, and in patients who have had myocardial infarction or breast surgery. It is usually rotator-cuff tendinitis that results in secondary limitation of movement of the glenohumeral joint in all planes. Frozen shoulder occurs in patients over 50 years of age and may present as a dull, aching pain of the shoulder, usually over the deltoid. It occurs more commonly in women. Initially, the patients have a normal range of motion but, as time progresses, an inflammatory stage of the disease leads to limitation of motion due to protective muscle spasm. This tightness may be a cause of brachial plexus compression (TOS). The pain is worse at night and markedly interferes with the patient's ability to sleep. The most notable clinical feature of this presentation is the inability of the patient to abduct the arm. With lack of antagonistic motion, the deltoid firmly pulls the humerus against the glenoid. Contracture of the tendon of the subscapularis 7 and the coracohumeral ligament results in even further restriction of external rotation.
der pain. On subsequent exam, one may notice atrophy of the supraspinatus and infraspinatus muscles. EMG evaluation is again indicated. X-rays may demonstrate osteoporosis resulting from disuse and some superior migration of the humeral head. Arthrography shows obliteration of synovial pouches. In almost every patient, the lesion resolves spontaneously with restoration of movement within 18 months. Therapy should be conservative, and may involve steroids, rest, and general physical therapy. Physical therapy in the acute stages can be aided by suprascapular nerve blocks and side arm traction. Manipulation, particularly under anesthesia, is to be avoided. Rarely, surgery is necessary to release the frozen shoulder.
Often, the patient will compensate for frozen shoulder with scapulothoracic movement. However, this may put traction on the suprascapular nerve in the suprascapular notch, further accentuating the shoul-
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1. Campbell JN, Dellon AL, Naff N: Thoracic outlet syndrome. Neurosurg Clin N Am 2:227, 1991 2. Dellon AL: Brachial plexus compression (not thoracic outlet syndrome): Treatment by supraclavicular plexus neurolysis. Presented at the Annual Meeting, Northeastern Society of Plastic Surgery, September, 1990 3. Mackinnon SE, Dellon AL: Multiple crush syndromes. In Surgery of the Peripheral Nerve, New York: Thieme 1988, chap 14 4. Cailliet R: Shoulder pain. In Reconstructive Microsurgery, 2nd ed. Philadelphia: FA. Davis, 1981, pp. 1-89 5. Herbert P, Kadefors R, Hogfors C, Sigholm G: Shoulder pain and heavy manual labor Clin Orthop 191:166, 1984 6. Neer CS, II: Impingement lesions. Clin Orthop 173:70, 1983 7. MacNab I: Rotator cuff tendinitis: "The frozen shoulder." In Everts, CM (ed): Surgery of the Musculoskeletal System, vol. 3.
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NY: Churchill Livingstone, 1983, pp 35-47 Cofield RH: Tears of the rotator cuff. In AAOS Instructional Course Lectures, XXX. St. Louis: CV Mosby, 1981, pp 258-273 Neviaser RJ, Neviaser TJ: Lesions of the musculotendinous cuff of the shoulder: Diagnosis and management. Part A: Tears of the rotator cuff. In AAOS Instructional Course Lectures, XXX.
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St. Louis: CV Mosby, 1981, pp 239-250 Bonica JJ: The Management of Pain, vol 1, Philadelphia: Lea & Febiger, 1990, pp 906-923 Rowe CR, Zarins BP: Recurrent transient subluxation of the shoulder. I Bone Joint Surg 63A:863, 1981 Uhthoff HK, Sarkar K, Maynard JA: Calcific tendinitis: A new concept of its pathogenesis. Clin Orthop 118:164, 1976 Francel TJ, Dellon AL, Campbell IN: Quadrilateral space syndrome: Diagnosis and operative decompression techniques. Plast Reconstr Surg 87:911, 1991
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