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Anterior Cruciate Ligament (ACL) Tear

Important Considerations – Don Wackwitz, M.D.

The Anterior Cruciate Ligament (ACL) is a strong cord like structure running down the center of the knee. It keeps the knee from sliding forward and over rotating. When it is torn it snaps back like a rubber band and the torn ends lose contact with each other. Because the torn ends do not touch, they cannot heal together. The ends are so shredded that the ligament cannot be repaired and therefore it must be reconstructed, that is, replaced with a graft, if we hope to have a stable knee once more.
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Publications – Advanced Arthroscopy

Acromioclavicular Joint Arthroscopy and Distal Clavicle Excision

The acromioclavicular (AC) joint is a common but sometimes overlooked source of shoulder problems. Degenerative disease of the AC joint frequently accompanies extrinsic impingement and cuff deterioration and must be addressed at the same time as decompression and/or cuff repair. Conversely, AC disease may also be isolated (osteolysis) and must be distinguished from and treated apart from the rest of the uninvolved shoulder. This chapter discusses the diagnosis and arthroscopic treatment of AC disease.
ANATOMY

The AC joint is an oval-shaped, synovial-lined articulation of the medial concave acromion and the lateral convex end of the clavicle. The joint allows gliding, shearing, and rotational motion. The normal joint has cartilage on the articular surfaces that evolves from hyalin to fibrocartilage as aging occurs.1 The acromial side is most often covered to a variable extent by a fibrocartilaginous disk as described by DePalma.2 His study associated early degenerative AC joint disease with lack of this meniscoid tissue.

The joint is stabilized by thick and strong superior and weaker inferior capsular thickenings—the AC ligaments. The posterior and superior portions of the capsule play the most important role in limiting anterior and posterior translation of the distal clavicle.3 The coracoclavicular ligaments function to stabilize the clavicle to the scapula, with the conoid ligament primarily preventing anterior and superior clavicular displacement. The trapezoid ligament is the primary constraint against compression of the distal clavicle into the acromion4 (Fig. 10.1).

FIGURE 10.1. Acromioclavicular (AC) and coracoclavicular anatomy. A: Superior and inferior AC ligaments. B: Coracoclavicular ligaments—conoid (medial) and trapezoid (lateral). C: Coracoacromial ligament.

The angle of the AC joint on anteroposierior (AP) view is variable. Urisl5 found 49% inclined from superolaleral to inferomedial, 27% vertically oriented, 21% incongruous, and 3% laterally oriented. The joint is also inclined a few degrees from anterolateral to posterior medial on the axillary view (Fig. 10.2).

FIGURE 10.2. AC joint orientation (Urist).

PATHOPHYSIOLOGY

FIGURE 10.3. Degenerative arthritis of the AC joint X-ray appearance.

The AC joint may become symptomatic secondary to a number of etiologies. Traumatic causes include AC separation and distal clavicle fracture. Mumford6 and Gurd7 independently reported in 1941 on resection of the distal clavicle for symptomatic AC joint dislocations. The open procedure gradually evolved into the treatment of choice for degenerative arthritis of the AC joint and for unresponsive osteolysis of the distal clavicle.

The pathoanatomy differs for posttraumatic or degenerative arthropathy as compared to repetitive use or traumatic osteolysis and has some bearing on the arthroscopic approach utilized. The degenerative process is characterized by loss of cartilage, joint space narrowing, osteophytes, and subchondral cysts (Fig. 10.3).

Osteolysis, however, demonstrates a wider joint secondary to an inflammatory hyperemic bone resorption with cystic changes and occasionally cupping of the AC joint8 (Fig. 10.4).

FIGURE 10.4. Radiographic appearance of AC osteolysis.

ASSOCIATED PATHOLOGY

Whether the process is degenerative or osteolytic, associated pathology must be carefully evaluated. Impingement syndrome as described by Neer9 is frequently associated with AC joint disease and must be treated with a concomitant decompression for successful results. Partial- and full-thickness cuff tears, superior labrum anterior to posterior (SLAP) lesions, biceps fraying or rupture, and glenohumeral degenerative disease have all been reported with impingement and AC arthritis.10-11 Similar pathology may also be found in patients with apparent isolated AC osteolysis if glenohumeral arthroscopy is performed at the time of resection.
DIAGNOSIS

Points of concern in the history include previous AC separation or clavicle fracture, the presence of degenerative or inflammatory arthritis, weight-lifting intensity and duration, and repetitive cross-arm usage.

Clinically, the patient will often present with pain radiating along the trapezius to the neck and laterally over the deltoid toward its humeral insertion. Sleeping on the affected side is troublesome, as the joint is compressed. The overlap with rotator cuff complaints is obvious. Discomfort with cross-chest adduction maneuvers is well documented but should localize to the superior aspect of the shoulder and not deep and anterior as found in anterior subcoracoid impingement as described by Gerber et al.12 The patient may complain of pain with extension, adduction, and internal rotation only when the degeneration of the AC joint localizes posteriorly. Weight lifters commonly have problems with bench and military presses.

Physical exam frequently demonstrates localized tenderness at the AC joint and often a prominence of the distal clavicle. Hawkins’s flexion and internal rotation impingement maneuver13 may be positive especially if inferior AC osteophytes are prominent. Straight flexion and abduction and external rotation maneuvers may localize pain at the AC area but not be impressive unless there is associated subacromial impingement. Injection of lidocaine in specific different locations about the shoulder can be very helpful in distinguishing AC disease from subacromial, rotator cuff, bicipital groove, and anterior subcoracoid pathology; 2 to 3 cc of a mixture of 1% lidocaine and 0.25% bupivacaine with a 25-gauge ( 5/8-inch) needle from a superior AC approach should prevent false-positive tests from inadvertent subacromial injection. Effective relief from pain with subsequent provocative maneuvers is a reliable indicator of AC disease.

Imaging Studies

Routine AP and Y (or outlet) lateral x-ray evaluation of the shoulder will often miss AC joint pathology. An AP radiograph of the AC joint with the x-ray beam directed 15 degrees cephalad and the voltage reduced by 30% to 50% will alleviate the superimposition of the joint on the scapular spine and its routine overexposure14,15 (Fig.10.5). Comparison AC views are often necessary for distinguishing the early narrowing and sclerosis of degenerative disease or the contrasting widening and osteopenia of osteolytic disease.

FIGURE 10.5.
A: Standard anteroposterior (AP) shoulder radiograph.
B: Anterior AC joint radiograph with 15-degree cephalad angulation and reduced exposure.

A good-quality axillary view is often the best radiograph for capturing the decreased posterior joint space and sometimes subtle posterior sclerosis noted in those patients with posterior AC arthritis with its associated pain with extension, adduction, and internal rotation. Magnetic resonance imaging (MRI) scans, which are frequently obtained for rotator cuff evaluation, are rarely needed but often available for AC review. Soft tissue enlargement and synovitis and encroachment of inferior joint osteophytes on the bursa and rotator cuff tendons can be appreciated. AC joint impingement, however, has become a popular radiographic diagnosis and needs to be carefully correlated with the patient’s clinical picture lest premature distal clavicle resection be performed. MRI findings associated with osteolysis include diffuse bone marrow edema, cortical thinning or irregularity, and tiny subchondral cysts of the distal clavicle.16 The most sensitive study for diagnosing osteolysis in equivocal cases is a magnesium bone scan, which will demonstrate increased uptake of radiotracer at the distal clavicle and AC joint.

TREATMENT

Nonoperative treatment, which is successful in a majority of cases, consists of (1) activity modification; (2) nonsteroidal antiinflammatories; (3) local steroid injection; (4) passive modalities such as ice, heat, and ultrasound; and (5) preventive therapeutic exercises to avoid atrophy or contracture. Weight lifters who resume, or persist with, their lifting activities generally fail the other nonoperative treatment modalities.8

Indications for operative treatment are failure of conservative care after 6 to 12 months of activity modification (or an unwillingness to give up weight training), localized tenderness with a positive injection test, and positive imaging studies. Debate exists regarding the advisability of either open or arthroscopic distal clavicle excision alone versus resection and stabilization (e.g., Weaver-Dunn or Bosworth procedure) in patients with chronic unstable AC separation.

ARTHROSCOPIC TECHNIQUE

There are two basic approaches to arthroscopic resection of the distal clavicle: superior and subacromial. Both techniques have advantages over the open technique in that they allow evaluation of the glenohumeral joint and subacromial space, permitting diagnosis of previously unrecognized pathology.10,11 They both preserve the deltoid origin, permitting quicker return to activities.17 One can combine these techniques with other arthroscopic or mini-open techniques for rotator cuff repair with less soft tissue trauma, less pain, and improved cosmesis.

Disadvantages of the arthroscopic techniques are that they are technically more demanding, equipment intensive, and have a longer learning curve. There is also the potential for increased morbidity if performed incorrectly (e.g., variable resection, rotator cuff and musculotendinous damage).

Superior Approach

First described by Lanny Johnson18 and championed more recently by Bigliani and Flatow,17,19,20 this technique approaches the AC joint from above through anterior-superior and posterior-superior AC portals. These authors routinely utilized interscalene regional anesthesia and placed the patient in the beach-chair position for this technique, although it can also be performed with the patient in the lateral decubitus position.

The AC joint position and inclination is exactly determined with three 22-gauge needles, and the joint is distended with normal saline. A 2.7-mm, 30-degree arthroscope is then inserted through a posterior-superior portal and a 2.0-mm resector placed through an anterior-superior portal to debride the meniscal remnant and debris. A 2.0-mm burr is then inserted, and removal of the distal clavicle is commenced. The scope and burr are then switched to the opposite portal and bone resection continued until the 4.0-mm arthroscope and larger tapered burr can be inserted. Electrocautery is used to “shell out” the distal clavicle from the surrounding soft tissues, but the capsule and ligaments are not incised. Final beveling of the bone surface is performed with an arthroscopic rasp.

Bigliani and Flatow attempt to resect 5 to 6 mm of distal clavicle with a uniform gap anteriorly and posteriorly. They report a 91% success rate in patients with arthritis or osteolysis with stable AC joints. Failures were due to retained posterior cortical ridges. Patients with previous second-degree AC separations and chronic AC pain faired poorly, with only 37% satisfactory results.20

The proposed advantages of this technique are direct visualization of the pathology “without violating the glenohumeral joint or subacromial bursa” and “precise bone resection and contouring.”20

The disadvantages of this technique are the following:

  1. It requires a small joint arthroscope and instruments.
  2. Arthritic and tight joints are difficult to operate in.
  3. The technique requires one to work backhanded, with the shaver coming toward the scope, with more potential equipment damage.
  4. The temptation exists not to examine the glenohumeral joint or the subacromial space, with associated pathology thus left undiagnosed.
  5. The posterior-superior portal with multiple passage of scopes, shavers, and burrs likely produces some injury to the most important part of the capsule, the posterior-superior AC joint ligament.

Subacromial Approach

Ellman21 and Esch et al22 were the first to describe the subacromial approach to the AC joint in conjunction with arthroscopic subacromial decompression. Modifications to their approach have been introduced by Tolin and Snyder23 Meyers,24 and Maki.25

All these techniques approach the AC joint while performing subacromial bursoscopy, resecting the medial bursal wall, the fat pad, and inferior AC joint ligament. With the joint exposed, a burr can be introduced posteriorly or laterally, removing that portion of the clavicle that can be pushed into view under the acromion with manual pressure from above. The remaining superior portion of the clavicle is resected from the anterior AC joint portal while viewing from the posterior or lateral portal.

The advantages of this technique are the following:

  1. It facilitates concurrent exam of the glenohumeral joint and subacromial bursa to diagnose and treat unrecognized pathology.
  2. It is easily performed in conjunction with arthroscopic subacromial decompression.
  3. It entails no injury to the posterior-superior capsule.
  4. It does not require small joint scopes or instruments.

The disadvantages of this technique are the following:

  1. It necessitates traversing and resecting a portion of nonpathologic bursa and inferior capsule in isolated AC joint disease.
  2. One or two more portals are necessary.
  3. A 70-degree scope may be needed.
  4. The technique entails more potential bleeding and fluid extravasation.
  5. It may be difficult to deliver the clavicle inferiorly with a medially inclined joint.

The subacromial approach is my preferred method for arthroscopic AC resection. I believe it is imperative to examine the glenohumeral joint and subacromial bursa even with presumed isolated AC joint disease. If this additional exam is performed, four portals rather than two are necessary for the superior approach, negating its major advantage. In addition, sacrifice of the weak inferior AC capsule rather than compromise of the thick and strong posterior-superior capsule is preferable. Finally, routinely switching from small-joint to standard-size arthroscopy equipment seems time-consuming and wasteful.

AUTHOR’S CURRENT SURGICAL TECHNIQUE

The patient is placed in the lateral decubitus position and rolled posteriorly 30 degrees to orient the glenoid parallel to the floor26 with an axillary roll and neutral head support (Fig. 10.6). The arm is abducted 25 to 30 degrees and flexed 10 to 15 degrees, and 10 pounds (15 in heavy or well-muscled patients) of traction applied.

FIGURE 10.6. Lateral decubitus position with axillary roll, padding, and head support exactly in neutral. Patient’s torso is angled posteriorly 25–30˚, orienting glenoid surface parallel to floor.

The next three steps vary with the type of patient:

  • Patients with Subacromial Symptoms
  • Patients with Apparent AC Disease
  • Patients with Either Technique.

Patients with Subacromial Symptoms

The scope is introduced through the standard posterior portal (2 cm inferior and 1 cm medial to the posterolateral corner of the acromion). An anterosuperior outflow cannula is introduced, and glenohumeral arthroscopy from both the anterior and posterior portals utilizing switching sticks is performed. Any intra-articular pathology is addressed (e.g., partial cuff tear, labral or biceps debridement).

The arthroscope is then inserted through the same skin incision into the subacromial bursa with the same anterior portal utilized for outflow and orientation at the anterolateral corner of the acromion, just under the coracoacromial ligament. A midlateral portal is made approximately 3.5 to 4 cm lateral to the acromion and directed slightly up at the undersurface of the acromion and directly at the AC joint (Fig. 10.7). A bursectomy and coracoacromial ligament release, or a subacromial decompression, is then performed, depending on the preoperative diagnosis and arthroscopic appearance.

FIGURE 10.7.
A: Portal position for right shoulder glenohumeral exam and subacromial decompression and distal clavicle resection. Scope posteriorly; gray cannula in lateral portal; blue cannula in anterior superior portal; needle at anterior AC portal.
B: Posterior view of debrided undersurface of right acromion with shaver tip on coracoacromial ligament. Anterior lateral corner of acromion to right.
C: Small amount of anterior and lateral acromial bone resected with burr on lateral edge of CA ligament.

If decompression is indicated, a two-portal, cutting block technique is routinely utilized (Fig. 10.8),27 except in a very thin, broad anterior hooked acromion where a lateral approach as described by Ellman21 would be utilized. After the acromion has been flattened with the burr from the posterior portal, the inferior one-third to one-half of the distal clavicle is often exposed. With the scope still in the lateral portal, the burr is then directed more medially and the lateral 1 to 1.5 cm of the inferior tip of the clavicle is resected. Manual pressure from above can usually deliver much of the remaining clavicle for resection (Fig. 10.8D).

FIGURE 10.8.
A. Scope placed laterally with burr introduced posteriorly for planing of the acromion.
B. Subacromial view of planing from posterior (left) to anterior (right).
C: Further planing with tip of clavicle visible under tip of burr.
D: Completed decompression with inferior clavicle partially resected—lateral view.

The scope is then placed posteriorly and rotated upward, visualizing the line of orientation of the AC joint and remaining superior clavicular bone. The burr (with the aid of an 18-gauge needle) is then introduced through an anterior and slightly inferior AC portal and directed from anterior to posterior and lateral to medial to remove the remaining superior cortical shell (Fig. 10.9).

FIGURE 10.9.
A: Scope placed posteriorly with burr introduced from anterior-inferior AC portal.
B: Posterior view of undersurface of acromion (right), AC joint line,
and clavicle (left) with inferior half of clavicle resected.
C: Burr resecting remaining superior clavicle.

Rotation of the scope from superior to medial exposes the posterior cortex and posterior-superior capsule to view (Fig. 10.10). If bursal tissue compromises visualization, either it can be debrided or the scope can be inserted through the lateral portal. If superior visualization is poor, a 70-degree scope can be utilized.

FIGURE 10.10.
A: Superior clavicle resected exposing superior capsule.
B: Scope rotated medially to view completed clavicle resection.
Posterior superior capsule intact.

Patients with Apparent Isolated AC Diseas

If the glenohumeral joint looks pristine from the posterior portal with the 30-degree scope, I may not utilize an anterior-superior portal and instead finish the 15-point glenohumeral exam with a 70-degree scope from posteriorly.

The scope is then redirected into the subacromial bursa from the posterior portal. If the bursa looks normal, again I will not utilize an anterior portal but still place a lateral portal and introduce a bipolar cautery/ablation tip or a shaver to debride the fat pad and inferior capsule of the AC joint.

Once the AC joint has been exposed, a burr is introduced from an anterior-inferior AC portal and directed from anterior to posterior and inferior to superior, resecting approximately 1.0 to 1.5 cm of the clavicle (and the medial acromial facet if the joint is inclined medially). The scope can be inserted through the lateral portal for visualization of the posterior clavicle if needed. It should be noted that for isolated AC joint disease, only three portals (posterior, lateral, and anterior inferior AC joint) are needed to perform a thorough glenohumeral exam, a subacromial bursoscopy (with minimal violation), and AC resection.

With Either Technique

The gap is then examined to make sure all cortical bone superiorly is removed and resection is even from anterior to posterior. It is measured with two parallel 18-gauge needles from above; 10 to 15 mm of bone is resected with more bone removed in patients with any previous AC instability (Fig. 10.11).

FIGURE 10.11.
A: Needles placed percutaneously in a parallel fashion to measure the amount of distal clavicle resection.
B: Arthroscopic view of gap with needles.
C: Lateral view of acromion (posterior to left) and resected end of clavicle.

The pump pressure is then reduced and hemostasis of larger vessels is obtained with the electrocautery device; 10 cc of 0.25% bupivacaine with epinephrine are instilled into the subacromial space and the incisions are closed with simple 4-0 nylon sutures. No immobilization is utilized unless associated rotator cuff repair is performed.

POSTOPERATIVE CARE

Passive support and motion of the affected shoulder is provided by the opposite arm if needed. Pendulum exercises are started the next day. Home range of motion exercises are utilized the first week. Physical therapy may or may not be utilized depending on the patient’s progress with the home program. Closed chain scapular stabilizing exercises are initiated at the end of week one. Gentle elastic tubing exercises for internal and external rotation are started at week two or three. Light-duty work is instituted early (1/2 to 2 weeks), but heavy labor usually begins at 6 to 12 weeks postoperatively. Sports activities are individualized and variable.

COMPLICATIONS

The complications associated with arthroscopic distal clavicle excision are the following:

  1. Inadequate resection.
  2. Heterotopic bone formation.
  3. Underlying muscle injury.
  4. Excessive bleeding

The amount of bone to be resected arthroscopically from the tip of the clavicle is still unresolved. If the posterior-superior AC ligaments are well preserved, the length of the clavicle to removed can be reduced.17 Bigliani20 found a 91% success rate in AC resection with just 5 to 6 mm of resection in patients with arthritis or osteolysis and stable joints. If the posterior and superior ligaments are violated or previously injured, then the remaining tip of the clavicle becomes more unstable and more resection is needed.3,4 Bigliani had only 37% satisfactory results in patients with painful AC joints after second-degree AC separations. However, he continued to perform minimal (5 to 6 mm) resections in this subgroup. Other investigators have had much improved results with second-degree and even third-degree separations with either open or arthroscopic technique when 1.5 to 2 cm of clavicle was resected.28,29

My present practice is as follows:

  • In AC joint disease with or without decompression with intact AC and coracoclavicular ligaments —10 to 12 mm of resection.
  • In AC joint disease with or without decompression with previous AC ligament injury but generally intact coracoclavicular ligament (second-degree separation or mild third-degree) — 15 to 17 mm of resection.
  • Chronic symptomatic, unstable, third-degree or fourth degree AC separation with both AC and coracoclavicular compromise — open modified Weaver-Dunn reconstruction and deltotrapezial fascial repair.

Care should be taken to measure the distance between the clavicle and the acromion with two 18-gauge needles from above; if needed, this should be performed at both the anterior and posterior aspect of the clavicle. It is easy to obtain an uneven gap in resection with more bone removed anteriorly than posteriorly.

Incomplete resection of the superior cortical bone during distal clavicle resection is not uncommon. Clear visualization of this area using either a 30-degree or 70-degree arthroscope is necessary to remove all the superior bone. If a cortical egg shell of bone is left behind, elevation and cross-chest maneuvers will remain painful, and the bone will also serve as a nidus of heterotopic bone formation (Fig. 10.12).

FIGURE 10.12.
Heterotopic bone formation.
A: Immediate postoperative x-ray with slight residual superior bone.
B: Six-month follow-up radiograph showing early heterotopic nidus.
C: Two-year postoperative radiograph demonstrating mature bone in AC interval.

Caution should be exercised when using burrs for resecting the tip of the clavicle. It is easy to wrap up the soft underlying cuff musculature in the instrument. I prefer to use a well-hooded burr with the open side always facing up or in toward the cancellous middle of the clavicle. Suction should be just enough to clear debris.

The vascularity around the tip of the clavicle and AC joint is plentiful. Cauterization of the fat pad underneath the AC joint before the debridement is helpful. It is also beneficial to outline the tip of the clavicle frequently with a cautery device as the clavicle is being resected medially because the periosteal vessels are numerous.

Other strategies can be utilized for the control of bleeding:

  • Inject 0.25% bupivacaine with epinephrine into the portals (2 cc) and subacromial space (10 cc) at the beginning of the case.
  • Incise skin only and avoid deeper muscle laceration.
  • Utilize a blunted conical trocar for penetration of muscle, joint, and subacromial space.
  • Add epinephrine, 10 mL (1:1,000 per 3-L bag to first irrigation bag only).
  • Utilize electrocautery immediately when significant bleeders are encountered.
  • Increase inflow with large bore sheath at scope. A pump with independent control of pressure and flow rate is helpful.
  • Decrease outflow to maintain pressure. Control suction on shavers and burrs to reduce “red out.” Integrated fluid deliver and shaver systems are helpful for this problem.
  • Reduce blood pressure, if the medical condition allows, to maintain a systolic pressure of less than 95 to 100 mm Hg.
  • Increase pressure on pump or elevate bags to level where bleeding is well controlled.

RESULTS

Ellman, Kay, and Harris21 reported on a series of 10 patients treated with the subacromial approach. All patients obtained a satisfactory outcome and returned to their previous level of sports participation. Bigliani17 had a 91% success rate in patients with isolated AC disease with stable clavicles.

My own series encompasses a period of time from 1991 to 1995 (minimum 2-year follow-up) and is composed of 35 cases of AC resection with varying degrees of decompression. The series includes patients with isolated AC disease and those with associated impingement. Excluded were cased with significant rotator cuff tears, biceps degeneration, or instability.

Thirty-five patients had well-documented preoperative and postoperative University of California at Los Angeles (UCLA) scores and returned for a long-term follow-up exam. An additional eight patients were doing well at last exam, had resumed work activities, were happy with their functional level, and did not return for long-term follow-up. One remaining patient complained of pain with light activities but had only slight restriction and could work above shoulder level (UCLA score 27).

In the 35 patients, preoperative UCLA scores averaged 14.83, and postoperative scores were 30.50. Eleven (31%) had excellent results, 19 (54%) good, 3 (9%) fair, and 2 (6%) poor. Of the five patients with fair or poor results, four were female with pain responsive to AC and subacromial injections but recurrent, and radiographic changes that were on the mild end of the spectrum. The one male with a fair result developed postoperative heterotopic bone and had some residual pain with light activities but only slight restriction.

SUMMARY

Arthroscopic AC resection is an increasingly popular technique, performed either primarily or in conjunction with an arthroscopic subacromial decompression. The learning curve for this procedure is steep and should not be underestimated. Two arthroscopic approaches were presented, and both can prove successful, with a more rapid recovery than with traditional open techniques. Diligent preoperative evaluation and intra-operative attention to potential complications will lead to positive surgical outcomes (Fig. 10.13).

FIGURE 10.13.
A: Pre- and postoperative radiograph of arthroscopic subacromial decompression.
B: Pre- and postoperative AP radiograph of AC resection.

REFERENCES

1. Tyurina TV. Age-related characteristics of the human acromioclavicular joint. Arkh Anat Gistol Embriol 1985;89:75.

2. DePalma AF. Biologic aging of the shoulder. In: DePalma AF, ed. Surgery of the shoulder. Philadelphia: JB Lippincott, 1983:235–240.

3. Klimkiewicz J, Sher J, et al. Biomechanical function of acromioclavicular ligaments in limiting anterior posterior translation of the acromioclavicular joint. Paper presented at the open meeting of the American Shoulder and Elbow Surgeons in 1997, San Francisco, CA.

4. Fukuda K, Craig EV, An K, et al. Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg 1986;68A:434–440.

5. Urist MR. Complete dislocation of the acromioclavicular joint. J Bone Joint Surg 1946;28:813–837.

6. Mumford EB. Acromioclavicular dislocation. A new operative treatment. J Bone Joint Surg 1941;23:799–802.

7. Gurd FB. The treatment of complete dislocation of the outer end of the clavicle. Ann Surg 1941;113:1094–1098.

8. Cahill BR. Osteolysis of the distal part of the clavicle in male athletes. J Bone Joint Surg 1982;64A:1053–1058.

9. Neer CS. Impingement lesions. Clin Orthop 1983;173:70–77.

10. Frick SL, Connor PM, D’Alessandro DF. The value of glenohumeral arthroscopy in surgical evaluation and treatment of impingement syndrome. Paper presented at the 16th annual meeting of the Arthroscopy Association of North America 1997, San Diego, CA.

11. Lewis DM, Arroyal JS, Pollock RG, et al. Early glenohumeral arthritis diagnosed at arthroscopy for impingement syndrome and rotator cuff disease. Paper presented at the 16th annual meeting of the Arthroscopy Association of North America, 1997, San Diego, CA.

12. Gerber C, et al. The role of the coracoid process in the chronic impingement syndrome. J Bone Joint Surg 1985;67B:703–708.

13. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Sports Med 1980;8:151–158.

14. Rockwood CA Jr, Szalay EA, Curtis RJ, et al. X-ray evaluation of shoulder problems. In: Rockwood CA Jr, Matesen FA III, eds. The shoulder. Philadelphia: WB Saunders, 1990:178–207.

15. Zanca P. Shoulder pain: involvement of the acromioclavicular joint. Analysis of 1000 cases. AJR 1971;112:493–506.

16. Patten RM. Atraumatic osteolysis of the distal clavicle: MR findings. J Comput Assist Tomogr 1995;19(1):92–95.

17. Flatow EL, Bigliani LU. Arthroscopic acromioclavicular joint debridement and distal clavicle resection. Oper Tech Orthop 1991;1:240–247.

18. Johnson LL. Shoulder arthroscopy. In: Johnson LL, ed. Diagnostic and surgical arthroscopy. St. Louis: CV Mosby, 1981: 1404.

19. Flatow EL, Cordasco FA, McClusky GM, et al. Arthroscopic resection of the distal clavicle via a superior portal: a critical quantitative radiographic assessment of bone removal [abstract]. Arthroscopy 1990;6:153–154.

20. Bigliani LU, Nicholson GP, Flatow EL. Arthroscopic resection of the distal clavicle. Orthop Clin North Am 1993;24(1): 133–141.

21. Ellman H. Arthroscopic subacromial decompression: analysis of one to three year results. Arthroscopy 1987;3:173–181.

22. Esch J, Ozerkis LR, Helgager JA, et al. Arthroscopic subacromial decompression: results according to the degree of rotator cuff tear. Arthroscopy 1988;4:241–249.

23. Tolin BS, Snyder SJ. Our technique for the arthroscopic Mumford procedure. Orthop Clin North Am 1993;24:143–151.

24. Meyers JF. Arthroscopic debridement of the acromioclavicular joint and distal clavicle resection. In: McGinty JB, ed. Operative arthroscopy. New York: Raven Press, 1991:557–560.

25. Maki NJ. Arthroscopic resection of the acromioclavicular joint: a new two portal technique. Paper presented at the 16th Annual Meeting of the Arthroscopy Association of North America, 1997, San Diego, CA.

26. Gross RN, Fitzgibbons TC. Shoulder arthroscopy: a modified approach. Arthroscopy 1985;1:156–159.

27. Sampson TG, Nisbet JK, Glick JM. Precision acromioplasty and arthroscopic subacromial decompression. Arthroscopy 1991; 7:301–307.

28. Smith MJ, Stewart MJ. Acute acromioclavicular separations: a 20 year study. Am J Sports Med 1979;7:62–71.

29. Jacobs B, Wade PA. Acromioclavicular joint injury — an end result study. J Bone Joint Surg 1966;48A:475–486.


Publications – Advanced Arthroscopy

Arthroscopic Subacromial Decompression: Lateral Approach

Arthroscopic subacromial decompression (ASAD) is becoming a widely performed surgical procedure of the shoulder. The technique has evolved from open anterior acromioplasty as described by Neer,1-2 Hawkins et al,3’4 Rockwood,5 and Bigliani et al.6 The transition from open to arthroscopic technique entails a definite learning curve and should not be underestimated. This chapter focuses on the technical aspects of the procedure and how to avoid complications.

HISTORICAL PERSPECTIVE

The arthroscopic technique for subacromial decompression was first described by Johnson7 in 1986. Ellman8 presented the first series with follow-up and detailed description of the operative technique. Esch et al9 evaluated their results with ASAD and related them to the severity of associated rotator cuff tears. Paulos and Franklin10 presented one of the largest early series (80 patients) and introduced the use of the midlateral subacromial portal.

All of these authors originally described the procedure with the scope viewing from the posterior portal and the instruments entering from a lateral approach.

Sampson et al11 first described the “cutting block” technique for precision acromioplasty in 1991. This technique places the scope laterally and introduces shaving and burring instruments from a posterior portal, using the posterior half of the acromion as a guide for resection. The authors also emphasized the importance of the supraspinatous outlet x-ray in both preoperative planning and postoperative evaluation and the benefits of evaluating the flatness of the cut from both the lateral and the posterior portals.

Many orthopaedists (myself included) who began performing arthroscopic acromioplasty from the originally described lateral approach now routinely utilize a technique incorporating the cutting-block principles. There are, however, still a number of cases where the posterior technique as described by Sampson et al will lead to complications, and the lateral approach with modifications is still preferable.

With either approach, the advantages of arthroscopic versus open subacromial decompression are evident and include the following:

  1. Less disruption of deltoid insertion and more rapid rehabilitation.
  2. Ability to assess both the articular and bursal surfaces of the rotator cuff and fully evaluate the glenohumeral joint for associated pathology.
  3. Ease of combining with other arthroscopic techniques (distal clavicle resection and/or rotator cuff de-bridement or repair).
  4. Improved cosmesis.
  5. Outpatient setting.

The disadvantages are the significant learning curve and the increased equipment needs of the arthroscopic procedure. Determination of the amount of bone resection especially with the lateral approach, may be more difficult than with open techniques. Complications, if encountered, may be harder to deal with arthroscopically than with an open procedure.

ETIOLOGY

Impingement is a nonspecific clinical syndrome with a number of different underlying etiologies. Accurate diagnosis is imperative to ensure appropriate nonoperative or surgical treatment. Patients complaining of pain with overhead activities are differentiated into one of the following categories:

  1. Primary impingement.
  2. Secondary impingement.
  3. Posterior superior impingement.
  4. Anterior subcoracoid impingement.
  5. Pseudoimpingement

Primary Impingement

Figure 2.1.1. Neer's impingement sign.

Neer1 introduced the concept of extrinsic impingement of the anterior acromion, coracoacromial arch, and the acromioclavicular joint on the underlying rotator cuff and biceps tendon. He also emphasized that forward flexion of the arm is the dominant functional position and that anterior decompression, not lateral acromionectomy, is the appropriate operative approach for significant cuff degeneration. His impingement sign is performed with the patient seated in front of the examiner, who stabilizes the scapula as the arm is elevated slightly lateral to the midline to impinge the tuberosity against the acromion (Fig. 2.1.1).

Pain thus produced is eliminated by injecting 10 cc of 1% Xylocaine into the subacromial bursa beneath the anterior acromion (impingement injection test) to confirm the diagnosis. Hawkins and Kennedy4 described a second impingement sign in which the arm is flexed forward 90 degrees and then forcibly internally rotated, jamming the supraspinatus tendon against the anterior edge of the coracoacromial ligament to produce pain.

Figure 2.1.2. Hawkins's flexion-internal rotation impingement

Patients with primary extrinsic impingement are usually in an older age group or have a bony architecture with an anterior acromial hook or spur that presses directly on the cuff and biceps with forward elevation of the arm. There is also a younger subgroup of overhead athletes who have benign bony anatomy but have a prominent or hypertrophied anterolateral band of the coracoacromial ligament.12 This produces an extrinsic irritation of the underlying bursa and cuff and occasionally a snap or click. Both of these types of patients have the most predictable operative success with arthroscopic subacromial decompression or coracoacromial ligament resection when conservative treatment has failed.

Secondary Impingement

The concept of secondary impingement originates with Codman,13 who proposed an intrinsic tendinous degeneration as the essential lesion in rotator cuff disease. The micro vascular studies by Rathbun and McNab,14 Moseley and Goldie,15 and Rothman and Parke16 support this concept. This vascular compromise results in tissue devitalization characterized as “angiofibroblastic hyperplasia” by Nirschl.17 The subsequent pain and weakness of the supraspinatus compromises its function as a humeral head depressor and allows the upward humeral migration forces of the deltoid to dominate, producing a secondary impingement of the cuff into the acromion.

F. Jobe et al18 enlarged this concept to include patients with underlying anterior glenohumeral ligament instability. As the humeral head subluxes anteriorly, the cuff is secondarily compressed against the coracoacromial arch.

Secondary impingement is more prevalent in a younger patient population actively involved in sports activities that entail overhead arm motion, and should be suspected when the bony architecture is unremarkable. The subluxation-relocation test, as described by Jobe et al18 is helpful in differentiating secondary causes of impingement (Fig. 2.1.3). With the arm abducted 90° and externally rotated, an anterior force is applied by the examiner’s hand on the posterior aspect of the humeral head. This accentuates the impingement pain in an unstable shoulder as the head and overlying cuff drive into the anterior edge of the acromial arch (subluxatiori). Conversely, posterior pressure on the head alleviates the impingement discomfort (relocation).

Figure 2.1.3. Jobe's subluxation-relocation test. Subluxation.

Figure 2.1.3. Jobe's subluxation-relocation test. Relocation.

Posterior Superior Impingement

Walsch et al19 and C. Jobe20 more recently have described another variety of impingement noted in overhead athletes that occurs when the arm is maximally externally rotated while abducted and extended (such as in the cocking phase of throwing). In this position the posterior superior articular surface fibers of the supraspinatus are placed under tension and sheer but are also compressed between the humeral head and adjacent glenoid rim, resulting in posterior superior synovitis and partial under-surface tears. Whether or not any underlying instability is a factor in this compression is still unresolved. While easily confused with primary or secondary anterior impingement, careful examination usually demonstrates pain more at the posterior-superior aspect of the rotator cuff with the arm abducted and externally rotated and extended, in contrast to the impingement positions of Neer and Hawkins. This apprehension position, although painful in this syndrome, does not elicit the usual anxiety found in patients with instability. However, there still may be a reduction of pain with the relocation maneuver of the subluxation-relocation test described by Jobe.

Anterior Subcoracoid Impingement

Gerber et al21 have described this type of anterior impingement between the humeral head and the coracoid process secondary to traumatic, iatrogenic, or idiopathic causes. Whatever the underlying etiology, the tip of the coracoid is positioned more lateral than normal, and as the arm is brought into forward flexion there is a compression of the rotator cuff between the humeral head and the tip of the coracoid. This produces pain with Neer’s forward flexion test, but it occurs usually between 80 and 130 degrees of flexion rather than at full flexion. Also Hawkin’s flexion and internal rotation test is consistently positive, but the pain is lower and more anterior than with superior impingement. The patient also demonstrates decreased horizontal adduction with pain similar to that found with acromioclavicular (AC) disease (Fig. 2.1.4), but the pain is again more at the tip of the coracoid and not at the AC joint.

Figure 2.1.4. Horizontal adduction test.

Pseudoimpingement

Gartsman22 coined the term pseudoimpingement syndrome for patients who demonstrated clinical history and physical findings of anterior superior impingement but in whom impingement was due to a lack of full external rotation. This restriction in range of motion does not allow the humerus to rotate externally with elevation, and the rotator cuff is compressed between the greater tuberosity and the acromion when the arm is elevated. This problem is easily confused with primary extrinsic compression but routinely resolves with therapy directed at regaining the lost external rotation.

ANATOMY

Knowledge of the coracoacromial anatomy is crucial both for diagnostic accuracy and operative facility, and the avoidance of complications.

The bony architecture is composed of the acromion, the AC joint, the coracoid process, and the greater humeral tuberosity. The shape of the acromion and contour of its undersurface is best evaluated with Neer’s supraspinatus outlet view (Fig. 2.1.5). Bigliani et al23 described three distinct acromial shapes: type 1, flat; type 2, curved; and type 3, hooked. They found an increased correlation between the type III hooked acromion and underlying full-thickness rotator cuff tears (69.5% for type 3 and 3% for type 1). This radiographic view is also valuable in determining the overall slope and thickness of the acromion, and in predetermining those cases where the cutting block technique of acromioplasty would be inappropriate.

Figure 2.1.5. Supraspinatus outlet view (right shoulder, anterior to right).

Rockwood and Lyons24 have described a modified anteroposterior (AP) view of the shoulder for differentiating the hooked acromion. This x-ray involves angulating the beam 30 degrees caudad to accentuate the anterior acromial protruberance (Fig. 2.1.6). Although this view is helpful in terms of diagnosis, it is not particularly useful in terms of preoperative planning or determining whether to use a lateral or a posterior approach for the acromioplasty.

The AC joint borders the coracoacromial space medially. As it degenerates, it may play an active role in the extrinsic impingement process. Osteophytic overgrowth on the undersurface of the distal clavicle and medial acromion can impinge on the underlying rotator cuff. The pain of an arthritic or osteolytic joint can also mimic that of anterior impingement. Careful preoperative evaluation is necessary to avoid residual pain at the AC joint after decompression.

Figure 2.1.6. A 30-degree caudal tilt view (right shoulder).

The coracoid process forms the anterior border of the subacromial space. It may be enlarged, fractured, or iatrogenically altered, such as occurs with a laterally positioned Bristow transfer of the coracoid tip onto the anterior glenoid rim. Fractures of the coracoid can occur with the recoil of a rifle into the shoulder in hunters. A posterior opening wedge osteotomy for instability also effectively lateralizes the coracoid tip relative to the humeral head. These changes, which can be associated with anterior subcoracoid impingement, are best noted on axillary view x-rays or a computed axial tomography (CAT) scan with the arm flexed 90 degrees and internally rotated.

The greater tuberosity of the humerus forms the floor of the coracoacromial space. It is important to note its size and shape, any osteophytic overgrowth, sclerosis, erosion, or cysts. It is best evaluated radiographically with an AP view with the arm in external rotation.

Soft Tissue Anatomy

It is important to remember that the subacromial bursa is an anterior structure. It extends from the anterior one-half to one-third of the acromion to just medial to the AC joint to 1 to 2 cm anterior to the acromion and 2 to 3 cm laterally (Fig. 2.1.7). The bursal wall is frequently thickened and troublesome posteriorly, and has been named the “posterior bursal curtain.” This curtain frequently “closes” as one backs the scope posteriorly to get a larger field of view of the subacromial bursa. It is frequently necessary to resect a portion of this structure when performing subacromial surgery.

Figure 2.1.7. Anterior view of latex injected subacromial bursa. Black arrow, anterior edge of bursa; white arrow, superolateral bursa; black wedge, coracoacromial ligament.

The anatomy of the coracoacromial ligament is pertinent to the technique of acromioplasty. It attaches to the front and undersurface of the acromion as a thick band and continues around the anterolateral corner to attach to the lateral ridge for a variable distance. Anteriorly the coracoacromial ligament attaches to the anterior inferior edge of the acromion, while the deltoid fascia attaches more superiorly (Fig. 2.1.8). As the coracoacromial ligament is detached, it falls away easily from the overlying anterior deltoid muscle and fascia. Laterally, however, the coracoacromial ligament blends inextricably with the deltoid muscle fascia along the lateral acromion. Care must be taken not to aggressively detach the fascia or resect too much bone laterally, as this may result in a deltoid detachment.

Figure 2.1.8. Lateral view of coracoacromial ligament and deltoid fascia attachment on anterior acromion.

Gallino et al26 found that the CA ligament has a variable thickness of insertion on the undersurface of the acromion, ranging from 2 to 5.6 mm. Those patients with excessively thickened ligaments would be the ones most likely to have anterior functional stenosis and/or snapping, as described by O’Boyle et al,12 and benefit from anterolateral band resection.

Edelson and Luchs25 and others have noted various degrees of transformation of the coracoacromial ligament into bone at its acromial insertion. Gartsman22labeled this phenomenon “anterior acromial protruberance.” Rockwood5 in his open technique recommends resecting 8 to 10 mm of full-thickness anterior bone and then reattaching the deltoid fascia. This technique of full-thickness anterior bone resection back to the level of the AC joint has insinuated itself into some authors’ description of subacromial decompression.26 For the most part the anterior acromial protruberance is really an inferior extension of calcification into the coracoacromial ligament insertion. One does not need to resect full-thickness acromial bone anteriorly to remove it, and in fact great care should be taken not to resect too much superior anterior bone, as this may detach the anterior deltoid fascia producing an operative disaster. The best radiographic views for determining the amount of anterior acromial protruberance are the axillary view and the supraspinatus outlet view (Fig. 2.1.9). The axillary x-ray is also an excellent view for evaluation of the AC joint, particularly for picking up posterior AC arthritis that may be missed on a routine AP view.

Figure 2.1.9. Anterior acromial protuberance on axillary view. Protuberance (shaded portion).

Figure 2.1.9. Anterior acromial protuberance on axillary view. Radiograph demonstrating anterior acromial protuberance.

DIAGNOSISM

The history is important. Pain with the cocking and acceleration phase of throwing is most likely secondary to an underlying instability or posterior superior impingement. Nocturnal and rest pain is often indicative of a rotator cuff, whereas patients with cuff tendinitis develop pain with progressive activity.27 Other causes of shoulder pain such as scapular thoracic bursitis, suprascapular nerve syndrome, cervical radiculopathy, and referred pain from the gallbladder, liver, lung, or heart also need to be differentiated.

The clinical signs and x-rays noted previously are the most valuable in making a diagnosis of impingement. Concomitant rotator cuff disease or AC joint disease can be evaluated with both an arthrogram or magnetic resonance imaging (MRI). The arthrogram may be more accurate in determining full-thickness rotator cuff tears but less sensitive in picking up partial-thickness lesions or intratendinous pathology. Isolated AC joint injection and/or bone scan may be helpful in differentiating AC joint versus sub-acromial disease. It is important to know the status of the AC joint prior to arthroscopic decompression so that residual pathology in this location is not left unattended.

TREATMENT

Conservative care should be diligent and prolonged. The goal is to diminish the inflammation in the tissues and then regain full range of motion and full strength in the scapular stabilizers and rotator cuff to balance the deltoid force couple. This is accomplished with rest, hot and cold modalities, massage, nonsteroidal antiinflammatories, and selective injection. Directed physical therapy and home treatment programs are beneficial. Various authors have recommended from 6 to 18 months of conservative care prior to consideration of operative intervention.

Operative Indications for Arthroscopic Subacromial Decompression

  1. Primary extrinsic impingement with type II or III acromion or coracoacromial ligament calcification. Clearly, this patient population has the most predictable success with either the open or arthroscopic operation.
  2. Secondary impingement with associated bony changes in conjunction with arthroscopic stabilization for anterior instability.
  3. Elderly patients with bony changes and full-thickness rotator cuff tears. If the cuff can technically be repaired and the patient can comply with the postoperative rehabilitation, then studies would indicate that the final outcome will be more favorable if this is performed either arthroscopically, mini-open, or as an open procedure with the ASAD. Unrepairable massive tears may also respond to decompression, as demonstrated by Rockwood for open procedures.28 When associated, however, with significant glenohumeral degenerative arthritis or superior migration of the humeral head, decompression is not recommended and maintenance of the coracoacromial arch with implantation of an oversized humeral hemiarthroplasty may prove more successful.
    In conjunction with arthroscopic or mini-open rotator cuff repair.

Indications for Bursectomy, CA Ligament Release, and Resection

  1. Younger patients with type I acromion but unresponsive subacromial pain and/or snapping with abduction and rotational maneuvers.
  2. Calcific tendinitis of the supraspinatus or subscapularis when associated with type III acromion.

Contraindications

  1. Secondary impingement with underlying instability in a young athlete with a type I acromion.
  2. Psuedoimpingement syndrome.
  3. Anterior subcoracoid impingement.
  4. Isolated AC osteolysis.
  5. Undersurface partial cuff tears with normal subacromial bursa and benign bony architecture.
  6. Association with massive rotator cuff tears and significant degenerative arthritis of the glenohumeral joint.

OPERATIVE TECHNIQUE

Careful preoperative evaluation is necessary to determine the appropriate operative approach and to avoid complications. Outlet and axillary views are the key to evaluating the acromion. The outlet view is utilized to determine the shape of the acromion (type II or type III) and the overall thickness.22,29 On the outlet view, lines are drawn on the undersurface of the acromion—one from the front tip of the acromion to the posterior edge, and a second line along the posterior half of the undersurface of the acromion extending out anteriorly. The distance between these two lines at the anterior margin approximates the amount of undersurface anterior bone that will be resected (Fig. 2.1.10).

Figure 2.1.10. Preoperative planning for ASAD. a, cutting block line.

The axillary view is used to determine the shape of the acromion (cobra versus square tipped) and whether there is any anterior acromial protruberance. If present, this protuberance will need to be resected at the time of coracoacromial ligament release.

If on the outlet view one notes a very thin or curved acromion, the cutting block line on the undersurface of the posterior half of the acromion may actually exit the superior aspect of the acromion, taking off too much anterior bone (Fig. 2.1.11). In these cases, the cutting block technique, as described by Sampson et al,11 would be inappropriate. Instead, the lateral approach (described below) would be more applicable, removing just a small anterior hook and not producing a type I flat acromion.

Figure 2.1.11. Thin curved acromion where cutting-block technique would not be appropriate. a, Original cutting-block line. b, Modified cut resecting only anterior hook, preserving deltoid fascia and not producing a type I flat acromion.

Poor visualization in the subacromial space is one of the more frustrating aspects of either approach and is usually secondary to either excessive bleeding or inadequate debridement of the subacromial space. Use of electrocautery is strongly recommended. Other strategies to control bleeding during arthroscopic subacromial decompression include the following:

  1. Inject 0.25% bupivacaine with epinephrine into the portals (2 cc) and subacromial space (10 cc) at the beginning of the case.
  2. Incise skin only and avoid deeper muscle laceration.
  3. Use a blunted conical trocar for penetration of muscle, joint, and subacromial space.
  4. Add epinephrine, 10 mL (1:1,000) per 3-L bag to first irrigation bag only.
  5. Avoid debridement of anterior medial acromion and the undersurface of the AC joint until late in the case.
  6. Use electrocautery immediately when significant bleeders are encountered.
  7. Increase inflow with large-bore sheath at scope. A pump with independent control of pressure and flow rate is helpful.
  8. Decrease outflow to maintain pressure. Control suction on shavers and burrs to reduce “red out.” Integrated fluid delivery and shaver systems are helpful for this problem.
  9. 9. Reduce blood pressure if medical condition allows, to maintain systolic pressure of less than 95 to 100 mm Hg.
  10. 10. Increase pressure on pump and elevate bags to level where bleeding is well controlled.

Operating Room Setup (Fig. 2.1.12)

I perform the procedure in an outpatient setting with the patient in the lateral decubitus position. I use general anesthesia. I don’t routinely use an interscalene nerve block, but this may ensure better postoperative pain control. The procedure may also be done in a beach-chair position with regional anesthesia as per surgeon preference.

The table is turned approximately 100 to 110 degrees from the anesthesiologist, who is then situated at the patient’s abdomen. Long anesthesia tubing is required. The TV monitor tower with contained video equipment is positioned directly anterior to the patient’s head and chest. The shoulder holder is attached to the operating table on the anterior side of the body near the foot. The inflow pump is positioned so that it can be observed by the surgeon during the procedure.

Figure 2.1.12

Patient Preparation

The patient is positioned in the modified lateral decubitus position as described by Gross and Fitzgibbons.30 This position rolls the patient back 25 to 30 degrees, placing the glenoid orientation parallel to the floor (Fig. 2.1.13). The patient is placed in the beanbag with the U position toward the head and the tails extending to the superior-anterior and posterior chest cephad to the axilla for support. The shoulder is isolated with large plastic U drapes, and traction is applied to the patient’s arm. An axillary roll and appropriate head support is utilized. The arm is positioned at approximately 30 degrees of abduction and 10 degrees of flexion with 7 to 15 pounds of traction applied depending on the patient’s size and muscularity. A second dual-traction apparatus may be applied if a stabilization procedure needs to be performed.

Figure 2.1.13A - Patient position with appropriate support for head and axillary roll.

Figure 2.1.13B - Roll-back position (Gross30 with permission)

PROCEDURE

Glenohumeral Diagnostic Arthroscopy

The anatomy of the shoulder is outlined with a marking pen prior to the operative procedure and the portals marked. The glenohumeral joint is then examined completely from both a posterior and a high anterior portal, established inside out at the superior aspect of the rotator interval. This will later be the anterior portal for the subacromial bursoscopy. Any pathology within the glenohumeral joint is appropriately addressed.

Figure 2.1.14.

Partial undersurface or small complete rotator cuff tears are frequently marked with a tag suture placed through an 18-gauge needle introduced from superiorly into the joint and retrieved out the anterior portal (Fig. 2.1.14). This suture marker is beneficial later when subacromial bursoscopy is performed, as it provides a quick reference to the questionable cuff area from the superior view. The scope is then removed from the glenohumeral joint and through the same posterior skin portal, redirected at a 10-degree caudad angle to the acromion into the subacromial bursa and far enough anteriorly to enter the chamber. If the bursa is easily entered and distended, then the inflow is brought in at the scope with a pump and a lateral portal is then made on the basis of an accurately placed 18-gauge needle.

If the bursa is significantly inflamed or not easily distended, with poor visualization, then the scope trocar and sheath is brought directly out anteriorly just lateral to the coracoacromial ligament to exit from the previously made high anterior skin portal. The outflow cannula is then placed on the tip of the trocar and pushed back into the subacromial space so that it lies under the anterior half of the acromion. The sheath is separated slightly, the scope is inserted into the posterior cannula, and flow and visualization are established. A lateral portal is then directed with an 18-gauge needle.

The bursa is then viewed from posteriorly and debrided from the lateral portal until good visualization is established. Any suspicious areas of the rotator cuff that may have been previously identified with a suture marker are debrided and examined from both the posterior portal and the lateral portal.

Lateral Approach for Subacromial Decompression

Preoperatively I will have decided whether I am going to use a modified lateral approach or a cutting-block approach for the decompression. If the patient has a thin curved acromion and a lateral approach is appropriate, I place my lateral portal 3.5 to 4 cm lateral to the acromion and about midway between the midportion of the acromion and the anterolateral corner. I make sure with an 18-gauge needle that I can get the shaver along the anterior-inferior edge of the acromion and a short distance down the anterolateral side, and that it can be directed slightly upward at the acromion for ease in burring and shaving.

The undersurface of the anterior half of the acromion is then debrided with an aggressive shaver and/or a cautery ablation system (Fig. 2.1.15). Care should be taken with either instrument to stay on the undersurface of the bone and not pop off anteriorly or laterally into the deltoid fibers, which are very vascular. The anterolateral corner of the acromion is identified with an 18-gauge needle directed from superiorly, and the debridement is started at this point and progresses medially toward the AC joint and also posteriorly.

Figure 2.1.15.

From the preoperative planning, the amount of bone to be resected is known, as is the diameter of the burr. Starting at the anterolateral corner, the appropriate amount of anterior hook is resected from anterior to medial. Care is taken not to remove full-thickness bone anteriorly and thereby detach the anterior deltoid fascia. This cannot be subsequently repaired as in open operative procedures. After the anterior bone is resected from lateral to medial, tapering of the remaining posterior bone is then accomplished from anterior to posterior to the midportion of the clavicle, or the scope can be placed laterally and the shaver introduced posteriorly to taper from posterior to anterior. Because of the thin and curved nature of the acromion, the goal is not to produce a completely flat undersurface but to perform a smooth and even taper (Fig. 2.1.16). Whether one tapers from anterior to posterior or posterior to anterior, the scope is always placed laterally to evaluate the decompression in two planes.

Figure 2.1.16A Preoperative outlet x-ray of think curved acromion with exuberant osteophyte.

Figure 2.1.16B Postoperative x-ray of anterior osteophyte and hook resection. Note increased anterior acromial-humeral distance in spite of nonflat acromial undersurface.

If there is no evidence of degenerative disease of the AC joint and no inferior osteophytes, I do not take the decompression into the joint or bevel it. If inferior osteophytes are present, then the undersurface of the AC joint is exposed and the osteophytes removed. Manual pressure from above will then deliver a portion of the distal clavicle to view and if it is noticeably arthritic, an arthroscopic distal clavicle resection can be performed. If the articular cartilage looks healthy, then the beveling alone would be performed.

Following adequate decompression, the pump pressure is reduced and hemostasis is obtained with the electrocautery unit. The subacromial space is then instilled with 10 cc of 0.25% bupivacaine with epinephrine and then 1 to 2 cc in each incision. The portals are closed with 4-0 nylon and a sterile dressing is applied.

Postoperative Care

Immediate postoperative motion is allowed and encouraged. No sling is utilized. On the first postoperative day, passive and active motion is encouraged to avoid the possibility of developing an adhesive capsulitis or captured shoulder, as described by Gross’s group.31 Patients are allowed to return to sedentary work as soon as possible. Heavy manual labor usually requires a slower progression and may take from 6 to 12 weeks.

RESULTS

I routinely utilize a two-portal cutting-block technique as described by Sampson et al.11 Although I orient the acromion on the top of the screen when I am in either the posterior or lateral portal, the principles of the procedure still apply. I have found this technique to be considerably more reproduceable and reliable than the traditional lateral approach as described herein and by Ellman8 and utilize it for at least 95% of my subacromial decompressions. On the rare occasions where a thin, broad, and curved acromion is encountered, then the cutting-block technique is inappropriate. The lateral approach as described above is still utilized with success.

REFERENCES

1. Neer CS. Anterior acromioplasty for chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg 1972;54A:41-50.

2. Neer CS. Impingement lesions. Clin Orthop 1983;173:70-77.

3. Hawkins RJ, Brock RM, Abrams JS, et al. Acromioplasty for impingement with an intact rotator cuff. J Bone Joint Surg 1986;70B:795-797.

4. Hawkins RJ, Kennedy JC. Impingement syndrome in athletes. Am J Spans Med 1980;8:151-158.

5. Rockwood CA Jr. Surgical treatment of the shoulder impingement syndrome: a modification of the Neer anterior acromioplasty in 71 shoulders. Orthop Trans 1990;14:251.

6. Bigliani LU, Delessandro DF, Duralde XA, et al. Anterior acromioplasty for subacromial impingement in patients younger than 40 years of age. Clin Orthop 1989;246:111-116.

7. Johnson LL. Shoulder arthroscopy. In: Johnson LL, ed. Arthroscopic surgery: principles and practice. St. Louis: CV Mosby, 1986;1371-1379.

8. Ellman H. Arthroscopic subacromial decompression: analysis of one to three year results. Arthroscopy 1987;3:173-181.

9. Esch J, Ozerkis LR, Helgager JA, et al. Arthroscopic subacromial decompression: results according to the degree of rotator cuff tear. Arthroscopy 1988;4:241-249.

10. Paulos LE, Franklin JL. Arthroscopic shoulder decompression development and application—five year experience. Am J Sports Med 1990; 18:235-244.

11. Sampson TG, Nisbet JK, Glick JM. decision acromioplasty in arthroscopic subacromial decompression of the shoulder. Arthroscopy 1991;7:301-307.

12. O’Boyle M, Newton PM, Arroyo JS, et al. Arthroscopic resection of the anterolateral and of the coracoacrornial ligament for impingement in the overhead athlete. Paper presented at the 16th Annual Meeting of the Arthroscopy Association of North America, San Diego, California, April 1997.

13. Codman EA. Rupture of the supraspinatus tendon and other lesions in or about the subacromial bursa. In: The shoulder. Boston: Thomas Todd, 1934;73-75.

14. Rathbun JB, McNab I. The microvascular pattern of the rotator cuff. J Bone Joint Surg 1970;52B:540-553.

15. Moseley HF, Goldie I. The arterial pattern of the rotator cuff on the shoulder. J Bone Joint Surg 1963;45B:780-789.

16. Rothman RH, Parke WW. The vascular anatomy of the rotator cuff. Clin Orthop 1965;41:176-186.

17. Nirschl RP. Rotator cuff tendinitis: basic concepts of pathoetiology. Instr Course Lect 1989;38:439-445.

18. Hibe FW, Kvitne RS, Giangarra CE. Shoulder pain in the overhand or throwing athlete: the relationship of anterior instability and rotator cuff impingement. Orthop Rev 1989;18:963-975.

19. Walsch G, Boylau P, Noel E, et al. Impingement of the deep surface of the supraspinatus tendon on the posterior superior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg 1992; 1:238-245.

20. Jobe CM. Posterior superior glenoid impingement: expanded spectrum Arthroscopy. 1995;11:530-536.

21. Gerber C, Terier F, Ganz R, The role of the coracoid process in chronic impingement syndrome. J Bone Joint Surg 1985; 678:703-708.

22. Gartsman GM. Arthroscopic acromioplasty for lesions of the rotator cuff. J Bone Joint Surg 1990;72A: 169-180.

23. Bigliani LU, Morrison DS, April EW. The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 1986;10:216.

24. Rockwood CA Jr, Lyons FR. Shoulder impingement syndrome: diagnosis, radiographic evaluation, and treatment with a modified Neer acromioplasty. J Bone Joint Surg 1993;75A: 409-424.

25. Edelson JG, Luchs J. Aspects of coracoacrornial ligament anatomy of interest to the arthroscopic surgeon. Arthroscopy 1995;11:715-719.

26. Gallino M, Vatiston B, Annaratone G, et al. Coracoacromiol ligament: a comparative arthroscopic and anatomic study. Arthroscopy 1995;ll:564-567.

27. Esch JC, Baker CL. Rotator cuff disease and impingement. In: Whipple TL, ed. Arthroscopic surgery—the shoulder and elbow. Philadelphia: JB Lippincott, 1993:161-163.

28. Rockwood CA Jr. Shoulder function following decompression and irrepairable cuff lesions. Orthop Trans 1984;8:92.

29. Wuh HCK, Snyder SJ. Modified classification of the supraspinatus outlet view based on the configuration and the anatomical thickness of the acromion. Paper presented at the Fifty-Ninth Annual Meeting of the American Academy of Orthopedic Surgeons, Washington, DC, February 1992.

30. Gross RM, Fitzgibbons TC. Shoulder arthroscopy: A modified approach. Arthroscopy 1985;1:156-159.

31. Mormino MA, Gross RM, McCarthy JA. Captured shoulder a complication of rotator cuff surgery. Arthroscopy 1996;12 457-461.


Publications – Surgical Techniques for the Shoulder and Elbow

Arthroscopic Subacromial Decompression
Posterior (Cutting Block) Approach

Indications

  1. Primary extrinsic impingement syndrome with subacromial bursitis and/or cuff tendinosis with type II or III acromion.
  2. Chronic secondary impingement with adaptive pathologic sub-acromial bony/soft tissue changes (e.g., anterior acromial traction spur or undersurface acromial fraying or bursal cuff degeneration).
  3. Lack of response to diligent conservative treatment program including scapular and rotator cuff retraining, non-steroidal anti-inflammatory drugs, subacromial injection, and activity modification for 6 to 12 months.

Contraindications

  1. Secondary impingement with underlying subluxation.
  2. Internal posterior-superior impingement with/without superior labrum anterior and posterior (SLAP) lesion.
  3. Anterior subcoracoid impingement.
  4. Pseudo-impingement.

Mechanism of Injury

Elevation of arm abuts the greater tuberosity against the prominent anterior acromial hook or coracoacromial spur, resulting in inflammation and bursal side degeneration/tearing of the rotator cuff and/or biceps tendon.

Physical Examination

  1. Pain with impingement maneuvers (Neer and Hawkins signs) relieved with subacromial injection of lidocaine.
  2. Tenderness to palpation of anterior acromion and anterior and superior cuff when arm is extended.
  3. Pain with resisted abduction and flexion (cuff tendinosis) and/or positive Speed’s test (biceps tendinosis).

Diagnostic Tests

  1. Standard shoulder radiographs including outlet, glenohumeral anteroposterior (AP), axillary, and acromioclavicular (AC) views to evaluate acromial morphology and AC disease.
  2. Magnetic resonance imaging, arthrogram, or ultrasound may be utilized to further evaluate rotator cuff and biceps tendon.
  3. Selective lidocaine injections into subacromial space versus AC joint versus bicipital groove to delineate pathology.

Special Considerations

Impingement symptoms in younger patients with benign bony morphology are likely secondary to underlying scapular or cuff/deltoid muscle imbalance or glenohumeral instability, and these problems should be addressed prior to consideration of arthroscopic subacromial decompression. Success with arthroscopic subacromial decompression (ASAD) can only be expected with extrinsic primary impingement, or chronic secondary as noted above.

Preoperative Planning and Timing of Surgery

  1. Outlet and axillary views are key to evaluating the acromion. AP of AC joint and axillary views are key for the AC joint.
  2. Determine the shape (should be type II or III or you are likely performing an inappropriate procedure) and thickness of acromion on outlet view. Draw two lines: one on the undersurface of the acromion from the front tip to the back edge; a second line along the posterior one half of the undersurface of the acromion extending through the anterior acromion. The distance between these two lines approximates the amount of undersurface anterior bone that will be resected (Fig. 10-1A).
  3. Figure 10-1 A. Radiographs allow determination of the shape and thickness of the acromion on the outlet view.

  4. Visualize the AC joint and acromion on the axillary view to determine the amount of anterior acromial protuberance that extends anterior to the AC joint. This approximates the amount of bone that will be taken off anteriorly :is one resects the AC spur in addition to the undersurface bone (Fig. 10-1B).
  5. Figure 10-1 B. The axillary view allows determination of the amount of a interior acromial rotuberance that will be removed. Co=coracoid, Cl=clavicle, Ac=acromion, H=humerus

  6. It is important on the outlet view to evaluate the thickness and shape of the acromion because those that are very thin and curved will not be candidates for the “cutting block” technique as too much bone would be resected, risking acromial fracture or deltoid detachment. A limited resection of the anterior hook would he more appropriate in these cases (Fig. 10-2).

Figure 10-2. In cases with a very thin and curved acromion, a limited resection of the anterior hook is more appropriate.

Special Instruments

  1. An arthroscopic eIectrocautery/ablation device is strongly recommended in the subacromial space to control hemorrhage, improve visualization, and aid in removal of soft tissue.
  2. A high-torque bone-cutting burr greatly facilitates anterior acromial resection.
  3. Anesthetic Options: General anesthesia. Scalene block.

Patient and Equipment Position

  1. Lateral decubitus.
  2. Anesthesia anterior to the abdomen for 180-degree surgical access to the superior shoulder with careful axillary and peroneal padding.
  3. Arm abducted 30 degrees and flexed 10 to 15 degrees with 7 to 15 pounds of distraction, depending on the patient’s body habitus.
  4. Patient rolled back 25 degrees to get the plane of the glenoid parallel to the floor.
  5. Beach chair position (alternative)

Surgical Approach

  1. After an exam under anesthesia and a thorough arthroscopic glenohumeral exam from both a standard posterior and high anterior approach, the scope is removed and redirected at a 15-degree caudad angle to the acromion. The scope is placed far enough anteriorly (under the anterior one half of the acromion) to enter the bursal chamber that is distended.
  2. With scope and flow posterior and outflow through anterior cannula (placed through previous high anterior portal with Wissinger rod), a lateral working portal is established 3 to 4 cm from the lateral border of the acromion, slightly anterior to the midpoint of the acromion and directed slightly upward so the shaver/ablator does not impinge on the lateral cortex.
  3. Define anterior one half of the bony acromion with shaver and cautery/ ablation from the lateral portal. Ablate or transect the coracoacromial ligament with the cautery unit or shaver and resect the anterior 3 to 4 mm of acromial bone from the anterolateral corner to the AC joint with burr. Also thin down the lateral border of the anterior one half of the acromion tapering posteriorly (Fig. 10-3). Eighteen-gauge needles at the anterolateral corner and AC joint aid in orientation.
  4. Figure 10-3. Remove the anterior 3 to 4 mm of acromion from the anterolateral corner to the AC joint. Thin down the lateral border of the anterior one half of the acromion, tapering posteriorly. (HH=humeral head, Ac=acromion, CL=clavicle, Co=coracoid.)

  5. Place scope in lateral portal to view arch of acromion and introduce burr through posterior portal directly on undersurface of posterior one half of the acromion. Using this as a “cutting block” the burr is advanced anteriorly with a sweeping motion medially to laterally (Figs. 10-4)
  6. Figure 10-4. The burr is advanced anteriorly using the posterior half of the acromion as a cutting block to remove the bone with a sweeping motion medially to laterally.

  7. The anterior hook of the acromion is resected and the undersurface flattened in AP plane (Figure 10-5). Take care not to advance the burr anteriorly into deltoid fibers or fascia (by sweeping more medially after flattening the acromion, the inferior portion of the clavicle can be excised if one desires to perform a concomitant Mumford distal clavicle resection).
  8. Figure 10-5. The anterior hook of the acromion is resected and the undersurface flattened in the AP plane.

  9. The scope is then placed posteriorly to view the acromion and ensure it is flat in the medial-lateral plane (Fig. 10-6). One can also view a burr from an anterior AC portal, resecting the superior remaining clavicle while performing a Mumford.
  10. Figure 10-6. The scope is placed posteriorly to view the acromion and ensure that it is flat in the mediolateral plane.

  11. The flow pressure is reduced and hemostasis obtained with the electrocautery unit.

Postoperative Care and Rehabilitation

  1. A simple absorptive sterile dressing is applied to the skin with foam tape and ice is used intermittently for 36 hours. Immediate active and passive range of motion and daily activities are allowed as tolerated, with sling usually not utilized unless associated cuff repair performed.
  2. Scapular stabilization and cuff exercises arc instituted at week 1.

Tips and Pearls

  1. Take care to keep the burr tightly on the undersurface of the posterior one half of the acromion as one comes forward on the “cutting block.” If portal is too low or soft tissue gets interposed posteriorly, the burr may falsely angle upward, resulting in excess anterior bone resection and risking subsequent acromial fracture or deltoid detachment (Fig. 10-7).
  2. Figure 10-7. Keep the burr flat against the undersurface of the posterior acromion to avoid incorrect resection angle.

  3. Resect 3 to 4 mm of anterior acromial bone from the anterolateral corner of the acromion to the AC joint and taper back along the lateral aminion from the lateral portal before placing the burr posteriorly to use the “cutting block.” This clearly outlines the bony anatomy, improves visualization, and lessens the potential for inaccurate resection (Fig. 10-3)
  4. If the AC joint is asymptomatic preoperatively and has no inferior osteophytes or degenerative changes on X-ray, an effort should be made not to violate the inferior capsule or joint as this may destabilize the joint and a percentage of these may become symptomatic postoperatively. If the AC joint is degenerative or has prominent inferior osteophytes, then beveling the inferior tip of the clavicle (co-planing) or arthroscopic distal clavicle resection (Mumford) is appropriate.

Suggested Readings

  • Gartsman GM. Arthroscopic acromioplasty for lesions of the rotator cuff. J Bone Joint Surg Am 1990;72:169-180.
  • Gerber C. Terrier F, Ganz R. The role of the coracoid process in the chronic impingement syndrome. J Bone Joint Surg Br 1985;B7:703-708,
  • Jobe KW, Kvitne KS, Giangarra CE. Shoulder pain in the overhand or throwing athlete: the relationship of anterior instability and rotator cuff impingement. Orthrop Rev 1989;18:963-975.
  • Neer CS. Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone joint Surg Am 1972:54:41-54.
  • Sampson TG, Nisbel JK, Glick JM. Precision acromioplasty in arthroscopic subacromial the decompression of the shoulder. Arthroscopy 1991;7;301-307.
  • Walch G, Boilean P, Noel E, Donell ST. Impingement of the deep surface of the supraspinatus tendon on the posterior or superior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg 1992;l:238-245.

Publications – Current Techniques in Arthroscopy

The technique of arthroscopic subacromial decompression (ASAD) and distal clavicle resection has become an increasingly common procedure for dealing with impingement and acromioclavicular (AC) joint disease. Many surgeons are now routinely combining these arthroscopic decompression techniques with either mini-open or, more recently, completely arthroscopic repair of rotator cuff tears. As with other open operations that have evolved arthroscopically, the learning curve for these procedures is significant and should not be underestimated.

Complications associated with shoulder arthroscopy in general are low. Small, in his 1986 study [1], found a complication rate in subacromial space surgery of 0.76%. However, the complication rate with anterior staple capsulorraphy was 5.3%. The rates excluded clinical failures. In his follow-up study in 1988 [2,3], reporting on complications relating to arthroscopy performed by experienced arthroscopists, the complication rate with shoulder arthroscopy was 0.7% overall, again with the highest rate in anterior capsulorraphy.

Curtis et al. [4] reviewed 711 shoulder arthroscopies and found an overall complication rate of 6%. Of the 43 complications, 19 were secondary to postoperative stiffness, six secondary to transient neurologic symptoms, five associated with wound hematomas, and six associated with bruising. One patient each had problems with hardware removal, reflex sympathetic dystrophy, laceration of the cephalic vein, pulmonary embolus, and painful posterior portal, corneal abrasion, and heterotopic bone. The rate increased from 4.5% for arthroscopic procedures to 8.0% for combined arthroscopic and open surgery (i.e., mini-open cuff repair or stabilization).

Several of the complications associated with shoulder arthroscopy are related to arthroscopic technique in general and are common to other joints that are arthroscopically examined [5]. In a survey sent to arthroscopy association members of the shoulder study group, however, some procedure-specific complications were also identified [6]. This chapter identities some of the difficulties inherent in these arthroscopic techniques and provides some suggestions for precautions and modifications that may help in their avoidance.

TECHNIQUE-RELATED COMPLICATIONS

Neurologic
For the most pant, neurologic complications have been associated with the lateral decubitus position for shoulder arthroscopy (Fig. 12-1). Neuropraxia involving traction injury to the brachial plexus may be secondary to the traction weight, direction of pull, and duration of the surgery. Five to 10 Ibs of distal traction is usually adequate for the average patient, and 15 Ibs is reserved for larger or well-muscled individuals. Increasing the weight to 20 Ibs or more, as was initially done in shoulder arthroscopy, results in changes in the somatosensory-evoked potentials of the musculocutaneous, median, ulnar, and radial nerves, with the musculocutaneous being the most sensitive at all arm positions and traction weights [7].

In a cadaver study, Klein et al. [8] demonstrated the greatest brachial plexus strain with the arm at 70° abduction and 30° of forward flexion. The minimum overall strain was noted at 90° of flexion and 0° of abduction, but this resulted in poor visualization. They recommended positions of 45° of forward flexion and either 0° or 90° of abduction, depending on the intra-articular region of interest.

Figure 12-1. The lateral decubitus position (solid) with necessary padding and support, and the dual traction technique (dotted) with the same padding and 7-10 lbs lateral distraction.

Dual traction as described by Gross and Fitzgibbons [9] (see Fig. 12-1) with low distal traction weights on a minimally abducted arm coupled with a laterally directed distraction force appeared to be associated with less compromise to somatosensory-evoked potentials in Pittman et al.’s study [7]. Gross and Fitzgibbons [9] also recommended rolling the patient back about 25° to 30° to orient the glenoid joint surface parallel to the floor. The rollback position coupled with 15° of additional flexion of the arm puts the direction of pull into Klein et al.’s safer zone [8]. No work has been specifically directed at determining the neurologic effects of the laterally directed distraction force in this set-up, but no reported complications have been associated with this type of traction.

For arthroscopic surgery in the subacromial space, minimal abduction (15° to 25°) and 15° of flexion from the rollback position opens up the space and yet does not put excessive strain on the brachial plexus. Excessive forward flexion of the arm brings the tuberosity into contact with the anterior acromial hook, making exposure difficult.

Careful attention needs to be given to the position of the head, which should be as close to exactly neutral as possible. Any sagging of the head down and away from the operative arm increases the strain on the brachial plexus. Overcompensation and excessive propping of the head away from the “down” arm can result in the opposite brachial strain. Careful padding and wrapping of the traction device at the wrist are necessary to avoid compression injury to the sensory branch of the radial nerve with resultant thumb numbness. Moreover, careful padding of the ulnar and peroneal nerves on the downside is necessary [10]. Time in traction is also a factor, and conversion to an open operation is recommended if the operation is extending past 2 hours or if distention is becoming severe.

The beach-chair position alleviates most of the neurologic concerns already stated [11], but careful positioning and support of the head are still necessary. A case of hypoglossal nerve injury has been reported with this position [12]. Exposure in the subacromial space, however, may be diminished because of loss of distraction. The dual traction technique is not possible with this position.

Anesthetic
General anesthesia provided to the patient in the lateral decubitus position appears safe relative to hypotensive and neurologic problems, so long as proper padding has been established. Interscalene nerve blocks are commonly used for either intraoperative anesthesia or additional postoperative pain relief. A temporary ipsilateral phrenic nerve palsy routinely results from this block but rarely causes pulmonary problems except in patients with preexisting pulmonary insufficiency [13,14].

Esch and Baker [15], however, reported on two patients requiring ventilatory support after interscalene block for ASAD. The anesthesia literature documents various relatively significant complications with interscalene blocks, including bilateral spread affecting both phrenics; complete spinal, bilateral cervical, and thoracic epidural blockade; prolonged Horner’s syndrome; auditory disturbance; and cardiac arrest [16-22]. Pneumothorax caused by incorrect needle placement has also been reported [23]. Complications associated with interscalene block appear to be more common when the block is performed after induction of a general anesthetic as opposed to when the patient is awake and a nerve stimulator has been used.

PORTAL PLACEMENT

Direct nerve injury can be associated with incorrect portal placement.

Posterior Portals
The traditional posterior portal as described by Andrews et al. [24] has become the standard position for the initiation of glenohumeral and subacromial arthroscopy. This penetrates the so-called soft spot approximately 1 cm medial and 1 to 2 cm inferior to the posterolateral corner of the acromion. The arthroscope should enter the joint approximately in the interval between the infraspinatus and teres minor muscles. This portal passes through the deltoid, ranging from 2 to 4 cm from the axillary nerve and the posterior humeral circumflex artery, and lies approximately 1 cm lateral to the suprascapular nerve and artery.

Inferior medial migration of this portal as described by Wolf [25] for the central posterior portal or inferior lateral migration for his modified posterior portal [26] places these structures at greater risk. Directing a blunted conical trocar toward the coracoid process provides some increased margin of safety for these posterior portals. Sharp trocars should generally be avoided for shoulder arthroscopy because of the increased risk of neurologic and chondral damage.

Anterior Portals
Several anterior shoulder arthroscopic portals have been described [24,25,27-30]. The anterior superior portals as described by Andrews et al. [24] and Wolf [25,26] and the superolateral portal described by Laurcncin et al, [30] are neurologically safe and most useful for subacromial surgery. They are also readily used to provide an anterior viewing portal for glenohumeral work. The central anterior portal in the superior recess above the subscapularis tendon as described by Matthews et al. [27] also appears to be safe relative to neurovascular structures. As the surgeon moves inferior to the tip of the coracoid process, the risk to neurovascular structures increases. These portals as described by Wolf (anterior-inferior portal) [25], Resch el al. [28], and Davidson and Tibonc [29] (anterior-inferior transubscapular) are more useful for arthroscopic instability surgery and are not generally used for subacromial or rotator cuff work (Fig. 12-2).


.

.

Figure 12-2.
External (A) and arthroscopic (B) views of the anterior portals, including the superolateral [30], anterior-superior [25], anterior [24], central anterior [27], anterior-inferior [25], and anterior-inferior trans-subscapular [28, 29] portals.

Superior Portal
The supraclavicular fossa portal was devised by Neviaser [31]; it allowed placement of an additional inflow portal at the posterior superior aspect of the joint, as well as access for superior instrumentation. The suprascapular nerve and artery lie deep and on the inferior surface of the supraspinatus muscle, approximately 2 cm medial to the path of the cannula. Too vertical a passage can injure the suprascapular nerve and artery; too lateral a passage can injure the rotator cuff tendon, particularly if the arm is abducted more than 30° [32]. This portal is no longer routinely needed or used, particularly for subacromial work (Fig. 12-3).

Subacromial Portals
Multiple subacromial portals have been described for decompression and for AC joint and rotator cuff surgery. These include the traditional posterior portal with angulation of the arthroscope or instrument superiorly into the subacromial bursa, the posterolateral portal [33], the central lateral portal [34], the anterolateral portal, the anterior and posterior AC joint portals [35], and the accessory high portals for anchor placement in rotator cuff surgery (see Fig. 12-3).

Figure 12-3. Subacromial and superior portals, including the posterior 24, posterolateral 33, central lateral 34, 50, anterolateral 33, superolateral 30, anterior-superior 25, anterior and posterior acromioclavicular (AC) 35, and superior 31 portals. Dotted line indicates course of axillary nerve 5cm lateral to the acromial edge.

The neurologic structure most at risk with the use of these portals is the axillary nerve, which traverses the underside of the deltoid muscle approximately 3 to 5 cm from the acromial margin. If the surgeon keeps the skin incision less than 5 cm from the acromion and directs the trocar toward the subacromial space, as opposed to directly down through the deltoid muscle, axillary nerve problems should be avoided [36]. These portals are best set up after preliminary placement and direct visualization of an 18-gauge needle to ensure the proper orientation for shaving or anchor placement.

Vascular
Problems related to hypotension have been associated with arthroscopy done with the patient in the beach-chair position, especially in elderly or hypertensive patients. Adequate fluid replacement and compression leg stockings may be beneficial to avoid premature termination of the procedure or switching to a lateral decubitus position. Although deep venous thrombosis is rare, it has also been reported with shoulder arthroscopy [37].

Likely, the most common vascular complication with subacromial surgery is bleeding. Because the subacromial area is extensively traversed by veins, frequently inflamed, and not a closed space, bleeding is more troublesome here than at almost any other arthroscopic site. Failure to control bleeding and to maintain visualization and orientation are common sources of complications in subacromial surgery. Use of electrocautery is strongly recommended. Strategies currently used for the control of bleeding include:

  • Inject 0.25% bupivacaine with epinephrine into the portals (2 ml) and subacromial space (10 mL) at the beginning of the procedure.
  • Incise only the skin to avoid deeper muscle laceration.
  • Use a blunted conical trocar for penetration of muscle, joint, and subacromial space.
  • Add epinephrine, 10 ml (1:1000) per 3-L bag to only the first irrigation bag.
  • Avoid debridement of anterior medial acromion and the undersurface of the AC joint until late in the case.
  • Use electrocautery immediately when significant “bleeders” are encountered.
  • Increase inflow with large-bore sheath at level of the arthroscope. A pump with independent control of pressure and flow rate is helpful.
  • Decrease outflow to maintain pressure. Control suction on shavers and burrs to reduce “red-out.” Integrated fluid delivery and shaver systems are helpful for this problem.
  • Reduce blood pressure, if the patients’ medical condition allows, to maintain systolic pressure of less than 95 to 100 mm Hg.
  • Increase pressure on pump or elevate bags to level at which bleeding is well controlled.

Pulmonic
Pneumothorax is a known complication associated with interscalene block anesthesia [23]. There have been rare cases of subcutaneous emphysema, pneumomediastinum, and potentially life-threatening tension pneumothorax associated with arthroscopic decompression [38].

Soft-Tissue Injury
Skin burns have been reported with shoulder arthroscopy if a noninsulated cautery tip is used with conductive solution. This problem can be avoided if the surgeon uses an insulated tip, or newer bipolar devices for ablation and cautery. These tips can be used safely even in conductive solutions such as normal saline or lactated Ringer’s solution.

Sterile water, which was used early on because of its nonconductivity, is injurious to soft tissues. Scattered reports exist of skin and muscle necrosis associated with extremely long procedures using water as an irrigating solution. Glycine (1.5%), used in urologic procedures, and less frequently as an arthroscopic medium, has been associated with transient blindness and is no longer recommended [39].

Extravasation and distention of the soft tissues with saline or lactated Ringer’s solution may sometimes produce alarming appearances. Studies have shown, however, that the intramuscular pressures rapidly return to normal at the end of the procedure [40,41]. The effect of soft-tissue distention on the nerves surrounding the shoulder has not been well-documented.

Infection
The infection rate resulting from arthroscopy in general is very low. Johnson et al. [42] reported less than one infection in 2000 new arthroscopies when using 2% glutaraldehyde as a sterilizing agent. Only four infection cases with shoulder arthroscopy have been noted in the literature to date [1,15,43].

Glutaraldehyde solution has been commonly used for instrument sterilization, especially in the outpatient setting. However, instruments must be thoroughly rinsed before use. Even trace amounts (such as may be found in arthroscopic rinse baths) can induce a severe synovial inflammatory reaction [44]. Because of this and because of concerns regarding HIV transmission through the use of glutaraldchyde, sterilization is increasingly being performed by automated sterilization units such as the Steris (peracetic acid; Steris Co, Mentor, OH) [45] or Sterad (gas plasma with hydrogen peroxide;
J & J Medical, Arlington, TX) [46].

Equipment Failure
The potential for an equipment failure increases with the complexity of the procedure. Cannulated suture hooks and punches, various suture retrievers, linear punches, and grasping forceps can break off in the joint. Keeping a retrieval instrument, such as the magnetic Golden Retriever suction device (Instrument Makar, Okemos, Ml), handy can considerably simplify recapture of metallic pieces.

PROCEDURE-RELATED COMPLICATIONS

Arthroscopic Subacromial Decompression
Complications of ASAD include 1) variable bone resection, 2) deltoid detachment, 3) heterotopic bone, and 4) residual coracoacromial ligament (CAL) snapping.

Variable Bone Resection
Variable hone resection is probably the most common complication of ASAD. Both inadequate decompression and excessive resection have been reported. Wolf [47] reviewed 35 patients with failed previous arthroscopic surgery of the shoulder. Of these patients, 60% failed because of previous inadequate ASAD; 20 of 21 had complete recovery after further ASAD [47]. Matthews et al. [27) and Esch [48] have reported on both acromial and clavicular fractures secondary to excessive resection.

Inaccurate decompression is usually secondary to inadequate preoperative planning with or without poor visualization and orientation during the procedure.

Preoperative Evaluation
Outlet and axillary views are key to evaluating the acromion. The outlet view is used to determine the shape of the acromion (type I, II, or III) and the overall thickness [49,50]. Rockwood and Lyons [51] have described a modified anterior shoulder view that, although helpful in making the diagnosis of impingement, is not beneficial in terms of preoperative planning. On the outlet view, two lines are drawn on the undersurface of the acromion – the first from the front tip of the acromion to the posterior edge, and the second along the posterior half of the under-surface of the acromion extending out anteriorly. The distance between these two lines at the anterior margin approximates the amount of undersurface anterior bone that will be resected (Fig. 12-4).

Figure 12-4. Preoperative determination of bone resection shown on an outlet-view radiograph. CAL - coracoacromial ligament. Shaded area between dotted lines denotes bone resection.

The axillary view is used to determine the shape of the acromion (cobra-shaped vs. square-tipped), as well as to determine whether there is any “anterior acromial protuberance” [52] anterior to the level of the AC joint (Fig. 12-5). This approximates the amount of bone that will be removed anteriorly in addition to the amount of bone that will be taken from the undersurface.

Figure 12-5. Preoperative evaluation (axillary view) of anterior acromial protuberance and the amount of resection. Shaded area between dotted lines denotes bone resection.

After these measurements have been determined, the two-portal technique of acromioplasty makes it relatively simple to reproduce this resection. It is difficult to obtain a flat acromion when visualizing only from the posterior portal because of the amount of curving away of the acromion from the arthroscope . The acromion may appear flat from medial to lateral and front to back, but may still have a considerable anterior-to-posterior concavity when later viewed from the lateral portal. Placing the arthroscope laterally and then bringing the shaver forward from the posterior portal using the posterior half of the acromion as a “culling block” [53] helps ensure a straight, flat cut in the sagittal plane. This technique reliably converts a type II or type III acromion to a type I flat surface as demonstrated on postoperative radiographs (Fig. 12-6). The surgeon should be sure to subsequently replace the arthroscope posteriorly and to confirm flatness of the acromion in the medial to lateral plane. The anterior lateral acromial comer is often difficult to visualize from the lateral portal. Good visualization from both portals assures a flat, smooth surface.

Figure 12-6
(A) Preoperative templating for arthroscopic subacromial decompression (ASAD) on outlet- view radiograph. Dolled line indicates correct line of bone resection.
(B) Postoperative radiograph of ASAD.

The surgeon should beware of the thin curved type acromion (type C) [50]. If, on the outlet view, a very thin or curved acromion is found, the cutting block line on the undersurface of the posterior half of the acromion may actually exit from the superior aspect of the acromion, taking off too much anterior bone (Fig, 12-7A) . In such cases, the cutting block technique would be inappropriate. In this situation, the original resection technique as described by Ellinan [33] is more applicable, that is, removing only a small anterior hook and not producing a type I flat acromion (Fig. I2-7B).

Figure 12-7.
Preoperative (A) and postoperative (B) radiographs of decompression on the thin, curved acromion. Dotted line in (A) indicates excessive bone resection with cutting-block technique. Postoperative radiograph demonstrates more conservative anterior resection with significant increase in anterior acromial humeral distance.

Inadequate Visualization
This finding is usually secondary to excessive bleeding (which can be managed as previously outlined), poor localization of the subdeltoid bursa, or inadequate debridement of the subacromial space. Remembering that the bursa is an anterior structure, the surgeon should make every effort when in the subacromial space to direct the arthroscope into what Wuh and Snyder [50] termed the room with a view. Time and care should be spent at the beginning of the procedure, debriding the bursitis and the thickened periosteum on the undersurface of the anterior half of the acromion. Some of the posterior bursal curtain may need to be resected to clearly visualize the bony architecture. Debridement can be done with a shaver-burr, or a cautery-ablation system, but the surgeon should be sure to stay on the acromial bone and not deviate into the deltoid fibers. Debridement should be performed from the anterior lateral corner of the acromion toward, but not into, the AC joint, and then posteriorly along the lateral edge of the acromion. Spinal needles are used in the anterior lateral corner and the AC joint to gain better clarification of the bony landmarks.

A burr should next be used to resect 3 to 4 mL of bone, again along the anterior margin of the acromion from the anterior lateral corner to the AC joint, then tapering posteriorly along the lateral edge of the anterior half of the acromion. This improves orientation and visualization when the arthroscope is placed in the lateral portal and the shaver is brought in posteriorly. The surgeon should not resect too much anterior bone – only enough to make it easy to delineate the anterior edge of the acromion as seen from the lateral portal. The surgeon should let the shaver from the posterior portal resect most of the bone, coming forward in a smooth, controlled, flat cut (Fig. 12-8)The amount of bone resected is easy to determine by comparing the anterior remaining ledge with the thickness of the burr.

Figure 12-8
Serial intraoperative views of arthroscopic subacromial decompression of the right shoulder.
A) Conservative anterior resection from the lateral portal with the shaver tip in the coracoacromial ligament.
B) Lateral view of the burr starting forward during cutting block resection.
C) Completed resection with flat acromial undersurface posterior to anterior and intact deltoid fascia.

The posterior portal (through the deltoid muscle) must be at the inferior edge of the acromion, and not further below with soft-tissue interposition, so that the shaver does not angulate superiorly in an excessive or artificial manner (Fig. 12-9). Although the same placement of posterior skin incision is used for both glenohumeral and subacromial arthroscopy, the burr needs to puncture the soft tissues right at the inferior edge of the acromion for successful two-portal cutting-block technique.

Figure 12-9A
Although the same skin incision is utilized for both the glenohumeral and subacromial examinations, the trocar penetrates the deeper soft tissues at different levels, so the shaver can be closely applied to the undersurface of the acromion.
Figure 12-9B
If portal or soft-tissue penetration is too inferior, the burr will angulate too far superiorly and excess resection will occur.

Deltoid Detachment
Deltoid detachment results from overly aggressive resection at the anterior aspect of the acromion. If no significant anterior acromial protuberance is seen on the axillary radiograph, then simply flattening the undersurface of the acromion will adequately decompress it.

When a protuberance does exist, it usually is an extension of calcification interiorly into the CAL. Resecting the ligament and the contained bone with subsequent flattening of the acromion will usually eliminate the anterior overhang. Routinely resecting 8 to 10 mm of full-thickness anterior bone (as described for open procedures [51]) from the lateral portal puts the deltoid attachment at significant risk. This damage cannot subsequently be repaired unless the shoulder is then opened. The surgeon should take a small amount of anterior bone from the lateral portal and the bulk of the bone from the posterior portal using the cutting-block technique, thus teasing the bone off anteriorly from the fascia. Deltoid detachment, either open or closed, is arguably the most devastating complication of shoulder surgery and should be avoided [54].

Heterotopic Bone
This finding has been reported to be associated with both acromioplasty and AC resection [55,56]. In the 10 cases reported by Berg et al. [55], eight developed recurrent impingement symptoms, with an apparent strong correlation with active spondylitic arthropathy or a profile of hypertrophic pulmonary osteoarthropathy – male, obese, smoker with chronic pulmonary disease. They recommended prophylactic measures (indomethacin or radiotherapy} with these two types of patient groups. The surgeon should also unplug clogged shavers and burrs (or use an accessory gravity drainage portal) to avoid debris (“clouds of snow”).

Coracoacromial Ligament
Continued snapping with abduction and rotation maneuvers from an inadequate resection and a rescarring of the CAL do occur occasionally. After bony decompression has been completed, another 5 to 10 mm of ligament can be resected using a shaver, basket punches, or an ablation device. This is especially appropriate if snapping of the biceps tendon or bursal fold on the CAL is an identifiable preoperative complaint. Partial release of the anterolateral band alone may be curative in some athletes engaged in overhead throwing maneuvers |57]. Care should be taken to avoid excessive release of the lateral extension of the ligament along the lateral edge of the acromion. The ligament and deltoid fascia are intimately connected at this location, and release risks the deltoid attachment [58-].

Resection should not be done in the presence of significant degenerative arthritis of the glenohumeral joint or cuff arthropathy with a massive cuff tear, or if future arthroplasty is contemplated [59].

Arthroscopic Distal Clavicle Resection
Thorough clinical and radiologic evaluation of the AC joint should be performed prior to decompression. Significant inferior osteophytes should be noted on the anteroposterior view, and narrowing and sclerosis (degenerative joint disease) or widening and cystic changes (osteolysis) should be noted on the anteroposterior and axillary views. Differential injection into the AC joint instead of into the subacromial bursa may be necessary to confirm AC involvement.

Depending on the findings listed above, a decision must be made preoperatively (if possible) regarding the AC joint and distal clavicle. The surgeon must decide whether to 1) leave the AC joint untouched, 2) bevel the distal clavicle, or 3) perform an arthroscopic distal clavicle resection.

Most early descriptions of ASAD recommended routine beveling of the distal clavicle [33,60]. However, this practice destabilizes the AC joint to a certain extent by resecting the’ weaker inferior ligaments. The author has seen two patients in his own practice (and anecdotal reports from others) who, after decompression and beveling, developed AC joint pain necessitating later distal clavicle resection. Prior to surgery, these patients appeared clinically and radiographically to have normal AC joint.

If there are significant inferior osteophytes off the clavicle, then there is likely already compromise of the inferior AC ligaments and enough direct irritation of the underlying cuff to warrant beveling the tip. As the beveling is performed, downward pressure on the clavicle will bring some of the articular surface into view. If it appears significantly arthritic, then a complete resection of 1.0 lo 1.5 cm of clavicle should be performed.

However, in patients with AC joints appearing normal on preoperative clinical and radiographic examinations, the author no longer routinely bevels the clavicle; instead, the medial acromial bone is leased off the capsule and cartilage, much as is done with the deltoid fascia during decompression.

Other complications associated with distal clavicle excision relate to )) heterotopic bone formation, 2) inadequate resection, 3) underlying muscle injury, and 4) excessive bleeding. Incomplete resection of the superior cortical bone during distal clavicle resection is not uncommon. Clear visualization of this area using either a 50° or 70° arthroscope is necessary to remove all the superior bone (Fig. 12-10).

Figure 12-10
A) View from the posterior portal looking up at the acromioclavicular (AC) joint (arrowhead) with the inferior half of the distal clavicle already resected from the right shoulder.
B) Posterior view of the AC space with the distal clavicle resected and two spinal needles placed externally to measure the distance between the clavicle tip and the medial edge of the acromion (right).
C) Lateral view of the clavicle resection with the posterior and superior ligaments intact (arrow).

If a conical eggshell of bone is left behind, elevation or cross-chest maneuvers by the patient will remain painful. The bone will also serve as a nidus of heterotopic hone formation (Fig. 12-11).

Figure 12-11
Heterotopic bone formation after distal clavicle resection (right shoulder).
A) Six month follow-up radiograph showing early heterotopic nidus.
B) Two-year postoperative radiograph demonstrating mature bone in the AC interval.

The optimal amount of bone to be removed arthroscopically from the tip of the clavicle remains unresolved. If the superior and posterior AC ligaments are well maintained with the resection, the length of clavicle 10 be removed can be reduced [61 ]. If the superior and posterior ligaments are violated, however, then the remaining tip of the clavicle becomes more unstable, and further resection is needed [62,63«|. Studies suggest that 1 lo 1.5 cm of bone resection would be adequate with use of the arthroscopic technique (Fig. 12-12); 1.5 cm of bone should be resected if the posterior-superior ligaments have been compromised.

Figure 12-12
Preoperative (A) and postoperative (B) radiographs of the acromioclavicular resection (right shoulder).

Care should be taken to measure the distance between the clavicle and the acromion with two 18-gauge spinal needles placed parallel through the skin from above. This should be performed at both the anterior and posterior aspects of the clavicle (see Fig. 12-10B). It is easy to obtain an uneven gap in resection with more bone removed anteriorly than posteriorly, which should he avoided.

Caution should be taken when using unhooded burrs to resect the tip of the clavicle because it is very simple to wrap up the soft underlying cuff musculature in the instrument. The author prefers to use a well-hooded burr with the open side always either facing up or in, toward the cancellous middle of the clavicle. Suction should be low, just sufficient to clear debris.

Vascularity around the tip of the clavicle and AC joint is plentiful. Cauterization of the fat pad beneath the AC joint before debridement is helpful. t is also beneficial to outline the tip of the clavicle frequently with the cautery device when it is being resected medially because periosteal vessels are numerous.

Arthroscopic Rotator Cuff Repair
The rotator cuff should be thoroughly evaluated arthroscopically both from the articular and bursal sides. Partial tears are usually well-managed with limited debridement and ASAD. Excessive debridement of partial tears can lead to complete rotator cuff tears if caution is not exercised. Evaluation is aided by placement of “suture markers” – an 18-gauge needle placed from a superior position through the cuff and into the joint with a #1 monofilament suture grasped in the joint and brought out through the anterior portal as the needle is removed. This allows the investigator to closely examine the exact area on the bursal surface of the cuff that corresponds to the torn area on the articular side. Nearly complete tears that will not heal with adequate strength should he completed and repaired [64|. Several clinical studies have demonstrated that repair of rotator cuff tears in conjunction with ASAD fares better in the long run when compared with simple debridement and decompression [52,64,65].

Failure of fixation of rotator cuff repair is a common problem with both open and arthroscopic repair. This may be due to mechanical factors, biological factors, or both.

Mechanical Considerations
Several factors related to technique can affect the mechanical strength of rotator cuff repair and increase the likelihood of success. Anchor fixation into bone can be improved by roughening the area of the tuberosity widely to increase the surface area for cuff repair, while decorticating lightly. Creation of deep troughs in the soft cancellous bone lead to anchor pull-out (or tunnel breakage during open techniques). St. Pierre et al. [66] demonstrated good healing in animal studies without the need of a deep trough.

Inserting the anchor at about a 45° angle to the direction of pull (Burkhart’s “deadman’s angle”) [67] results in increased resistance to pull-out and puts the anchor under the stronger subchondral bone medially. Recent studies also suggest that simple suture may be stronger than mattress sutures in the fixation of tendon to bone in the rotator cuff area [68].

With the 45° “deadman’s angle” approach to the bone, the suture is pulled at an acute angle, with repetitive tension over the medial lip of the anchor hole. If the edge is too sharp, fraying and breaking of the suture may ensue. If the initial drill has a slight bevel at the stop point or if the hole is subsequently chamfered, the results of this problem may be diminished.

Biologic Considerations
The vascular involvements of rotator cuff repairs in older patients are always in question. Factors that may affect the blood supply to the repair should be kept in mind. Debriding the edges of a rotator cuff back to bleeding tissue stimulates an acute healing response.

Reducing tension on the rotator cuff repair in its early healing phase improves circulation and healing potential. This reduction can be accomplished by fixing small tears where they appear (i.e., more medially than the normal tuberosity attachment). Burkhart has described the principle of “margin convergence” [69] in the reduction of tension on rotator cuff tissue and repairs. By repairing the larger tears with side-to-side sutures medially and then working laterally to fix the remaining Y-shaped or L-shaped tissue to bone using anchors, tension on the repair and susceptibility to anchor pull-out are reduced. This appears to be a valid principle in the author’s practice.

The larger the tear, the more beneficial an abduction pillow may be to improve blood flow to the “critical zone” and again reduce tension on sutures. Careful monitoring of postoperative rehabilitation is essential. The goal is to protect the repair and to avoid development of excessive scar tissue formation in the subdeltoid space – a “captured shoulder,” as described by Mormino et al. [70]. Passive motion is less stressful on the repair in the early phases. Debate exists as to when to allow active abduction; this decision should be influenced by the size, pattern, and vascularity of the tear, as well as the stability of fixation.

Incorrect Diagnosis
Symptoms that persist despite adequate decompression or distal clavicle excision may be secondary to incorrect diagnosis. Decompression in a patient with secondary impingement from underlying anterior instability may often be unsuccessful until the underlying instability has been addressed. Posterior superior impingement is not likely to respond to anterior decompression. Underlying glenohumeral arthritis in weightlifters may negate the beneficial effects of distal clavicle excision for osteolysis. Suprascapular nerve syndrome must be diagnosed using specific neurologic modifications of standard electromyographic technique. A high index of suspicion for this entity must be maintained. Radicular cervical disease, metastatic carcinoma of the scapular neck, Pancost’s tumors of the lung, and referred pain to the shoulder from visceral structures are also part of the differential diagnosis. Postoperative pain associated with a cracking sensation is most likely secondary to a fracture of the acromion.

Norwood and Fowler [71] reported on four cases of recurrent symptoms after technically well-performed shoulder arthroscopy, secondary to persistent cuff tears. These appeared to be related to inadequate healing on the articular side of the tendinous portion of the cuff at the posterior portal site. Because larger cannulae are now being used routinely, this problem may become increasingly noted, both anteriorly and posteriorly. If persistent or recurrent pain and weakness occur after arthroscopy, repetition of the arthrogram may be worthwhile. If results are positive, an open repair is likely to be beneficial.

Inadequate Surgical Preparation
Surgical preparation entails not only physician training, preoperative planning, and equipment requirements, but also patient education. Many patients have unrealistic expectations as to the results that arthroscopic surgery can accomplish relative to the shoulder. Education about soft-tissue healing times and scar tissue maturation should help temper unwarranted enthusiasm and activity. Because pain associated with arthroscopic procedures is often reduced, careful monitoring of postoperative activity, especially with rotator cuff repair, is necessary.

Physician preparation is mandatory for successful surgical results. Training at meetings and cadaver laboratories, such as the Orthopedic Learning Center (Chicago, IL), is prudent before attempting new techniques in one’s practice. These procedures are equipment intensive, and a step-wise progression from open to mini-open to arthroscopic technique is recommended.

CONCLUSION

Arthroscopic subacromial decompression, distal clavicle excision, and rotator cuff repair are demanding operative procedures. It is hoped that diligent preoperative planning and intraoperative attention to the possible complications presented will increase the potential for successful surgical outcomes.

REFERENCES AND RECOMMENDED READING

Recently published papers of particular interest have been highlighted as:

* Of Interest
** Of Outstanding Interest

  1. Small NC, Committee on Complications of the Arthroscopy Association of North America: Complications in arthroscopy: the knee and other joints. Arthroscopy 1986, 2:253-258.
  2. Small NC: Complications in arthroscopic surgery performed by experienced arthroscopists. Arthroscopy 1988, 4:215-221.
  3. Small NC: Complications in arthroscopic surgery of the knee and shoulder. Orthopedics 1993, 16:985-988.
  4. Curtis AS, Delpezio W, Ferkle RD, et al:: Complications of shoulder arthroscopy. Paper presented at the 59th Annual Meeting of the American Academy of Orthopedic Surgeons. Washington, DC; February, 1992.
  5. Bigliani LU, Flatow EL, Deliz DD: Complications of shoulder arthroscopy. Orthop Rev 1991, 20:743-751.
  6. Rogerson JS: Avoiding complications in subacromial surgery. Presented at the AANA Specialty Day at the 61th Annual Meeting of the American Academy of Orthopedic Surgeons. New Orleans, LA; 1994.
  7. Pitman MI, Nainzadeh N, Ergas E, et al.: The use of somatosensory evoked potentials for detection of neuropraxia during shoulder arthroscopy. Arthroscopy 1988, 4:250-255.
  8. Klein AH, Franc JC, Mutschlen TA, et al.: Measurement of brachial plexus strain in arthroscopy of the shoulder. Arthroscopy 1987, 3:45-52.
  9. Gross RM, Fitzgibbons TC: Shoulder arthroscopy: a modified approach. Arthroscopy 1985, 1:156-159.
  10. ** Stanish WD, Peterson DC: Shoulder arthroscopy and nerve injury: pitfalls and prevention. Arthroscopy 1995, 11:458-466.
  11. Excellent analysis of all the different etiologies of nerve injuries, including portal placement, traction set-ups, and anesthesia techniques.
  12. Skyhar MJ, Altchek DW, Warren RF, et al.: Shoulder arthroscopy with the patient in the beach-chair position. Arthroscopy 1988, 4:256-259.
  13. Mullins RC, Drez D, Cooper J: Hypoglossal nerve palsy after arthroscopy of the shoulder and open operation with the patient in the beach-chair position: a case report. J Bone Joint Surg Am, 1992, 74:137-139.
  14. Urmey WF, Talts KH, Sharrock NE: One hundred percent incidence of hemi-diaphragmatic paresis associated with interscalene brachial plexus anesthesia as diagnosed by ultrasonography. Anesth Analg 1991, 72:498-503.
  15. Urmey WF, McDonald M: Hemidiaphragmatic paresis during interscalene brachial plexus block: effects on pulmonary function and chest wall mechanics. Anesth Analg 1992, 74:352-357.
  16. Esch JC, Baker CL: Complications and pitfalls. In Arthroscopic Surgery – the Shoulder and Elbow. Edited by Whipple TL. Philadelphia: JB Lippincott; 1993:221.
  17. Dutton RP, Eckhardt WF, Sunder N: Total spinal anesthesia after interscalene blockade of the brachial plexus. Anesthesiology 1994, 80:939-941.
  18. Gologorsky E, Leanza RF: Contralateral anesthesia following interscalene block. Anesth Analg 1992, 75:311-312.
  19. Tuominen MK, Pere P, Rosenberg PH: Unintentional arterial catheterization and bupivacaine toxicity associated with continuous interscalene brachial plexus block. Anesthesiology 1991, 75:356-358.
  20. Cook LB: Unsuspected extradural catheterization in an interscalene block. Br J Anaesth 1991, 67:473-475.
  21. Edde RR, Deutsch S: Cardiac arrest after interscalene brachial plexus block. Anesth Analg 1997, 56:446-447.
  22. Sukhani R, Barclay J, Aasen M: Prolonged Horner’s syndrome after interscalene block: a management dilemma. Anesth Analg 1994, 79:601-603.
  23. Rosenberg PH, Lamberg TS, Tarkkila P: Auditory disturbance associated with interscalene brachial plexus block. Br J Anaesth 1995, 74:89-91.
  24. Abrams SE, Hogan QH: Complications of nerve blocks. In Anesthesia and Perioperative Complications. Edited by Benumof JL, Saidman LJ. St. Louis: Mosby; 1992:69-70.
  25. Andrews JR, Carson WG, Ortega K: Arthroscopy of the shoulder: technique and normal anatomy. Am J Sports Med 1984, 12:1-7.
  26. Wolf EM: Anterior portals in shoulder arthroscopy. Arthroscopy 1989, 5:201-208.
  27. Wolf EM: Arthroscopic shoulder stabilization using suture anchors: technique and results. Presented at the 15th Annual Meeting of the Arthroscopy Association of North America. Washington, DC; 1996.
  28. Matthews LS, Zarrens B, Micheal RH, et al.: Anterior portal selection for shoulder arthroscopy. Arthroscopy 1985. 1:33-39.
  29. Resch H, Wykypiel HF, Maurer H, et al.: The antero-inferior (transmuscular) approach for arthroscopic repair of the Bankart lesion: an anatomic and clinical study. Arthroscopy 1996, 12:309-322.
  30. Davidson PA, Tibone JE: Anterior-inferior (5 o’clock) portal for shoulder arthroscopy. Arthroscopy 1995, 5:519-525.
  31. Laurencin CT, Deutsch A, O’Brien SJ, et al.: The superolateral portal for arthroscopy of the shoulder. Arthroscopy 1994, 10:255-258.
  32. Neviaser TJ: Arthroscopy of the shoulder. Orthop Clin North Am 1987, 18:361-367.
  33. Souryal TO, Baker CL: Anatomy of the supraclavicular fossa portal in shoulder arthroscopy. Arthroscopy 1990, 6:297-300.
  34. Ellman H: Arthroscopic subacromial decompression. Arthroscopy 1987, 3:173-181.
  35. Paulos LE, Harner CD, Parker RD: Arthroscopic subacromial decompression for impingement syndrome of the shoulder. Tech Orthop 1988, 3:33-39.
  36. Flatow EL, Cordasco FA, McCluskey GM, et al.: Arthroscopic resection of the distal clavicle via a superior portal: a critical, quantitative radiographic assessment of bone removal. Arthroscopy 1990 6:153-154.
  37. Brian WJ, Schauder KK, Tullos HS: The axillary nerve in the relationship to common sports medicine shoulder procedures. Am J Sports Med 1986, 14:113-116.
  38. Burkhart SS: Deep venous thrombosis after shoulder arthroscopy. Arthroscopy 1990, 6:61-63.
  39. Lee HC, Dewan N, Crosby L: Subcutaneous emphysema, pneumomediastinum and potentially life threatening tension pneumothorax: pulmonary complications from arthroscopic decompression. Chest 1992, 101:1265-1267.
  40. Burkhart SS, Barnett CR, Snyder SJ: Transient postoperative blindness as a possible effect of glycine toxicity. Arthroscopy 1990, 6:112-114.
  41. Lee YF, Cohen L, Tooke SM: Intramuscular deltoid pressure during shoulder arthroscopy. Arthroscopy 1989, 5:209-212.
  42. Ogilvie-Harris DJ, Boynton E: Arthroscopic acromioplasty: extravasation of fluid into the deltoid muscle. Arthroscopy 1990, 6:52-54.
  43. Johnson LL, Schneider DA, Austin MD, et al.: Two-percent glutaraldehyde: a disinfectant in arthroscopy and arthroscopic surgery. J Bone Joint Surg 1982, 64(suppl B)237-239.
  44. Ticker JB, Lippe RJ, Barkin DE, et al:: Case report: infected suture anchors in the shoulder. Arthroscopy 1996, 12:613-615.
  45. Harner CD, Mason GC, Few HF, et al.: Cidex induced synovitis. Am J Sports Med 1989, 17:96-102.
  46. Seballos RJ, Walsh AL, Mehta AC: Clinical evaluation of a liquid chemical sterilization system for the flexible bronchoscope. J Bronchology 1995, 2:192-199.
  47. Caputo RA, Fisher J, Jurzynski V, et al.: Validation testing of a gas plasma sterilization system. Med Dev Diagn Ind 1993, 15:132-138.
  48. Wolf EM: Causes of failed shoulder arthroscopy: a review of 35 revision cases. Presented at the 16th annual meeting of the Arthroscopy Association of North America. San Diego, CA; 1997.
  49. Esch JC: Arthroscopic subacromial decompression and post-operative management. Orthop Clin North Am 1993, 24:161-171.
  50. Bigliani LU, Morrison DS, April EW: The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 1986, 10:216-228.
  51. Wuh HCK, Snyder SJ: Modified classification of the supraspinatus outlet view based on the configuration and the anatomical thickness of the acromion. Paper presented at the 59th Annual Meeting of the American Academy of Orthopedic Surgeons. Washington, DC; February 1992.
  52. Rockwood CA Jr, Lyons FR: Shoulder impingement syndrome: diagnosis, radiographic evaluation, and treatment with a modified Neer acromioplasty. J Bone Joint Surg Am 1993, 75(suppl A):409-424.
  53. Gartsman GM: Arthroscopic acromioplasty for lesions of the rotator cuff. J Bone Joint Surg Am 1990, 72:169-180.
  54. Sampson TG, Nisbet JK, Glick JM: Precision acromioplasty in arthroscopic subacromial decompression. Arthroscopy 1991, 7:301-307.
  55. Groh GI, Simoni M, Rolla P, et al.: Loss of the deltoid after shoulder operations: an operative disaster. J Shoulder Elbow Surg 1994, 3:243-254.
  56. Berg EE, Ciullo JV, Oglesby JW: Failure of arthroscopic decompression by subacromial heterotopic ossification causing recurrent impingement. Arthroscopy 1994, 10:158-161.
  57. Snyder SJ, Banas MP, Karzel RP: The arthroscopic Mumford procedure: an analysis of results. Arthroscopy 1995, 11:157-164.
  58. Arroyo JS, Rodosky MW, Pollack RG, et al.: Arthroscopic resection of the antero-lateral band of the coracoacromial ligament for impingement in the overhead athlete. Presented at 16th Annual Meeting of the Arthroscopy Association of North America. San Diego, CA; 1997.
  59. * Edelson JG, Luchs J: Aspects of coracoacromial ligament anatomy of interest to the arthroscopic surgeon. Arthroscopy 1995, 6:715-719.
  60. Discusses the anatomic differences between the anterior and the lateral insertion of the coracoacromial ligament and the deltoid fascia and their pertinence to decompression technique.
  61. Arntz CT, Jackins S, Matsen FA: Prosthetic replacement of the shoulder for the treatment of defects in the rotator cuff and the surface of the gleno-humeral joint. J Bone Joint Surg Am 1993, 75(suppl A):485-491.
  62. Esch JE, Ozerkis LR, Helgager JA, et al.: Arthroscopic subacromial decompression: results according to the degree of rotator cuff tear. Arthroscopy 1988, 4:241-249.
  63. Flatow EL, Bigliani LU: Arthroscopic acromioclavicular joint debridement and distal clavicle resection: Oper Tech Orthop 1991, 1:240-247.
  64. Fukuda K, Craig EV, An K, et al.: Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am 1986, 68:434-440.
  65. * Klimkiewicz J, Sher J, et al.: Biomechanical function of the acromioclavicular ligaments in limiting anterior posterior translation of the acromioclavicular joint. Presented at the Open Meeting of the American Shoulder and Elbow Surgeons. San Francisco, CA; 1997.
  66. Demonstrates the importance of the posterior and superior acromioclavicular ligaments for stability.
  67. Weber SC: Arthroscopic versus open treatment of significant partial thickness rotator cuff tears. Presented at the 13th Annual Meeting of the Arthroscopy Association of North America. Orlando, FL: 1994.
  68. Ryu RK: Arthroscopic subacromial decompression: a clinical review. Arthroscopy 1992, 8:141-147.
  69. * St. Pierre P, Olson FJ, Elliott JJ, et al.: Tendon healing to cortical bone versus a cancellous trough: a biomechanical and histological model in the goat. Presented at the 14th Annual Meeting of the Arthroscopy Association of North America. San Francisco, CA; 1995.
  70. Comparative study of tendon-to-bone biologic healing techniques.
  71. Burkhart SS: The deadman theory of suture anchors: observations along a south Texas fence line. Arthroscopy 1995. 11:119-123.
  72. Burkhart SS, Fisher SP, Nottage WN, et al.: Tissue fixation security in transosseous rotator cuff repairs: a mechanical comparison of simple versus mattress sutures. Arthroscopy 1996. 12:704-708.
  73. * Burkhart SS, Athanasiou KA, Wirth MA: Margin convergence: a method of reducing strain in massive rotator cuff tears. Arthroscopy 1996, 12:335-338.
  74. Biomechanical analysis of an important rotator cuff repair concept.
  75. Mormino MA, Gross M, McCarthy JA: Captured shoulder, a complication of rotator cuff surgery. Arthroscopy 1996, 12:457-461.
  76. Norwood LA, Fowler HL: Rotator cuff tears: a shoulder arthroscopy complication. Am J Sports Med 1989, 17:837-841.

Hip Education – Arthritis and Hip Replacement

The purpose of this pamphlet is to help you understand hip replacement surgery. We will discuss how arthritis affects the hip and causes pain and stiffness. Further, we will describe hip replacement surgery and the usual recovery process. Finally, we will explain the typical results of the operation and possible complications which may occur. It is our hope and intention that this knowledge will assists you in making an informed decision concerning your own need for hip replacement surgery.

Hip Anatomy and Function

The hip is the largest ball & socket joint in the body. It is formed by the meeting of two bones, the femur (thigh bone) and pelvis. The pelvis contains the acetabulum or socket which covers the head (ball) of the femur. Ligaments and muscles hold these bones together and provide joint stability. All of the moving surfaces of the hip joint are covered with surface (articular) cartilage. The contact of cartilage on cartilage provides a smooth, cushioned, low friction surface. The combined structures of bone, cartilage and muscle allow smooth, painless motion as you walk, bend and sit using your hip.

Effects of Arthritis

Arthritis is the condition which results from gradual deterioration and loss of the joint surface articular cartilage. This deterioration of cartilage may occur due to the effects of previous injury or from progressive wear and tear which occurs with aging. In addition, inflammatory conditions such as rheumatoid arthritis, may destroy joint surface cartilage.

Mild arthritis causes joint stiffness and some discomfort. As the cartilage deterioration progresses, nearly constant pain and permanent stiffness occur. At this point, normal activities of daily living become difficult to carry out. Patients with advanced arthritis are only able to walk short distances before needing to rest, have difficulty going up and downstairs, and need assistance getting out of a chair or car.

Orthopedic Evaluation

Your orthopaedic evaluation assesses the severity of your arthritis. This evaluation leads to a treatment recommendation.

The evaluation begins with questions concerning the severity of your hip pain. We attempt to discover how your hip pain and stiffness limits your usual daily activities such as walking, stair climbing and driving and riding in a car. We also ask about previous treatments such as medications, cortisone shots and the use of a cane.

Examination of the hip includes assessment of the range of motion and the presence of any fixed contractures (stiffness). In addition, ability to walk and the presence of a limp are noted.

X-rays are very useful in determining the severity of arthritis. As arthritis and cartilage deterioration progresses, the “cartilage space” between the bones decreases in size and may disappear altogether (“bone rubbing on bone”). When this occurs pain usually becomes significant. Abnormal calcifications or spurs also develop as arthritis progresses.

After completion of the orthopedic examination (symptoms, exam, x-rays) the various treatment options and specific recommendations can be discussed.

With mild arthritis, some moderation of activities and arthritis medications may be adequate. Occasional use of a cane may be helpful and exercise and weight loss are often recommended. Physical therapy or a Cortisone injection into the affected joint may occasionally be of benefit.

As arthritis progresses, the hip pain and loss of function usually becomes more resistant to conservative or nonoperative treatment.

Arthritic Hip and a Normal Hip

The question as to when to proceed with hip replacement surgery is a highly individual matter. This depends on the patient’s pain threshold, their activity level, their social situation, and the help that they may have available at home.

Most patients choose to proceed with hip replacement when their pain becomes generally disabling. This usually occurs when pain is present everyday and often with every step and interferes with realistic activities for the patient’s age. Night pain that interferes with sleep is a significant disability and usually prompts people to seek operative intervention. Most patients who come to hip replacement surgery have difficulty tying their shoes, going up and down stairs and getting in and out of a car. They are frequently dissatisfied with their general quality of life. One final factor that frequently is considered in joint replacement surgery is if the hip arthritis is aggravating arthritis elsewhere in the body, such as the knee or the spine to a significant degree.

As the pain becomes more severe or constant, and the inability to carry out daily activities increases, surgery with hip replacement may be the recommended treatment.

Hybrid Hip Prosthesis

Non-Cemented Hip Prosthesis

Hip Prosthesis

The standard hip replacement consists of two basic components. The acetabular or socket component is a high density polyethylene plastic which has an indentation for the metal ball of the femoral component. The socket component often includes a thin metal shell around the surface of the plastic where it meets the bone to help provide more stability. The femoral component is a long peg that extends down into the shaft of the femur or thigh bone. The top of the stem is made up of a round highly polished ball that articulates with the plastic socket. The ball is held into the socket by the muscles of the hip and gradually a new capsule around the ball is formed after surgery as the healing process occurs.

Total hip replacement surgery requires replacement of the damaged joint surfaces with metal and plastic components (prosthesis). Metal on plastic artificial joints have proven to be self-lubricating and show minimal wear despite years of use.

The artificial hip components are held to the bone with a plastic cement. In younger patients, components which allow “bone ingrowth” will be placed without cement. A more recent trend in hip replacement involves implanting a noncemented “bone ingrowth” acetabular (socket) component and cemented femoral component —- a “hybrid” total hip. Recommendations regarding the use of cement versus bony ingrowth fixation will be made on an individual basis preoperatively based on your age, weight, activity level and bone density.

Results of Hip Replacement

After hip replacement you can expect nearly complete relief of pain. While an artificial hip is not a normal hip, you can expect to resume most activities of daily living with comfort and ease. Studies have confirmed that approximately 95% of all hip replacements can expect a very good result. Unlimited walking tolerance without pain is usually the case. Recreational activities such as bicycling, swimming and golf are likely to be possible. More strenuous sports such as jogging, tennis and skiing could damage the artificial hip and are not recommended.

Many patients notice a significant improvement in their over-all energy level when the strain of constant pain is eliminated. Less dependence on others is another frequent benefit noted after total hip replacement.

Potential Risks of Hip Replacement

No surgery is without risk. Understanding the risks of surgery is necessary in order to make an informed decision about your desire for surgery.

Anesthesia in surgery places increased stress on the body. Serious complications such as heart attack, stroke or even death have been reported. Fortunately, these occurrences are extremely rare. A thorough medical evaluation prior to surgery minimizes these risks.

Infection is also a very serious complication of joint replacement. Many precautions are taken to avoid infection and as a result, the risk of infection is very low (less than 0.5%). Further surgery would be necessary if infection should occur.

Blood clots can occur after hip surgery but this occurrence has been minimized by the routine use of special “pump” stockings and either aspirin or blood thinners used after surgery. Even rarer complications could include artery or nerve damage or fractures of the bones near the hip.

Most patients want to know how long they can expect their artificial hip to last. Over an extended period of time, the hip prosthesis may work loose from the bone. This occurs when the bond between the bone and the plastic cement breaks down. Even though this is the most common cause of artificial joint failure, it is quite unusual. More than 90% of artificial hips continue to function well after 10 years. If an artificial hip becomes loose and painful, it can usually be repaired with a second operation. Only rarely does a hip prosthesis become loose prior to 10 years.

Preparation for Surgery

Once you have made a decision to proceed with hip replacement surgery, a number of arrangements will be made. A date for surgery will be determined and scheduled at Meriter Hospital. Many patients have similar arthritis in both hips and will require replacement surgery of each hip. Usually we recommend performing one hip replacement and having the patient recover from the initial surgery before proceeding to the second operation. The usual time interval between the first hip operation and a second would be three to six months. If, however, a patient is wheelchair bound and would not be able to walk or rehabilitate his first hip operation, then we might proceed during the same hospitalization to replace the second hip.

A thorough pre-surgical medical evaluation needs to be completed within one month of your surgery by your primary care physician. You will also be seeing my physician assistant approximately two weeks preoperatively for a thorough evaluation and exam. During this session, your surgical procedure and the pre and postoperative routine will be discussed. Data will also be collected for a hip study we are conducting. Lab tests, chest x-ray and EKG will be ordered at that time and reviewed. We will also arrange for you to be seen in the Physical Therapy Department prior to your hospitalization so that you can obtain either a walker or crutches and be instructed on the exercises that you will be doing in the hospital postoperatively. You should practice using the correct technique with the walker or crutches prior to being admitted to the hospital.

You should not take aspirin, Ibuprofen or other nonsteroidal anti-inflammatory medication during the two weeks prior to surgery. These medications thin your blood and increase your risk of bleeding complications. You may take acetaminophen (Tylenol), propoxyphene (Darvon or Darvocet) or codeine for pain if needed. Stopping smoking preoperatively helps decrease the chance of postoperative lung problems.

You will be admitted to the hospital the morning of surgery. You will have further instructions on that day by the orthopedic nurses.

One of the anesthesiologists will see you and discuss the type of anesthesia that is recommended. He/she can also answer your questions concerning anesthesia and the risks involved. The nurses will orient you to the nursing unit and usual daily activities while you are hospitalized. You may again be seen by one of the physical therapists who will review your hip exercises with you.

If for some reason the laboratory tests, chest x-ray or EKG have not been previously completed prior to your hospitalization, they will be done prior to surgery.

Blood transfusions may be necessary with hip surgery, particularly in the uncemented variety. Many patients in this day and age are concerned about getting blood transfusions from unknown donors. With the present screening techniques used by the blood bank, the risk of getting hepatitis, AIDS or other blood borne diseases is extremely low. An alternative to getting bank blood is to donate your own blood preoperatively and have it stored in a liquid or frozen state until the time of your operation. These donations have to be coordinated with the time of your surgery. We will discuss these options with you preoperatively. My secretary will then arrange for your donation appointments if you decide on “auto-transfusion.”

We routinely use a “cell saver” during the operative procedure to return irrigated blood into your system after it has been filtered. We are also often using a postoperative wound drainage auto transfusion device to try to diminish your need for transfusions. If you have given your own blood preoperatively, you will likely receive this as a transfusion postoperatively.

Day of Surgery

Your hip surgery will either be performed at 8:00 in the morning or 1:00 in the afternoon, depending on the availability of the operating room. You will be informed of the expected time of surgery when scheduled. You will not be allowed to eat or drink after midnight the evening before surgery. You may desire a sleeping pill the night before surgery and this is fine.

On the morning of surgery, you will be taken to the operating room approximately 30 minutes before surgery. Your family may accompany you and will be directed to the family waiting room near surgery. The actual surgical procedure takes 1-1/2 to 2-1/2 hours. You will then spend another 1 to 2 hours in the recovery room where you will be closely observed as you awaken from anesthesia. When you are awake (but often very drowsy) and your vital signs are stable, you will be returned to your room. Five to six hours may have elapsed since you first left your room.

When you are back in your room, you will be aware of moderate pain in your hip. This pain can be greatly relieved by the use of a “PCA pump” which allows you to administer your own pain relieving medication. By simply pushing a button, a predetermined amount of pain medication is pumped into your IV line, which has been started in surgery. This provides rapid relief of pain without the usual discomfort and delay of a “hypo.” In some circumstances, however, hypos are still used, particularly if the patient has a problem with nausea and vomiting. Your IV line is usually left in place for at least 48 hours so that you can be given adequate fluids and also so that necessary antibiotics can be given. Antibiotics help to prevent infection in your new hip. After surgery you will have a bulky dressing on your hip. You will also have 1 or 2 drains coming out of the skin, which collect any blood within the joint or subcutaneous tissues. These will generally be removed the morning of the second postoperative day.

In addition, you will have a triangular pillow between your thighs to prevent you from crossing your legs and dislocating your hip.

After Surgery

Most patients will be allowed and encouraged to get out of bed the first day after surgery. The increased activity in the upright position of sitting encourages the lungs to expand fully and helps eliminate any fever. You will likely be given a “tri-flow” device to help expand your lungs every 2 hours during the day.

On the second postoperative day, your drain is usually removed and you will now begin the important rehabilitation process. The success of this program depends greatly on the cooperation and enthusiasm of the patient. The goals of therapy are to increase hip range of motion, increase strength in the hip and thigh muscles, learning to walk with crutches and become independent with daily activities such as climbing stairs and using the bathroom.

The muscle strengthening exercises include attempts to tighten the thigh muscle (quad sets) and then to lift the leg off the bed with the knee straight (straight leg raise). These exercises should eventually be done in sets of 10, at least 6 to 10 times daily, if possible.

Your nurses, therapists, and doctor can help you with these exercises. Don’t be discouraged. It takes most patients several days before they are able to independently lift the operative leg off the bed. Physical therapists will instruct you and assist you in walking with crutches or walker. The therapist will also direct you as to how much weight you can put on the operative leg. This varies depending on whether the prosthesis is cemented or the bony ingrowth variety. Some patients start with a walker and then progress to crutches; others prefer the walker and never use the crutches. By the time you are discharged from the hospital, you should be able to walk with the walker or crutches without assistance. You should also be able to handle a few stairs. Your therapist will work with you at least twice daily on these activities.

Several other important points about your hospital stay should be noted. Following major lower extremity surgery, there is a risk of blood clots forming in the leg. To minimize the risk of this occurrence, most patients are placed on one aspirin per day and also placed in special sequential compression stockings that continually assist in externally pumping the blood through the legs.

If you have had a previous history of blood clots or thrombophlebitis, a blood thinner called Coumadin may be used during your hospitalization. A blood sample must be drawn every morning so that the proper dose of Coumadin can be determined; thus you should not be surprised if you need daily blood tests in the hospital. The Coumadin is often continued for several weeks when you are discharged from the hospital. You will need to have your blood tested on an outpatient basis and adjustments made in your Coumadin level.

Elastic stockings (TED hose) are also used to minimize risks of blood clots and control swelling in the lower leg and foot. If possible, we like these stockings worn during the day but they may be removed at night for comfort.

Small metal staples are used to close your incision. These will be removed approximately 7 to 10 days after surgery. This process is relatively painless.

Hip Precautions

It is important for several weeks following total hip replacement surgery that care be taken to keep from dislocating the hip prosthesis. For six weeks following surgery, the patient should not bend at the hip past a 90° position. A pillow may need to be placed in a soft chair to add support so that bending does not pass 90°. For at least eight weeks following surgery, the patient should not cross his or her legs. It is important that the hip is not internally rotated. This position will be shown to the patient during hospitalization. The abduction splint or a pillow should be placed between the legs while sleeping for the first 4 weeks after the time of surgery.

Hospital Discharge

Most patients are able to return home 7 to 10 days after surgery. At this time we expect you to be able to walk independently with crutches (or walker), get in and out of a chair or bed and to lift your leg with the knee extended straight. The following instructions are intended to make your return home as comfortable as possible. Please read them carefully and ask either my physician assistant or myself if you have any further questions.

Exercises

We encourage you to be as active as possible. You should not spend much time in bed other than at night to sleep. You should walk several times daily. These walks are by far the most important exercise you can do. As your recovery progresses, you should be able to walk longer distances and with less fatigue. Be careful not to push yourself too hard, too quickly. Conversely, remember not to sit for extended periods of time, as this tends to retard the venous drainage from your leg. It is better to get up and move around, walking every 30 to 45 minutes. Exercise as noted previously. Walking is the most important exercise. You should also continue to do straight leg raises. Try to lift your leg with the knee straight and hold it up for 10 seconds (do this 10 repetitions, 6 to 10 times a day).

Bathing

You may begin to shower as soon as you return home. Bathing in a tub is difficult and should be avoided for the first two months. Neither a shower or a bath is harmful to your incision.

Incision

Usually the incision is well healed at the time of discharge and requires no special care at home. f the incision becomes excessively swollen, red or begins to drain, you should call us. It is not unusual for the thigh and hip to remain swollen and feel warm for several months after surgery.

Elastic Stockings (TEDS)

Please continue to wear the elastic stockings while you are awake for the first 2 to 3 weeks after discharge.

Return Appointment

Your first return examination in our office will occur after about 5 weeks. In most instances, you will be given an appointment card at the time of discharge. If for some reason you did not receive an appointment card or if your appointment time is not convenient, please call our office during the normal office hours for an appointment time. (608-231-3410).

Driving

We do not recommend that you drive a car until after your first office appointment after surgery.

Traveling

It is reasonable to travel by car or plane soon after leaving the hospital, however you will need a pillow under your buttocks so that you do not sink down and flex the hip greater than 90°. When traveling long distances, you will be more comfortable if you stop and walk a little every hour. Airport security metal detectors are generally not set off by these artificial joints. We can, however, give you a card stating that you have a joint replacement to keep with you just in case.

Medications

Most patients still require the use of pain medication for a period of time following discharge from the hospital. We will provide a prescription for an appropriate medication. In addition, you should resume any other medication you were taking prior to hospitalization unless otherwise instructed by a physician.

Dental or Urologic Care

If you require dental work (including regular cleaning) or any urologic evaluation after surgery, you should take a short course of antibiotics. Many of the bacteria in the mouth are susceptible to Penicillin. There may be a number that are resistant, so at the present time I am utilizing a combination of Pen VK 500 mg., two tablets orally one hour before and six hours after the procedure. In addition, I prescribe Keflex 500 mg., one tablet one hour before and six hours after the procedure. If the patient is allergic to Penicillin, Erythromycin 1 gm. orally, one hour before and then 500 mg. six hours after the initial dose, would be substituted.

Precautions

It is extremely important after total joint replacement to be very careful regarding infections. There have been reports of infections elsewhere in the body that have shed bacteria into the blood stream which then infect the joint replacement, even years after the initial procedure. Therefore, it is imperative after a total joint replacement that infections are treated aggressively. This includes pneumonias, bronchitis, urinary tract infection or external skin sores that may become infected. The usual sore throat associated with some nasal drainage is frequently a viral infection and of no major concern. However, if you develop marked sore throat or fever, suggestive of a strep throat, you should see your family doctor immediately to be tested for strep throat and placed on antibiotics if your culture is positive. In general, if you have questions as to whether or not you may have an infection that should be treated, please call my office so that we can discuss this with you.

Summary

Don’t forget that you have a new hip but it is not a completely normal hip. Your healing pattern will be somewhat cyclical. It is common for you to feel very good for several days, overdo it and then have the leg swell or stiffen up slightly. This will improve and go through a number of cycles until you are finally healed. Don’t look at your progress on a day by day basis, but more on a week to week basis. Don’t get too excited or depressed by the cyclical variations.

If you find when you go home that there is something new or different that you have a question about, please feel free to contact me. I am concerned about you as a person as well as a patient and would be happy to answer any questions that you may have.

Good luck with your new hip.


Metal-on-Metal Articulation – PROPOSED METAL DEFENSE PROTOCOL

Keith A. Brewster Norman
Oklahoma, USA
kbrews@cox.net
www.ActiveJoints.com
Revised, June 28, 2002

Introduction

While considering metal-articulated hip resurfacing surgery, and continuing after the fact, I sought to understand the possible impact of having metal components in the body. This document contains the result of my research on the issue and relates the steps I’ve decided to take as a sort of insurance measure to protect against any potential long-term effects of having a foreign body in my system. To date there seems to have been no mention in the literature of any proactive actions for the patient beyond limiting wear-producing activity.

Modern metal articulating surfaces are manufactured from an alloy of cobalt, chrome, and other minor constituents. A typical alloy is prescribed by the American Society for Testing and Materials (ASTM) as ASTM-F75, cast cobalt chrome, composed of approximately 65% cobalt, 28% chrome, 6% molybdenum, and less than 1 percent each of several other elements. Cobalt-chrome alloys are extremely hard, resistant to corrosion, and can be machined to a smooth, wettable surface. Additionally, these alloys have the property that they are self-polishing. That is, small defects will tend to become smoothed out over time, rather than growing with additional contact. The body’s natural fluid, the synovial fluid, lubricates the articulating surfaces. Despite the lubrication, tiny metal debris can be shed from the surfaces, and the metals may spread through the body as micron-sized (millionths of a meter) particles or metal ions (e.g., Case et al., 1994).

Experiments with hip simulators and various metal-metal hip prostheses have shown that the maximum wear rate occurs in the first one-half to one million cycles (meant to represent walking steps), when the volumetric wear rate is about 0.5-4.0 mm3 million cycles (e.g., Chan et al., 1999, Nelson et al., 2000). On the average, the hip patient takes about two million steps per year (one million cycles per joint), though there is quite a bit of variance (Schmalzried et al., 1998, Schmalzried et al., 2000). Certainly during the recovery period, the hip patient will have a less-than-average activity level. Thus, the maximum rate of wear would be expected in the first year or two. There is some evidence that the rate of wear may be related to the degree of sphericity of the joint and the extent of clearance between the ball and cup (e.g., Chan et al., 1999, Nelson et al., 2000). The relative lack of machining accuracy available with 1960s technology is thought to be responsible for some of the problems experienced by early metal-on-metal articulating joints in that era (McKee-Farr joints), though some of those joints have gone on to last over 30 years in some patients.

Cobalt (Co) is an essential element in the body as it is a constituent of Vitamin B-12. Vitamin B-12 is involved in the production of red blood cells. There is no recommended daily allowance (RDA) for cobalt, but the RDA for Vitamin B-12 is 6 meg per day. Cobalt can be found in liver, kidneys, milk oysters, fish, clams, or sea vegetables. Cobalt is also found in some beer, teas and coffees.

The effects of cobalt on the human body through drinking water and supplementation and other exposures are reviewed by a UK Expert Group on Vitamins and Minerals (2000). Cobalt is processed by the kidneys and excess cobalt is quickly eliminated from the body, with a monitored individual showing 90-95% eliminated after 48 hours, and 99% after 30 days (UK EGVM, 2000). There is some evidence from animal studies and from the mid-60s when cobalt chloride was commonly added to beer that cobalt could accumulate in the myocardium. This accumulation was increased by the consumption of alcohol and may have been related to a deficiency in proteins (including L-cysteine) and/or other trace minerals in the diet (Sandusky et al, 1981). The metal may also affect the thyroid as rare cases of patients receiving very high-dose long-term therapeutic cobalt salt treatments (0.17 to 3.9 mg/kg/day) experienced hypothyroid symptoms.

Chromium (Cr) is an essential metal in the body. It is involved in the process of converting sugar and fat to energy by insulin. Chromium deficiencies can result in high blood glucose levels. There is no official RDA for chromium, but the National Academy of Sciences defined an Adequate Intake (based on average intake by healthy subjects) as 35 meg for young males (NAS 2001). Chromium is a trace metal found in certain vegetables and meats, including brewers yeast, mushrooms, broccoli, calf s liver, mollusks, crustaceans, American cheese and wheat germ. It is included in many all-in-one vitamin and mineral formulas (e.g., Centrum™ contains 65 meg, other formulas contain up to 200 meg). Chromium exists in two common oxidation states, Cr(III) and Cr(VI), and as metallic chromium, which also can be denoted Cr(0). One form, Cr(VI), also known as hexavalent chromium, is a known carcinogen; Cr(VI) is the presumed cancer risk raised by some orthopedic surgeons when considering metal-metal components.

The effects of chromium on humans through drinking water and other exposure are reviewed by Morry (1999). Much of the concern regarding Cr (VI) arises from occupational exposure by welders and other steel workers exposed to airborne chromium dust or vaporized chromium through working with stainless steel, an alloy of iron that contains chromium and other metals. Under such conditions, chromium can be inhaled and chronic exposure can lead to cancer of the respiratory system. Oral ingestion of hexavalent chromium has shown a slightly increased rate of cancer in the forestomachs of rats (Borneff et al., 1968). No studies have shown a link of oral ingestion Cr(III) to cancer. Rats that ingested Cr(III) showed no adverse effects from consuming up to 1468 mg/kg per day of Cr(III) over a 600 day period (Ivankovich and Preussmann, 1975). Furthermore, it is believed that hexavalent chromium is rapidly reduced to other valence forms in acidic environments such as in the stomach and blood stream (Kerger et al., 1997, D’Agostini et al., 2000, DeFlora, 2000). Chromium is primarily eliminated by the kidney (Donaldson and Rennert, 1981, Kerger et al., 1997). Metal-metal articulation is contra-indicated for those with chronic kidney failure.

Statistical Studies

There have been a few statistical studies concerning cancer risk among patients with artificial hip implants. Besides metal-metal articulating surfaces, there are other aspects of artificial hip components that have raised concern. Metals can be released by corrosion of hip stems, fretting between components in modular hip systems can shed metal debris, and metals can leech from the bone-implant surfaces of uncemented components. The International Agency for Research on Cancer (1999) and Tharani et al. (2001) present a comprehensive review of the studies that have been done, and combines the results of several to show no significant difference in cancer rates between those with hip replacements and the general population. In one particular study, Visuri et al. (1996), the registry of hip patients in Finland were studied and they found no difference in mortality between those with metal-metal articulated hips and those who had metal on plastic joints. The rate of cancer was slightly higher in the metal-metal group, but was no different than in the general population, and no sarcomas were found near the prosthesis. There was an elevated occurrence of leukemia, but due to the small number of cases overall, the result was not statistically significant. Sulzer Medica of Switzerland has over 100,000 metal-metal articulated hip implanted in Europe; no alarming health trends have been noted due to the metal-metal articulation thus far, though there is not a coordinated effort of follow-up.

There is concern that the statistical studies are too narrow in their cultural and genetic scope (many rely on Scandinavian disease records) and that in time new trends might arise due to possible latency between chromosomal damage and clinically apparent cancers.

Elements of Proposed Metal Defense Protocol

Given the concerns of the possible carcinogenic effects of Cr(VI) and the possible ill-effects of accumulation of metals in tissues, it seems prudent to maintain levels of nutrients in the body that could ensure the rapid the conversion of any Cr(VI) to Cr(III) and to ease the elimination of the metallic ions via the kidneys and liver. I propose the following five-element protocol to get a leg up on any detrimental effects of metals that may result from the hip prosthesis.

1. Discontinue Chromium Multi-vitamins

If you are taking a multi-vitamin, discontinue use if you find it contains chromium. Many multi-vitamins contain 65 mg of Cr, some may contain up to 200 mg. This eliminates an unnecessary source of the metal, but obviously, you’ll lose any benefit you had been getting from the other ingredients.

2. Water

Its generally a good idea to drink several cups of water per day, and this should also help keep the kidneys well hydrated and perhaps better able to flush cobalt from the system. Personally, I am not taking any specific action in this regard, but generally, I like to have some ice water, dilute fruit juice or a soft drink at my desk while I work in the office or at the computer at home. I recognize that soft drinks may not help the hydration issue, but I’m allowed some vices.

Water from your tap or mineral water can contain cobalt or chromium; if you happen to live in an area with high concentrations of these metals, you might consider finding another source for your drinking water. The EPA requires your water treatment plant to measure and report levels of chromium in your drinking water to its costumers. The EPA maximum concentration limit for drinking water is 100 ppb (parts per billion, or micrograms per liter); the State of California and the World Health Organization sets this limit at 50 ppb. The practical measurement limit is 10 ppb. These limits are established in order to prevent excess Cr(VI) ingestion without specifically requiring the monitoring of the separate valence forms of Cr present. If you have a well, you might investigate if you can have it tested for chromium and avoid drinking it if it is has high levels of Cr.

3. Vitamin C and anti-oxidants

Vitamin C, known in the literature as ascorbic acid, is a powerful anti-oxidant. The anti-mutagenic and anti-carcinogenic effects of Vitamin C are well known. Furthermore, Vitamin C is the most effective antidote for cases of Cr(VI) poisoning (Hathaway, 1986).

The National Academy of Science RDA for Vitamin C is 90 mg for adult males and 75 mg for adult females (excluding pregnancy and lactation, which require higher levels). There is evidence that serum levels of Vitamin C are saturated at an intake of 200 mg per day (NAS, 2000). The tolerable upper limit for Vitamin C has been established at 2000 mg per day (NAS, 2000).

I seek then, to get at least 200 mg of Vitamin C per day through diet or supplementation. Many fruits and vegetables contain Vitamin C; a small sample is listed in the following table. In addition, Vitamin C supplements are available everywhere and are very inexpensive. However, the most commonly found products contain 500 mg or 1000 mg tablets.



Fruit

mg
Vitamin C/Serving

Grapefruit (half)
44

Cantaloupe (eighth)
29
Guava 165

Honeydew Melon (eighth)
20
Kiwi
fruit
74
Mango 57

Orange
70
8 oz
Orange Juice
96

Papaya
47

Tangerine
26

Tomato
23

Watermelon (large slice)
27

Although no specific benefits of Vitamin A and E have been uncovered specific to cobalt and chrome, it seems reasonable to have a team of anti-oxidants on the job, also these vitamins are not as quickly flushed from the system as the water soluble Vitamin C. The following table is a specific anti-oxidant formula (Spring Valley, price: ~$6.00 for 60 softgel tablets) I found at Wal-Mart, but I have seen similar combinations in other products at chain drug stores. One can get the serum-saturating dose of Vitamin C as well from one of these tablets.


Nutrient


Amt per tab


Adult


Vitamin A

10,000 I.U.

200%

Vitamin C

250 mg

277%

Vitamin E

200 I.U.

667%

Zinc
7.5
mg
50%

Selenium

15 mcg
21%

Copper

1 mg

50%

Manganese

1.5mg
75%

4. NAC (N-Acetyl-L-Cysteine)

NAC is an amino acid that is used in the production of glutathione (GSH). GSH has an important role in binding reactive metals. NAC has been shown to increase the anti-oxidant properties of Vitamin C (Agostini et al., 2000), and the combination of ascorbic acid and GSH has been shown to decrease the production of Cr(V) in the reduction of Cr(VI) by ascorbic acid in mice (Liu et al., 1995). The production of reactive Cr(V) has been suggested as a step in the carcinogenic mechanism of Cr(VI). In short, there are circumstances in which Vitamin C can actually act as a pro-oxidant but when combined with NAC, the pro-oxidant effect is effectively neutralized. NAC has also been shown to effective in increasing the body’s immune response to the influenza virus (De Flora et al.,1997). NAC, when injected in the abdomens of rats, has been shown to increase the rate of cobalt excretion in the urine and to decrease the accumulation of cobalt in the liver and spleen, and it overall it was the most effective among five tested chelators (Llobet et al., 1988). No studies have been done to establish the long-term safety of NAC supplementation.

NAC is naturally produced in the body and is contained in animal proteins, but supplementation can help to insure the body has adequate supplies. I take 1200 mg per day. Label directions suggest taking 1 to 2 of the 600 mg tablets per day. I buy NAC at my local General Nutrition Center, two bottles of 60 600 mg capsules cost about $28.00 including sales tax and the discount for buying two bottles at one time.

Chromium can also be bound by other chelating agents such as EDTA. A chelating agent works in a way that is analogous to soap, it binds certain insoluble molecules and makes them soluble so that may be processed and potentially eliminated. It has been suggested that EDTA treatments (which must be done intravenously, by administration of calcium-EDTA) might increase chromium elimination from the body. EDTA is best known as a treatment for lead poisoning. In one study of humans (Anderson et al., 1996) EDTA treatments did not increase the elimination of chromium. In a study of metal workers (Sata et al., 1998) EDTA treatments did increase the elimination of chromium but also increased the elimination of lead, zinc and magnesium. In another study (Araki et al., 1998) the EDTA treatments increased the chromium elimination by just 10% but increased the rate of elimination of lead, manganese, zinc and cadmium by much higher rates. Zinc and manganese are necessary trace minerals, for which the additional elimination would be considered a detrimental side effect for the orthopedic patient without additional sources of these trace minerals. EDTA does not seem to be well suited for preferentially eliminating chromium.

5. Blood Donation

Once every two months I go to the local office of the Red Cross and donate a unit (approximately 1 pint) of blood. The average human has 9-11 pints of blood in their system, so if there are any metals in my bloodstream, the result of each donation is a reduction by about one-tenth of the total amount of metal in the bloodstream. (Since it will be diluted about 1-to-9 in the body of the recipient, so I am not concerned about any ill effects on the recipient). The reduction may seem small, but the cumulative effect can be dramatic, especially considering that the period of run-in wear may be limited.

If you are concerned about the potential effects on the recipient you may be able to opt to have your blood held back from distribution. The Red Cross has a system of confidential notification that the donor believes their blood may be a risk to the recipient. If you choose to withdraw your blood donation you may want to make a tax-deductible contribution to the Red Cross to cover their costs for drawing your blood. Alternatively, it might be possible to obtain a prescription to have your blood drawn periodically as is done for those with hemochromatosis. Given the lack of demonstrable risk, it may be difficult to obtain such a prescription, however.

Summary

Some nutritional supplements and actions have been identified that might mitigate any possible effects of metal ion activity for those with implanted metals. There are few known side effects to the proposed protocol with possible beneficial side effects identified for many of the actions. The cost of the protocol is quite reasonable, and the supplements are available in the United States through many sources.

 
Target Dose/ Frequency

Intent

Positive
Side Effects

Negative
Side Effects

Estimated
Monthly Cost

Vitamin C

250-500 mg
1 x/day

Anti-oxidant

Cold and flu defense

Considered safe below 2000 g/day

$1.00

Anti-oxidant Formula

1 softgel/day

Anti-oxidant
   
$3.00

NAC
n-acetyl-1-cysteine

600 mg 2x/day

Anti-oxidant Cobalt
chelator

May reduce flu symptoms
 
$14.00

Blood Donation

1 Unit/ 8 weeks

Dilution

Medical benefits to
blood recipients
 
1-2 hours of time every two months

It is not my intent to raise the fear level over metal, rather provide some positive action that may make the patient feel more in control of any possible risks.

Note, it is beyond the scope of this report to consider reproductive health issues. Consult your OS or Ob-Gyn for possible risk factors. Some information on the subject can be found online at Reprotox.org.

Although the author believes this to be a safe and defensible protocol, much of the research evidence is based on animal and in-vitro experiments. This protocol has not been clinically proven, nor has it been reviewed in any way by the U.S. Food and Drug Administration. It is beyond the author’s knowledge to judge the methods and other details of the cited publications, for a few only the abstract was readily accessible. Any treatment should be done in consultation with a medical professional. Taking any nutritional supplements could affect test results or interact with medications; keep your physician informed of your actions.

References

Anderson R.A., N.A. Bryden, and R. Waters, 1999: EDTA chelation therapy does not selectively increase chromium losses. Biol. Trace Elem. Res., 70, 254-272.

Agostini, F.D., R.M. Blansky, A. Camoirano, and S. De Flora, 2000: Interactions between N-Acetylcysteine and ascorbic acid in modulating mutagenesis and carcinogenesis. Int. J. Cancer, 88, 702-707.

Araki S., H. Aono, and K. Murata, 1986: Mobilisation of heavy metals into the urine by CaEDTA: relation to erythrocyte and plasma concentrations and exposure indicators. Br. J. Ind. Med., 43, 636-641.

Boraeff, I, Engelhardt, K, Griem, W, et al. (1968). [Carcinogenic substances in water and soil. XXII. Mouse drinking study with 3,4-benzpyrene and potassium chromate]. Arch.Hyg. 152, 45-53. (German) {As reported in Morry, 1999}

Case C.P., V.G. Lingkumer, C. James, M.R. Palmer, AJ. Kemp, P.P. Heap, L. Solomon 1994: Widespread dissemination of metal debris from implants. J Bone Joint Surg (Br.); 76 (B), 701-712.

Chan, F.W., J.D. Bobbin, J.B. Medley, JJ. Krygier, S. Yue, M. Tanzer, Engineering issues and wear performance of metal on metal hip implants, Clin. Orthop. Res., 333, 996-107.

De Flora, S., C. Grassi, and L. Carati, 1997: Attenuation of influenza-like
symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment. Eur. Resp. J., 10, 1535-1541.

DeFlora, S., 2000: Personal communication.

Gillespie, W.J., D.A. Henry, D.L. O’Connell, S. Kendrick, E. Juszczak, K. Mclnneny and L. Derby, 1996: Development of hematopoietic cancers after implantation of total joint replacement. Clin. Orthop., 329 SuppL, S290-S296.

Hathaway, 1986: Treatment of acute chromium poisoning. In D.M Sernone, (ed.), Chromium symposium 1986: an update, pp. 87-99. Industrial Health Foundation, Pittsburgh. (Cited by D’Agostini etal., 2000.)

International Agency for Research on Cancer (IARC), 1999 Evaluation of cancer risks to humans: Surgical implants and other foreign bodies. IARC Monographs, Volume 74.

Ivankovic, S and R Preussmann, 1975: Absence of toxic and carcinogenic effects after administration of high doses of chromic oxide pigment in subacute and long-term feeding experiments in rats. Food Cosmet. Toxicol., 13, 347-351. (As reported in Morry, 1999}

Kerger, B.D., B.L. Finley, G.E. Corbett, D.G. Dodge, D.J. Paustenbach, 1997: Ingestion of chromium (VI) in drinking water by human volunteers: Absorption, distribution, and excretion of single and repeated doses. J. Toxicol. Environ. Health, 50, 67-95.

Llobet J.M., J.L. Domingo, and J. Corbella, 1988: Comparative effects of repeated parenteral administration of several chelators on the distribution and excretion of cobalt. Res. Commun. Chem. Pathol. Pharmacol, 60, 225-233.

Mathiesen, E.B., A. Ahlbom, G. Bermann, and J.U. Lindgren, 1995: Total hip replacement and cancer. A cohort study. J. Bone Joint Surg. Br., 77, 345-350.

Morry, D., 1999: Public Health Goal for Chromium in Drinking Water, Report of Office of Environmental Health Hazard Assessment, State of California Environmental Protection Agency. 26 pp.

National Academy of Science (U.S.), Institute of Medicine 2000: Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids, National Academy Press, Washington, D.C., available online at http://www.nap.edu/books/0309069351/html/index.html

National Academy of Science (U.S.), Institute of Medicine 2001: Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc National Academy Press, Washington, D.C., available online at http://www.nap.edu^oks/0309072794/html/index.html

Sata F., S. Araki, K. Murata, and H. Aono, 1998: Behavior of heavy metals in human urine and blood following calcium disodium ethylenediamine tetraacetate injection: observations in metal workers. J. Toxicol. Environ. Health, 54, 157-178.

Schmalzried T.P., E.S. Szuszczewucz, M.R. Northfield, K.H. Akizuki, R.E. Frankel, G. Belcher, and H.C. Amstutz, 1998: Quantitative assessment of walking activity after total hip or knee replacement. J. Bone Joint Surg., 80, 54-59.

Schmalzried T.P., E.F. Shepherd, F.J. Dorey, W.O. Jackson., M. dela Rosa, F. Fa’vae, H.A. McKellop, C.D. McClung, J. Martell, J.R. Moreland, and H.C. Amstutz, 2000: Wear is a function of use, not time. Clin. Orthop., 381, 36-46.

Shamberger, R.J., 1984: Genetic toxicology of ascorbic acid. Mutat. Res., 133, 135-159.

Tharani, Ravi, F.J. Dorey, and T. P. Schmalzried, 2001: The Risk of Cancer Following Total Hip or Knee Arthroplasty, J. Bone J. Surgery, 83,774-780.

United Kingdom Expert Group on Vitamins and Minerals, 2000: Review of Cobalt. 21 pp. Available online at: http://www.foodstandards.gov.uk/committees/evm/papers.htm

Visuri T., E. Pukkala, P. Paavolainen, P. Pulkkinen and E.B. Riska, 1996: Cancer risk after metal on metal and polyethylene on metal total hip arthroplasty. Clin. Orthop., 329 Suppl., S280-289.

©2001 Keith A. Brewster
www. Active Joints. com


Metal-on-Metal Articulation – A CAUSE FOR CONCERN IN METAL-ON-METAL BEARINGS?

Joshua J. Jacobs, MD; Nadim J. Hallab, PhD; Anastasia K. Skipor, MS; and Robert M. Urban, AS

In the majority of patients, orthopaedic implants are biocompatible. However, there is an increasing recognition that, in the long-term, permanent orthopaedic implants may be associated with adverse local and remote tissue responses in some individuals. These adverse effects are mediated by the degradation products of implant materials. The recent reintroduction of metal-on-metal bearings for total hip arthroplasty has heightened concerns about the biologic response to metal degradation products in light of the fact that the serum and urine metal concentrations in patients with these implants typically are higher than those seen in patients with conventional metal-on-polyethylene bearings. From previous studies of long-term metal-on-metal McKee-Farrar implants, it seems that these elevated levels may persist for the duration of the implant’s lifetime. This is of particular concern in the younger and more active patient in whom life expectancy after implantation may exceed 30 years. The association of metal release from orthopaedic implants with any metabolic, bacteriologic, immunologic, or carcinogenic toxicity currently remains conjectural because cause and effect have not been established in human subjects. However, continued surveillance of patient populations with metal implants, particularly those with metal-metal bearings, is warranted.

Joint replacement prostheses have a long history of safety and effectiveness when used for the appropriate indications and when implanted properly. It is recognized, however, that in the long-term, these implants may be associated with adverse local and remote tissue responses in some individuals. These adverse effects are mediated by the degradation products of these implant materials that may be present as:

  • (1) particulate wear and corrosion debris
  • (2) metal-protein complexes
  • (3) free metallic ions
  • (4) inorganic metal salts or oxides,
  • (5) sequestered in an organic storage form such as hemosiderin.12’13

Much of the interest in the long-term effects of implant materials has centered on the metallic components because of their tendency to undergo electrochemical corrosion resulting in the formation of chemically active degradation products. Concern about the release and distribution of metallic degradation products is attributable to the known potential toxicities of the elements used in modern orthopedic implant alloys, particularly Co and Cr. Metal toxicity may be mediated by metabolic alterations, alterations in the interaction between host and parasite, immunologic interactions of metal moieties by virtue of their ability to act as haptens (specific immuno-logical activation), antichemotactic agents (nonspecific immunologic suppression), or lymphocyte toxins, and by chemical carcinogenesis.13 The association of metal release from joint replacement components with any metabolic, bacteriologic, immunologic, or carcinogenic toxicity currently remains conjectural because cause and effect have not been established in human subjects or animal models. This may be attributable to the difficulty of observation; most symptoms caused by systemic and remote toxicity can be expected to occur in a finite frequency in any population of patients.

We will address the question of whether the metal degradation products originating from the current generation of metal-on-metal bearings are associated with adverse, clinically significant toxicologic sequelae.

Metal Particles

Particulate debris comprises a substantial portion of metal degradation products generated by joint replacement prostheses. The degradation products of ceramics and polymers are exclusively in particulate form, because these classes of materials generally are considered insoluble in physiologic environments. Although PE particles generally are recognized as the most prevalent particles in the periprosthetic milieu, metallic and ceramic particulate species also are present in variable amounts and may have important sequelae. When present in sufficient amounts, particulates generated by wear, corrosion, or a combination of these processes induce the formation of an inflammatory, foreign body granulation tissue with the ability to invade the bone-implant interface. This may result in progressive, periprosthetic bone loss that threatens the fixation of cemented and cementless devices, limiting the survivorship of total joint replacement prostheses. Consequently, particulate wear debris of polymers, ceramics, and metal alloys used in prosthetic components have been the subject of intense study concerning their role in bone resorption and aseptic loosening.14’15

Willert et al43 reviewed their collection of retrieved metal-on-metal hip joints (nine McKee-Farrar, seven Muller, and three Huggler prostheses) and associated periprosthetic tissues. The calculated annual wear was low compared with conventional surfaces. The cellular reaction to metal wear particles was regarded as mild. Likewise, Doom et al6 concluded that the capsular and interface tissues retrieved from short-term and long-term metal-on-metal THRs had less intense granulomatous inflammation and foreign body giant cell reaction in comparison with tissues from patients with metal-on-polyethylene bearings. However, a more recent comparison study of periprosthetic tissues from metal-on-metal (n = 25) and metal-on-polyethylene (n = 10) THRs showed that tissues from patients with metal-on-metal bearings had more extensive and severe ulceration of the synovial surface with a predominant lymphocytic infiltrate accompanied by abundant plasma cells. Furthermore, metal-on-metal bearings were associated with a striking pattern of perivascular inflammation with prominent lymphocytic cuffs, especially deep to areas of surface ulceration. These findings raise the specter of a metal hypersensitivity-induced vasculitis, which has been reported previously in cases of metal-on-metal THRs and in a case of a severely corroded modular femoral stem.38’42 The prevalence and clinical importance of these observations are subjects of continued scrutiny.

The morphologic features of particulate debris from metal-on-metal bearings also have been a topic of considerable interest. Doom et al5 reported on a transmission electron microscopic analysis of metal particulate debris retrieved from 13 patients having revision of a metal-on-metal THR. The majority of the Co-alloy wear particles were less than 50 nm in size (range, 6-834 nm), approximately one order of magnitude smaller than what has been reported for retrieved PE particles. Based on reported volumetric wear rates from metal-on-metal bearings, this translates into 6.7 X 1012 to 2.5 X 1014 particles per year. This is 13 to 500 times the number of particles produced by a typical metal-on-polyethylene bearing.5 Therefore, even though the volumetric wear rate is lower for metal-on-metal bearings in comparison with metal-on-polyethylene bearings, the number of particles actually is greater, because of the smaller particle size. It is unknown whether these nanometer-sized particles are more or less bioreactive than micrometer-sized particles because of the difficulty of isolation of nanometer particulate debris for study in cell culture. The very small (nanometer) size of metallic debris released by metal on metal bearings,5 combined with the fact that the bio-availability of metal is thought to be a function of the total surface area of the released debris rather than on its volume or weight,33 casts doubt on the supposition that the net adverse biologic response will be reduced by modem metal-on-metal designs even though the volumetric wear is reduced.

Less attention has been focused on particles generated by corrosion, perhaps because evidence of macroscopic corrosion in the current generation of single-part components is rare. Willert et al43 reported that the preponderance of particles in the periprosthetic tissues of 19 patients with failed metal-on-metal THRs were corrosion products, based on a reversal of the Cr/ Co ratio in the tissues relative to the alloy. In addition, there has been a report of corrosion product deposition on a retrieved McKee-Farrar metal-on-metal bearing.35 Although characteristics (composition, size, morphologic features) and biologic response to corrosion debris from metal-on-metal bearings has yet to be determined, there have been several reports indicating that modular femoral THR components can undergo severe corrosion at the tapered interface between their head and neck4,8,27 and produce solid products of corrosion that are similar, if not identical, to that produced by metal-on-metal bearings.40 In the setting of modular femoral head corrosion, the corrosion products have been well-characterized and were determined to be an amorphous chromium (III) orthophosphate. This debris has been recovered from osteolytic lesions adjacent to corroded modular femoral stems20 and has been shown to be capable of inducing the release of proinflammatory cytokines from macrophage cell culture and bone resorption in organ culture.24 Furthermore, similar debris generated from corrosion of modular stainless steel femoral intramedullary nails has been associated with diaphyseal osteolysis, in the absence of PE wear debris, in the adjacent femur.22 The elucidation of the role of solid corrosion products in the clinical performance of metal-on-metal bearings will require additional study of implants and periprosthetic tissues retrieved post mortem and at revision surgery.

Metal Ion Release

Metallic implants, or wear debris generated from implants, may release chemically active metal ions into the surrounding tissues. Although these ions may stay bound to local tissues, metal ions also may bind to protein moieties that then are transported in the bloodstream and/or lymphatics to remote organs. Broad reviews of the toxicology of the elements used in orthopaedic metal alloys are available elsewhere.7,10,21,23,36,44 However, when considering the litany of documented toxicities of these elements, it is important to remember that the toxicities generally apply to soluble forms of these elements and may not apply to the chemical species that result from the degradation of prosthetic implants.

Multiple studies have shown chronic elevations in serum and urine Co and Cr after total joint replacement.17,29,37 In addition, transient elevations of urine and serum Ni have been observed immediately after surgery.37 This hypernickelemia and hypernickeluria may be unrelated to the implant because there is such a small percentage of Ni within these implant alloys. Rather, this may be related to the use of stainless steel surgical instruments (that contain a relatively higher percentage of Ni in the alloy) or metabolic changes associated with the surgery. Chronic elevations in serum Ti concentrations in subjects with total joint replacements with Ti-containing components also have been reported.16 Serum and urine V concentrations have not been found to be elevated in patients with total joint replacements partially because of the technical difficulty associated with measuring the minute concentrations present in serum.17

There is an increasing body of data available on systemic metal concentrations in patients with metal-on-metal articulating surfaces. One of the earliest reports was published approximately three decades ago when Coleman et al3 reported approximately threefold elevations of Cr in whole blood, 11-fold elevations of Co in whole blood, and 15-fold elevations of Cr in urine in nine patients with CoCr metal-on-metal THRs in comparison with their preoperative values. No such elevations were observed in patients with metal-on-polyethylene THRs. For three patients for whom longitudinal data were provided, a strong pattern of time dependent Cr and Co concentration increases in blood and urine were observed. With the reintroduction of the new generation metal-on-metal THRs there has been a resurgence of interest in systemic distribution of metal degradation products. Brodner et al2 in a prospective study with a follow up of 2 years, reported that all of the 27 patients with metal-on-metal THRs had detectable serum Co values after surgery. These values were significantly higher than in patients with ceramic-on-polyethylene articulating surfaces. Their data show than in the majority of patients, serum Co levels increased at the 2-year follow up interval compared with the 3- and 6-month intervals. The authors suggested that the wear-in period for these devices may exceed 2 years. In a follow up study at 5 years postoperative, these authors suggested that the serum Co levels were relatively constant, and no “wear-in” period could be ascertained.

Schaffer et al32 retrospectively studied 76 patients with stable metal-on-metal THRs. The patients were grouped according to their postoperative period of 1, 2, and 3 years. A group of patients about to have surgery served as controls. These investigators measured Cr and Co in whole blood and urine. Their data indicate that Co and Cr concentrations in blood were elevated at selected postoperative intervals and that urinary concentrations for Co and Cr were increased significantly at all periods postoperative compared with the concentrations observed in controls. Gleizes et al11 also reported on serum Co levels in patients with metal-on-metal articulating surfaces. Their follow up ranged from 2.6 to 35 months with a mean follow up of 12.9 months. All of the patients with metal-on-metal implants had higher serum Co values than a group of patients with no implants. They observed that patients who had a follow up of greater than 18 months were likely to have higher serum Co values than those whose follow up was less than 18 months. They attributed this increase to increased activity after 18 months after surgery.

MacDonald et al25 reported erythrocyte metal levels in a randomized, controlled study of 41 patients having metal-on-metal versus metal-on-polyethylene THRs at a minimum of 2-years of follow up. In comparison with patients with PE inserts, patients with metal inserts had a 5.3-fold increase in erythrocyte Co, no increase in erythrocyte Cr, a 35.1-fold increase in urine Co, and a 17.4-fold increase in urine Cr. Forty-one percent of patients with metal-on-metal implants had increasing metal levels at the most recent follow up.

Metal-on-metal resurfacing arthroplasty has become increasingly popular as a more conservative option for hip reconstruction. It is of interest to determine the impact of the altered geometry of surface replacements (absence of modularity, larger head size and smaller femoral stem size in comparison to total hip replacements) on the serum and urine metal concentrations. In a preliminary study with 1 year postoperative follow up, the serum and urine Co and Cr concentrations in patients with metal-on-metal surface replacements were within the same range as those from patients with metal-on-metal THRs.34 For both surface replacement and THR, however, the concentrations were considerably higher than those present in patients with conventional metal-on-polyethylene THRs using identical analytic techniques (Fig 1).

Fig 1. This figure summarizes several longitudinal and cross sectional cohort studies on serum Cr levels in patients having total hip reconstruction with either metal-on-metal resurfacing arthroplasty (Conserve plus,34 McMinn/Wagner18), metal-on-metal THA (Perfecta, McKee-Farrar18), or metal-on-polyethylene THA19 (hybrid, extensively porous-coated cementless CoCr, proximally porous-coated cementless Ti/CoCr head). All of these studies used identical analytic techniques. Metal-on-metal bearings were associated with approximately 6-fold to 10-fold elevations in serum Cr with respect to metal-on-polyethylene bearings, even in patients with clinically successful long-term (> 20 years) McKee-Farrar implants. Serum Cr levels in patients with contemporary metal-on-metal THRs.

It should be pointed out, however, that in contrast to surface replacements, several THR designs, including the one in the aforementioned study, have two metal-on-metal modular taper connections (in the acetabular and femoral component), which are potential sources of metal release.13,19 Therefore, it is not possible to isolate the amount of metal generated from the bearing versus the amount generated from other sources.

In a unique long-term (> 20-year follow up) study examining serum and urine metal levels in eight patients with well-functioning McKee-Farrar metal-on-metal THRs, it was shown that these patients had 9-fold elevations in serum Cr, 35-fold elevations in urine Cr and at least 3-fold elevations in serum Co with respect to control subjects without implants.18 With respect to a longitudinal cohort of patients with well-functioning metal-on-polyethylene implants studied up to 3 years postoperative using identical analytic techniques,19 the patients with long-term metal-on-metal bearings have approximately 6.4-fold elevations in serum Cr, 4-fold elevations in urine Cr and 3.5-fold elevations in serum Co (Fig 1). This study suggests that the elevated serum and urine Co and Cr concentrations observed in the recent studies on the newer generation of metal-on-metal bearings may persist throughout the lifetime of the implant. This only can be established with continued follow up of patients with such devices.

Hypersensitivity

Dermal hypersensitivity to metals is fairly common, affecting approximately 10% to 15% of the population.14 The term hypersensitivity refers to the induction of the immune system by a sensitizer. This response can be humoral (initiated by antibody or formation of antibody-antigen complexes) that takes place within minutes (Type I, Type II and Type III reactions), or cell-mediated (a delayed-type hypersensitivity (DTH) response) that occurs over days (Type IV). Dermal contact and ingestion of metals have been documented to cause immune reactions.14

Data from numerous investigations regarding the prevalence of metal sensitivity, albeit with heterogeneous patient populations and testing methodologies, have been compiled. The combined results of approximately 50 studies shows that the prevalence of metal sensitivity among the general population is approximately 10% to 15%, with Ni sensitivity the highest (approximately 14%).14 Because the cross reactivity of these antigens is high, the prevalence of metal sensitivity generally is considered to be 10%, the approximate average of the three metals. Cross reactivity between Ni and Co is the most common.14

The incidence of metal sensitivity among patients with well-functioning and poorly-functioning implants is approximately twice as high (approximately 25%) as that of the general population. Furthermore, the prevalence of metal sensitivity among patients with a failed implant, compiled from five investigations, is 50% to 60%, approximately five times the incidence of metal sensitivity observed in the general population and two to three times that of all patients with metal implants.14 The increased prevalence of metal sensitivity among patients with loose prostheses has prompted the speculation that immunologic processes may be a factor in implant loosening. Currently, however, it is unclear whether metal sensitivity caused the increased prevalence of implant loosening or whether implant loosening results in the development of metal sensitivity. It currently is unknown whether metal sensitivity exists only as an unusual complication in a few susceptible patients, or is more common and plays a contributory role in implant failure. These considerations are of particular concern in patients with metal-on-metal bearings, which consistently have serum metal concentrations that are higher than in patients with metal- or ceramic-on-polyethylene bearings. Patients with metal-on-metal bearings also have had a higher prevalence of metal sensitivity as determined by patch testing.14

Carcinogenesis

The carcinogenic potential of the metallic elements used in orthopaedic implants has historically been of interest. This particularly is true for joint replacement components because the large surface areas of cementless porous coated devices are intended for implantation in younger, more active patient populations that may have life expectancies exceeding 30 years. Animal studies have documented the carcinogenic potential of orthopaedic implant materials; small increases in rat sarcomas were observed to correlate with metal implants that had high Co, Cr, or Ni content.28 Furthermore, lymphomas with bone involvement were more common in rats with metallic implants.28 Implant site tumors in dogs and cats, primarily osteosarcoma and fibrosarcoma, have been associated with stainless steel internal fixation devices.1

The occurrence of tumors at the site of metallic implants in humans also has been reported. In a review of the literature that included publications up until 1992, 24 cases of malignancies adjacent to a total joint replacement device were cited. The most common lesion was malignant fibrous histiocytoma.16 Because of the large number of joint replacement devices inserted up until that time, this would seem to be a relatively small number of cases. This suggests that the occurrence of periimplant malignancies may be coincidental. However, because many such cases may go unreported and because these tumors may have relatively long latency periods, additional surveillance and broad-based epidemiologic studies are warranted.

There have been several human epidemiologic studies of systemic and remote cancer incidence in the first and second decades after THR. In two studies, slight increases in the risk of lymphoma and leukemia were observed in patients who had a Co-alloy THR, particularly in those patients who had a metal-on-metal device.9,41 Larger, more recent studies have showed no significant increase in leukemia or lymphoma;26,30 however, these studies did not include as large a proportion of subjects with metal-on-metal prostheses. Interestingly, studies have shown a decreased incidence of certain tumors, including breast carcinoma,9 sarcoma31 and stomach30,41 in recipients of total joint replacements.

Therefore, it may be that there are constitutive differences in the populations with and without implants that are independent of the implant. This clearly confounds the interpretation of these epidemiologic investigations. In a recent review on the relationship between cancer and TJR, Tharani et al39 have highlighted the serious limitations in the available data stemming from insufficient periods of follow up, a lack of information regarding dose-response, the presence of confounding comorbidities, and the dearth of data from populations outside of Scandinavia. Currently, the association of metal release from orthopaedic implants with carcinogenesis remains conjectural because causality has not been definitely established in human subjects.

Discussion

Implants fabricated from nonbiologic engineering materials continue to be crucial tools in the armamentarium of the orthopaedic surgeon. When used for the appropriate indications and when inserted with proper technique, these implants have been successful with few serious short-term and long-term clinical sequelae. However, as more experience is gained with these devices, it is evident that, in certain situations, adverse biologic effects may occur that may compromise the clinical outcome.

Characterization of the bioavailability and bioreactivity of the metal species that have been released from prosthetic materials is the next step in this line of investigation. Central to this determination is the speciation of the metal moieties present in body fluids and tissue stores that result from implant degradation, because many of the metals used in implants have valence and ligand dependent toxicities in mammalian systems. Such studies represent an enormous challenge because of the technical complexities of working with nanometer-sized particles and ion concentrations in the parts per billion range. Current technologic tools (graphite furnace Zee-man atomic absorption spectrophotometry and inductively coupled plasma-mass spectrometry) can measure only the concentration of the element and provide no information on the chemical form or biologic activity. Currently, there is limited information in the literature that describes the physical chemical form of the degradation products of metallic joint replacement prostheses. Ultimately, specific toxicologic investigation of relevant species can be used in animal models and cell cultures to delineate the biologic effects of these degradation products.

Finally, longer-term multicenter epidemiologic studies are required to fully address the issues of metal implant associated carcinogenesis, hypersensitivity, and remote toxicity. Additional advances in molecular biology and materials science, applied to the study of the host tissue response to implanted devices, promises to increase our understanding of the critical determinants of implant biocompatability. This will provide new opportunities for the development of improved biomaterials, novel diagnostic and screening modalities, and pharmacological strategies to modify host response. Ultimately, this promises to lead to improved clinical outcomes for patients requiring implanted devices.

Acknowledgements

We thank our collaborators at the Joint Replacement Institute/Orthopaedic Hospital in Los Angeles, CA who provided access to materials from their patients with metal-on-metal bearings: Harlan Amstutz, MD, Thomas P. Schmalzried, MD, and Patricia Campbell, PhD.

References

1. Black J: Orthopaedic Biomaterials in Research and Practice. New York, Churchill Livingstone 1988: 292-295.
2. Brodner W, Bitzan P, Meisinger V, et al: Elevated serum cobalt with metal-on-metal articulating surfaces [published erratum appears in J Bone Joint Surg 79B:585, 1997]. J Bone Joint Surg 796:316-321, 1997.
3. Coleman RF, Henington J, Scales JT: Concentrating of wear products in hair, blood and urine after total hip replacement. BMJ 1:527-529, 1973.
4. Collier JP, Suiprenant VA, Jensen RE, Mayor MB, Surprenant HP: Corrosion between the components of modular femoral hip prostheses. J Bone Joint Surg 746:511-517, 1992.
5. Doom PF, Campbell PA, Worrall J, et al: Metal wear particle characterization from metal on metal total hip replacements: Transmission electron microscopy study of periprosthetic tissues and isolated particles. J Biomed Mater Res 42:103-111, 1998.
6. Doom PF, Mirra, JM, Campbell PA, Amstutz HA: Tissue reaction to metal on metal total hip prostheses. Clin Orthop 329(Suppl):S187-S205, 1996.
7. Elinder CG, Friberg L: Cobalt. In Friberg L, Nordberg GF, Vouk VB (eds). Handbook of the Toxicology of Metals. Vol 2. Amsterdam, Elsevier 211-232, 1986.
8. Gilbert JL, Buckley CA, Jacobs JJ: In vivo corosion of modular hip prosthesis in mixed and similar metal combinations: The effect of crevice, stress motion and alloy coupling. J Biomed Res 27:1533-1544, 1993.
9. Gillespie WJ, Frampton CMA, Henderson RJ, Ryan PM: The incidence of cancer following total hip replacement. J Bone Joint Surg 708:539-542, 1988.
10. Gitelman HJ: Aluminum and Health: A Critical Review. New York, Dekker 1989.
11. Gleizes V, Poupon J, Lazennec JY, Chamberlin B, Saillant G: [Value and limits of determining serum cobalt levels in patients with metal on metal articulating prostheses]. Rev Chir Orthop Rep-aratrice Appar Mot 85:217-225, 1999.
12. Hallab NJ, Jacobs JJ, Skippr AK, et al: Systemic metal-protein binding associated with total joint replacement arthroplasty. J Biomed Mater Res 49:353-361,2000.
13. Jacobs JJ, Gilbert JL, Urban RM: Current concepts review: Corrosion of metal orthopaedic implants. J Bone Joint Surg 80A:268-282, 1998.
14. Jacobs JJ, Goodman SB, Sumner DR., Hallab NJ: Biologic Response to Orthopaedic Implants. In Buck-waiter JA, Einhom TA, Simon SR (eds). Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System. Ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons 401—426, 2000.
15. Jacobs JJ, Roebuck KA, Archibeck M, Hallab NJ, Giant TT: Osteolysis: Basic science. Clin Orthop 393:71-77, 2001.
16. Jacobs JJ, Rosenbaum DH, Hay RM, Gitelis S. Black J: Early sarcomatous degeneration near a ce-mentless hip replacement: A case report and review. J Bone Joint Surg 746:740-744, 1992.
17. Jacobs JJ, Skipor AK, Black J, Urban RM, Galante JO: Release and excretion of metal in patients who have a total hip-replacement component made of n’tanium-basealloy. J Bone Joint Surg 73A:1475-1486, 1991.
18. Jacobs JJ, Skipor AK, Doom PF, et al: Cobalt and chromium concentrations in patients with metal on metal total hip replacements. Clin Orthop 329 (Suppl):S256-S263, 1996.
19. Jacobs JJ, Skipor AK, Patterson LM, et al: Metal release in patients who have had a primary total hip arthroplasty: A prospective, controlled, longitudinal study. J Bone Joint Surg 80A: 1447-1458, 1998.
20. Jacobs JJ, Urban RM, Gilbert JL, et al: Local and distant products from modularity. Clin Orthop 319: 94-105, 1995.
21. Jandhyala BS, Horn GJ: Minireview: Physiological and pharmacological properties of vanadium. Life Sci 33:1325-1340, 1983.
22. Jones DM, Marsh JL, Nepola JV, et al: Focal os-teolysis at the junctions of a modular stainless-steel femoral intramedullary nail. J Bone Joint Surg 83A:537-548, 2001.
23. Langard S, Norseth T: Chromium. In Friberg L, Nordberg GF, Vouk VB (eds). Handbook of the Toxicology of Metals. Vol 2. Ed 2. Amsterdam, Elsevier 185-210, 1986.
24. Lee S-H, Brennan FR, Jacobs JJ, et al: Human monocyte/macrophage response to cobalt-chromium corrosion products and titanium particles in patients with total joint replacements. J Orthop Res 15:40-49, 1997.
25. MacDonald SJ, McCalden RW, Chess DG, et al: Metal-on-metal versus polyethylene in hip arthroplasty: A randomized clinical trial. Clin Orthop 406:282-296, 2003.
26. Mathiesen EB, Ahlbom A, Bermann G, Lindgren JU: Total hip replacement and cancer: A cohort study. J Bone Joint Surg 776:345-350, 1995.
27. Mathiesen EB, Lindgren JU, Blomgren GGA, Reinholt FP: Corrosion of modular hip prostheses. J Bone Joint Surg 736:569-575, 1991.
28. Memoli VA, Urban RM, Alroy J, Galante JO: Malignant neoplasms associated with orthopaedic implant materials in rats. J Orthop Res 4:346-355, 1986.
29. Michel R, Hofrnann J, Loer F, Zilkens, J: Trace element burdening of human tissues due to the corrosion of hip-joint prostheses made of cobalt-chromium alloys. Arch Orthop Trauma Surg 103:85-95, 1984.
30. Nyren O, McLaughlin JK, Gridley, C, et al: Cancer risk after hip replacement with metal implants: A population-based cohort study in Sweden. J Nat Cancer Inst 87:28-33, 1995.
31. Paavolainen P, Pukkala E, Pulkkinen P, Visuri T: Cancer incidence in Finnish hip replacement patients from 1980 to 1995: A nationwide cohort study involving 31,651 patients. J Arthoplasty 14:272-280, 1999.
32. Schaffer AW, Pilger A, Engelhardt C, Zweymueller K, Ruediger HW: Increased blood cobalt and chromium after total hip replacement. J Toxicol Clin Toxicol 37:839-844, 1999.
33. Shanbhag AS, Jacobs JJ, Black J, et al: Macrophage/ particle interactions: Effect of size, composition and surface area. J Biomed Mater Res 28:81-90, 1994.
34. Skipor AK, Campbell PA, Patterson LM, et al: Serum and urine metal levels in patients with metal on metal surface arthroplasty. J Mater Sci Mater Med 13:1227-1234, 2002.
35. Smethurst E, Waterhouse RB: Causes of failure in total hip prostheses. J Mater Sci 12:1781-1792, 1977.
36. Sunderman FW: A pilgrimage into the archives of nickel toxicology. Ann Clin Lab Sci 19:1-16, 1989.
37. Sunderman Jr FW, Hopfer SM, Swift T, et al: Cobalt, chromium, and nickel concentrations in body fluids of patients with porous-coated knee or hip prostheses. J Orthop Res 7:307-315, 1989.
38. Svensson O, Mathiesen EB, Reinholt FP, Blomgren G: Formation of a fulminant soft-tissue tumor after uncemented hip arthroplasty: A case report. J Bone Joint Surg70A: 1238-1242, 1988.
39. Tharani R, Dorey FJ, Schmalzried TP: The risk of cancer following total hip or knee arthroplasty. J Bone Joint Surg 83A:774-780, 2001.
40. Urban RM, Jacobs JJ, Gilbert JL, Galante JO: Migration of corrosion products from modular hip prostheses: Particle microanalysis and histopatho-logical findings. J Bone Joint Surg 76A:1345-1359, 1994.
41. Visuri T, Pukkala F, Paavolainen P, Pulkkinen P, Riska EB: Cancer risk after metal on metal and
polyethylene on metal total hip arthroplasty. Clin Orthop 329(Suppl):S280-S289, 1996.
42. Willert HG, Buchhom GH, Fayyazi A, Lohmann CH: Histopathological changes around metal/metal joints indicate delayed type hypersensitivity: Preliminary results of 14 cases. Osteologie 9:2-16,2000.
43. Willert HG, Buchhorn GH, Gobel D, et al: Wear behavior and histopathology of classic cemented metal on metal hip endoprostheses. Clin Orthop 329 (Suppl):S160-186, 1996.
44. Williams DF: Biological Effects of Titanium. In Williams DF (ed). Systemic Aspects of Biocompati-bility. Vol 1. Boca Raton, FL, CRC Press 169-177, 1981.

CLINICAL ORTHOPAEDICS AND RELATED RESEARCH
Number 417, pp. 1-9
© 2003 Lippincott Williams & Wilkins, Inc.


Metal-on-Metal Articulation – TWO YEAR METAL ION LEVELS IN PATIENTS WITH METAL-ON-METAL ARTHROPLASTY


Anastasia K. Skipor1, Patricia A. Campbell2, Harlan C. Amstutz2 and Joshua J. Jacobs1
1Orthopedic Surgery, Rush Presbyterian St. Luke’s Medical Center, Chicago II 60612
2Joint Replacement Institute, Orthopedic Hospital, Los Angeles CA 90007

Introduction

Metal-on-metal articulation is becoming a more accepted alternative in hip replacement surgery. It is also intended for the younger and more active patient where polyethylene wear and its accompanying osteolysis of the more conventional metal-on-polyethylene bearings is of most concern. Surface arthroplasty of the hip is a conservative procedure designed to retain valuable femoral bone stock in younger patients. In this study we examine serum chromium (SrCr) and cobalt (SrCo) and urine chromium (UrCr) in patients with metal-on-metal surface arthroplasty (SA) of the hip.

Materials and Methods

This is a prospective study. Nine patients with metal-on-metal surface arthroplasty of the hip are presented. The patients were implanted with the Conserve+® surface arthroplasty. The acetabular component consists of one piece and has sintered CoCr (F75) beads on the outer surface designed for interference fitting to obtain initial stability. The femoral component is a CoCr (F75) hemispheric shell with a chamfered cylindrical interior design and a short tapered stem to enhance alignment and stability. The femoral head size ranged from 40 to 52 mm. There were 6 males and 3 females with an average age at implantation of 45 years (range 28 – 59 years). The components were manufactured by Wright Medical Technology Inc. (Arlington, TN, USA) Serum and urine samples were collected pre-operatively and at 3, 6 and 12 months post implantation. Serum was assayed for Cr and Co and urine for Cr concentration using graphite furnace atomic absorption spectrophotometry. The detection limits in serum were 0.03 ng/ml (ppb) for Cr and 0.3 ppb for Co and 0.015 ppb for Cr in urine.

Results

The concentration for SrCr, UrCr and SrCo for the nine cases, are shown in Figs. 1-3, respectively. The data indicate that for SrCr, levels are still elevated at 12 months postoperatively and then decrease. Five of the nine cases had lower values at 24 months post operatively than their previous sampled time period. A similar trend is seen for SrCo but the change is more dramatic following the 6 month postoperative time period (Fig 3). Of the nine cases 7 had SrCo levels at 24 months post operatively lower than their previous sampled time period, (Fig 2). UrCr levels increase up to 12 months and then begin to decline. Six of the 8 cases for which we had urine levels at 24 months post operatively demonstrated lower values than their previous sampled time period.

Discussion

This group of patients is a subset of a larger group that we are following prospectively. As can be seen with the exception of SrCo all post-operative time periods had elevated levels compared to their pre-operative levels, and these levels are higher than those observed in patients with metal-on-poly bearings1. However over 50% of these individuals had lower levels at their latest follow-up compared to their previous sampled time period. In the case of SrCo two cases have already returned to their pre-operative levels by 24 months post-operative. The data demonstrate that the values by two years begin to decline. It is still early to tell with any certainty due to the small sample size but the wear in period of these devices is longer than the accepted 1-year or 1 million cycles generally observed in metal-on-poly bearings.

While the wear properties of metal-on-metal bearings are better than those observed in metal-on-poly bearings, the wear particles generated by these bearings are greater in number and smaller in size. Therefore for a given wear volume many more particles will be released into the surrounding tissue and be available for corrosion and subsequent release of metal ions into the system. The decline in metal ion levels in most of these patients supports the anticipated low steady state wear in well functioning metal-on-metal bearings.

References

1. Jacobs, J.J. et. al. JBJS 80-A:1447-1458.
2. Doom, P.P. et. al. JBMR 442:103-111


Metal-on-Metal Articulation – Biological Issues in Metal-Metal Total Hip Arthroplasty.

Published in the Biomaterials Forum
Thomas P. Schmalzried, M.D.
Patricia Campbell, Ph.D. ‘ Frank W. Chan, Ph.D.

Metal-metal technology for total hip replacements has become a viable alternative bearing combination to metal-conventional polyethylene articulating couples since polyethylene wear particle-induced osteolysis was identified in the early 1990s as the leading problem in total hip arthroplasty. Extensive research and development has provided the orthopaedic community with an increased understanding of the engineering issues related to good metal-metal wear performance.4 Despite this and state-of-the-art manufacturing leading to reproducible, low-wearing metal-metal couples, the biological issues of this technology remain in the spotlight.

The wear rate of metal-metal hips is a fraction of the wear rate of metal-conventional ultra-high molecular weight polyethylene (UHMWPE) implants.25,29. However, the cobalt chromium alloy (CoCr) particles found within macrophages around metal-metal total hips are in the nanometer-size range, one order of magnitude smaller than typical polyethylene particles.6 Because smaller particles will have relatively larger surface area, there may be potential clinical ramifications as total particle surface area can possibly influence dissolution rate and biological activity. Surface area has been identified as a variable affecting the macrophage response to particles.28

The focus of concern, therefore, has been the wear particles generated from the intended motion of the joint, the ball moving relative to the socket. Practically, however, numerous wear particles can also be generated from other, non-articulating surfaces in what is referred to as mode four wear.21 This includes particles generated from relative motion due to loosening, modular connections, and neck-socket impingement, which can be orders of magnitude greater than that generated by a well-functioning hip articulation. Studies have shown that mode four wear can potentially cause adverse local and systemic tissue reactions31 including rapid osteolysis26, resulting in the need for revision despite little wear of the primary metal-metal bearing.16 With regard to adverse biological reactions, the malfunctioning joint is a greater threat to the host than the intended wear of the metal-metal articulation.

Although the actual nature of the metallic wear particles and organometallic complexes formed in vivo is still under investigation, recent studies have attempted to utilize more clinically relevant models, for example, by exposing particles to serum prior to use in vitro, employing particles extracted from periprosthetic tissues, or using particle doses similar to those occurring in vivo.12,20,27 While experiments conducted with variable cell types, particles, and analytical methods often lead to conflicting results,15 it consistently appears that, at clinically relevant concentrations, the wear products from CoCr implants are able to modulate cytokine expression in macrophages10,11,15,33 and may have inhibitory effects upon osteoblasts,1 neutrophils,24 and T cells9 but do not induce cytotoxic effects.1,14,33 In contrast to the latter observation from cell culture models is the frequent observation of necrosis in the periprosthetic tissues of metal-metal total hips.2’7,8,19 However, a direct correlation between necrosis and visible metallic particles has not been established and extensive necrosis is also seen in tissues around failed metal-UHMWPE total hips.7

Studies of the levels of cobalt and chromium in the hair, blood, and urine have shown that metallic content in patients with metal-metal total hips are generally higher than in patients with metal-UHMWPE articulations.5 This finding has been repeated in more recent studies of serum and urine metal levels that employed analytical instruments with increased sensitivity and stringent methods to avoid contamination of the samples.17,18 These studies indicated that cobalt ions are rapidly transported from the implant site and mostly eliminated in the urine while chromium tends to be stored in the tissues and eliminated more slowly. While the release of cobalt and chromium ions from metal-metal total hips has been verified, the clinical significance of this finding is still unclear.

Cobalt and chromium wear particles have been shown to induce carcinoma in animal models,13 giving rise to the concern that such alloys could have the same effect if present in sufficient amounts in human tissue for a sufficient length of time. Elevated levels of cobalt and chromium have been found in human tissues surrounding orthopaedic implants and in tissues at remote sites.3 The concern, therefore, is that metal-metal bearings used in total hip arthroplasty may pose a higher risk of malignant degeneration because of an increased exposure to metal particles and ions. Although metal particles and ions have been the prominent concern, there have also been reports of cancer induction with polymethylmethacrylate (bone cement)23 and polyethylene22 in animal models. Overall, the available epidemiological data do not demonstrate an increase in cancer risk following total hip replacement.32 At the same time, it is important to recognize the limitations of the available data with regard to sample size, length of follow-up, and lack of stratification for other co-morbidities.30

The issue of delayed-type hypersensitivity (DTH) to the main elements in metal-metal total hips – cobalt, chromium, and nickel -was addressed in the 1960s and 1970s using skin patch testing. Although this is now recognized as unreliable for the assessment of hypersensitivity to implants, this type of testing has shown that cobalt, chromium, and nickel are associated with contact dermatitis, and as many as 15% of the population is estimated to be sensitive to cobalt and nickel and 8% to chromium. Because there is a higher reported incidence of metal sensitivity in patients with loose components, the association between metal sensitivity and loose implants has fueled a long-standing debate: does hypersensitivity cause loosening or does loosening cause hypersensitivity? Either way, it does appear that a small number of patients with metal-metal total hips develop an adverse local tissue response and present with unexplained pain and chronic effusions that resolve when the metal-metal bearings are exchanged for metal-UHMWPE hips. The histology of abundant lymphocytes and plasma cells is highly suggestive of an immune response. Therefore, caution should be taken in the implantation of a metal-metal bearing in patients with a known sensitivity to metals.

Further investigations of the local and systemic effects related to the wear of the primary articulating surface are needed. It should be emphasized, however, that clinical success is multifactorial. Patient selection, surgical technique, component fixation, and the other aspects of the prosthetic joint will influence the clinical performance of any articulation.

References

1. Alien MJ,,Myer BJ, Millett PJ, and Rushton N: The effects of particulate cobalt, chromium and cobalt-chromium alloy on human osteoblast-like cells in vitro. J Bone Joint Surg 79B: 475-482, 1997.
2. Campbell P, McKellop H, Lu B, Park SH, Doom P, Dorr L, and Amstutz HC: Clinical wear performance of modern metal-on-metal hip arthroplasties. Trans Soc forBiomatls 24: 210, 1998.
3. Case CP, Langkamer VG, James C, Palmer MR, Kemp AJ, Heap PF, and Solomon L: Widespread dissemination of metal debris from implants. J Bone Joint Surg 76B: 701-712, 1994.
4. Chan FW, Bobyn JD, Medley JB, Krygier JJ, and Tanzer M: Wear and lubrication of metal-on-metal hip implants. Clin Orthop 369: 10-24, 1999.
5. Coleman RF, Herrington J, and Scales JT: Concentration of wear products in hair, blood, and urine after total hip replacement. BrMedJ 1: 527-529, 1973.
6. Doom PF, Campbell PA, Worrall J, Benya PD, McKellop HA, and Amstutz HC: Metal wear particle characterization from metal on metal total hip replacements: Transmission electron microscopy study of periprosthetic tissues and isolated particles. J Biomed Mater Res 42: 1013-1111, 1998.
7. Doom PF, Mirra JM, Campbell PA, and Amstutz HC: Tissue reaction to metal on metal total hip prostheses. Clin Orthop 329 Suppl: S187-205, 1996.
8. Evans EM, Freeman MAR, Miller AJ, and Vernon-Roberts B: Metal sensitivity as a cause of bone necrosis and loosening of the prosthesis in total joint replacement. J Bone and Joint Surg 56B: 626-642, 1974.
9. Faleiro C, Godinho I, Reus U, and de Sousa M: Cobalt-chromium-molybdenum but not titanium-6aluminium-4vanadium alloy discs inhibit human T cell activation in vitro. Biometals 9: 321-326, 1996.
10. Goodman SB, Lind M, Song Y, and Smith RL: In vitro, In vivo and tissue retrieval studies on particulate debris. Clin Orthop 352: 25-34, 1998.
11. Haynes DR, Boyle SJ, Rogers SD, Howie DW, and Vernon-Roberts B: Variation in cytokines induced by particles from different prosthetic materials. Clin Orthop 352:223-230, 1998.
12. Haynes DR, Rogers SD, Hay S, Pearcy MJ, and Howie DW: The differences in toxicity and release of bone-resorbing mediators induced by titanium and cobalt-chromium-alloy wear particles. J Bone and Joint Surg 75A: 825-834, 1993.
13. Heath JC, Freeman MAR, and Swanson SAV: Carcinogenic properties of wear particles from prostheses made in cobalt-chromium alloy. Lancet 564-566, 1971.
14. Horowitz SM, Luchetti WT, Gonzales JB, and Ritchie CK: The effects of cobalt chromium upon macrophages. J Biomed Mater Res 41: 468-473, 1998.
15. Howie DW, Rogers SD, McGee MA, and Haynes DR: Biologic effects of cobalt chrome in cell and animal models. Clin Orthop 329 Suppl: S217-232, 1996.
16. lida H, Kaneda E, Takada H, Uchida K, Kawanabe K, Nakamura T: Metallosis due to impingement between the socket and the femoral neck in a metal-on-metal bearing total hip prosthesis. A case report. J Bone and Joint Surg 81A: 400-403, 1999.
17. Jacobs J, Skipor A, Black J, Hastings C, Schavocky J, Urban R, and Galante J: Metal release and excretion from cementless titanium total knee replacements. Trans Soc forBiomatls 13:199, 1990.
18. Jacobs JJ, Skipor AK, Paterson LM, Hallab NJ, Paprosky WD, Black J, and Galante JO: Metal release in patients who have had a primary total hip arthroplasty. J Bone and Joint Surg 80A: 1447-1458, 1998.
19. Jones DA, Lucas HK, O’Driscoll M, Price CHG, and Wibberley B: Cobalt toxicity after McKee hip arthroplasty. J Bone and Joint Surg 57B: 289-296, 1975.
20. Kim KJ, Hijikata H, Itoh T, and Kumegawa M: Joint fluid from patients with failed total hip arthroplasty stimulates pit formation by mouse osteoclasts on dentin slices. J Biomed Mater Res 43: 234-240, 1998.
21. McKellop HA, Campbell P, Park S, Schmaizried TP, Amstutz HC, and Sarmiento A: The origin of sub-micron polyethylene wear debris in total hip arthroplasty. Clin Orthop 311: 3-20, 1995.
22. Memoli VA, Urban RM, Alroy J, and Galante JO: Malignant neoplasms associated with orthopedic implant materials in rats. J Orthop Res 4: 346-355, 1986.
23. Oppenheimer BS, Oppenheimer ET, and Danishefsky I: Further Studies of Polymers as Carcinogenic Agents in Animals. Cancer Res 15: 333-340. 1955.
24. Rae T: The action of cobalt, nickel and chromium on phagocytosis and bacterial killing by human polymorphonuclear leukocytes; its relevance to infection after total joint arthroplasty. Biomatls4: 175-180, 1983.
25. Schmaizried TP, Peters PC, Maurer BT, Bragdon CR, and Harris WH: Long duration metal-on-metal total hip replacements with low wear of the articulating surfaces. J Arthroplasty 11: 322-331, 1996.
26. Schmaizried TP, Zahiri CA, and Woolson ST: The significance of stem-cement loosening of grit-blasted femoral stems. Orthopedics 23: 1157-1164, 2000.
27. Shanbhag AS, Dowd JE, Jacobs JJ, Tramaglini DM, Giant TT, Black J, and Rubash HE: Biological response to particulate debris: In vitro and in vivo studies. Cells and Mails 7: 175-182, 1997.
28. Shanbhag AS, Jacobs JJ, Black J, Galante JO, and Giant TT: Macrophage/particle interactions: effect of size, composition and surface area. J Biomed Mater Res 28: 81-90, 1994.
29. Sieber HP, Rieker CB, and Kottig P: Analysis of 118 second-generation metal-on-metal retrieved hip implants. J Bone and Joint Surg 81 B: 46-50, 1999.
30. Tharani R, Dorey FJ, and Schmaizried TP: The risk of cancer following total hip or total knee arthroplasty. In press, J Bone and Joint Surg (Am), May 2001.
31. Urban RM, Jacobs JJ, Tomlinson MJ, Gavrilovic J, Black J, Peoc’h M: Dissemination of wear particles to the liver, spleen, and abdominal lymph nodes of patients with hip or knee replacement. J Bone and Joint Surg 82A: 457-477, 2000.
32. Visuri T: Cancer risk after metal on metal hip prosthesis. In Rieker C and Wyss U eds. Metasul A Metal-on-Metal Bearing. Bern, Hans Huber, pp 149-154, 1999.
33. Wang JY, Wicklund BH, Gustilo RB, and Tsukayama DT: Titanium, chromium and cobalt ions modulate the release of bone-associated cytokines by human monocytes/macrophages in vitro. Biomatls 17: 2233-2240, 1996.