Revision shoulder stabilization: 2- to 10-year results.

We evaluated 43 patients who underwent revision shoulder stabilization between 1978 and 1992. Twenty-three shoulders in 23 patients had unidirectional anterior shoulder instability (group A), whereas 21 shoulders in 20 patients exhibited multiple directions of shoulder instability (group B). Within group A recurrent instability developed at a mean of 35.5 months after the initial stabilization. Recurrence was traumatic in 12 patients. Revision surgery included a Bankart repair in 19 patients (coupled with capsular shift in 15 and a Bristow in 1) and capsular shift alone in 4. Within group B recurrent instability developed at a mean of only 16 months after the initial stabilization and was traumatic in only 2 patients. Revision surgery included capsular shift in 11 patients, Bankart repair in 5, anterior/posterior graft reconstruction in 3, and posterior bone block in 2. All patients had significant capsular laxity. A Bankart lesion was found in only 24% of patients. The mean follow-up from revision was 77.3 months (range 24 to 196 months) in group A. The results were excellent in 8 patients, good in 7, fair in 4, and poor in 4. Three of the 4 failures, however, had undergone successful reoperation before follow-up, improving the number of good or excellent results to 18 (78%). In contrast, at a mean follow-up of 61.5 months, only 9 (39%) good or excellent results occurred in group B despite multiple reoperations. Four patients ultimately went on to have glenohumeral fusion. Revision shoulder stabilization is a reliable procedure for patients who have recurrent anterior instability; however, it is unpredictable in patients who have multidirectional instability, with surgical failure and reoperation occurring frequently.

Osteonecrosis in the rheumatoid femoral head.

OBJECTIVE: To define the prevalence and pathological spectrum of femoral head osteonecrosis in patients with rheumatoid arthritis (RA) and to correlate its presence with disease related clinical and therapeutic factors. METHODS: A total of 545 primary total hip arthroplasties performed in 507 patients with RA were identified. A historical review of each patient's rheumatoid disease and treatment as well as pathological review of each femoral head specimen was performed. RESULTS: Osteonecrosis was identified in 66 specimens (12.1%) in one of 2 discrete forms. Thirty-two specimens (5.9%) contained classic subchondral avascular necrosis. Thirty-four specimens (6.2%) contained osteonecrosis in association with degenerative changes (within regions of sclerotic and eburnated subchondral bone), but not classic avascular necrosis. Remaining femoral head specimens were characterized by inflammatory arthritis (431 specimens) or degenerative joint disease (48 specimens). Corticosteroid therapy was used in 81% of patients with avascular necrosis and 68% with degenerative osteonecrosis. This was significantly greater prevalence than in patients without osteonecrosis (33%). Average daily prednisone dosage was 8 mg and no association between dosage and the presence of osteonecrosis was identified. No correlation between pathological findings and clinical disease severity was identified. In 5 of 27 specimens showing classic avascular necrosis and 11 of 34 containing degenerative osteonecrosis, no steroid treatment had been administered. CONCLUSION: Femoral head osteonecrosis is present in about 12% of patients with RA at hip arthroplasty, and occurs in 2 forms -- classic avascular necrosis and degenerative necrosis. Both forms are significantly associated with corticosteroid use. "Low dose" therapy does not protect patients against the development of osteonecrosis. Additionally, baseline prevalence of osteonecrosis of about 3% occurs in the absence of steroid use and may be related to the underlying inflammatory diseases. Despite its association with osteonecrosis the net effect of corticosteroid therapy on the natural history of rheumatoid hip disease remains unclear.

Hemiarthroplasty of the shoulder for rotator cuff arthropathy.

Sixteen patients underwent hemiarthroplasty for rotator cuff arthropathy between June 1989 and March 1992, and evaluations obtained before and after surgery in all patients were compared. A modular head large enough to articulate with the coracoacromial arch but not so large as to prevent approximately 50% of humeral head translation on the glenoid was used in these cases. Each patient was evaluated with Neer's limited goals rating scale after an average follow-up of 33 months (24 to 55 months). Ten patients were rated as successful and six as unsuccessful. Four of the six unsuccessful patients had undergone at least one attempt at rotator cuff repair with acromioplasty before the index procedure, and two of these four patients had deficient deltoid function after this rotator cuff surgery as a result of postoperative deltoid detachment. Also, three of these four patients who had previously undergone acromioplasty subsequently had anterosuperior subluxation after hemiarthroplasty. Hemiarthroplasty did not provide for a successful outcome in all patients with rotator cuff arthropathy. However, 10 of the 12 patients in this series with good deltoid function and an adequate coracoacromial arch were rated as successful by Neer's limited goals criteria. In addition, this study illustrates that formal acromioplasty carried out during attempts at rotator cuff repair in such patients may jeopardize the subsequent success of hemiarthroplasty.

The role of CD4+ helper T cells in the destruction of microencapsulated islet xenografts in nod mice.

Islet transplants for large numbers of patients with diabetes will require xenografts. Microencapsulation is an appealing method for islet xenografting. However, graft function has been limited by a cellular reaction, particularly intense in spontaneously diabetic, NOD mice. The purpose of this study was to elucidate the mechanism of this reaction. Poly-1-lysine-alginate microcapsules containing 4000-12,000 dog or 1800-2000 rat islets were xenografted intraperitoneally into streptozotocin (SZN)-diabetic C57BL/6J and NOD mice, with or without recipient treatment with GK 1.5 (anti-CD4 monoclonal antibody) (20-30 microliters i.p. every 5 days, begun on day -7. Grafts were considered technically successful if random blood glucose (BG) was normalized (less than 150 mg/dl) within 36 hr. Graft failure was defined as BG greater than 250 mg/dl. Dog and rat islets in microcapsules normalized BG in both SZN and NOD mice within 24 hr routinely. Empty microcapsules and GK 1.5 treatments alone did not affect BG. NODs destroyed both microencapsulated dog and rat islets more rapidly than did SZN-diabetic mice (P less than .01). Graft biopsies showed an intense cellular reaction, composed of lymphocytes, macrophages and giant cells, and no viable islets. GK 1.5 treatment significantly prolonged both dog-to-NOD and rat-to-NOD grafts (P less than 0.01). Biopsies of long-term functioning grafts (on days 65-85) demonstrated viable islets and no cellular reaction around microcapsules; 1/4 rat and 1/8 dog islet xenografts continued to function indefinitely in NOD recipients, even after cessation of GK 1.5 therapy. Prediabetic NODs receiving encapsulated dog or rat islets mounted a moderate cellular reaction to grafts. Empty microcapsules excited no cellular reaction in diabetic or prediabetic NODs. We conclude that the NOD reaction to microencapsulated xenogeneic islets is helper T cell-dependent, and that the target of this reaction is not the microcapsule itself, but the donor cells within.

A fluorinated glucose analog, 2-fluoro-2-deoxy-D-glucose (F-18): nontoxic tracer for rapid tumor detection.

Rapid uptake of F-18 FDG was observed in a variety of transplanted and spontaneous tumors in animals. The tumor uptake reached a peak by 30 min and remained relatively constant up to 60 min, with a very slow wash-out of F-18 activity from the tumor thereafter. Tumor-to-normal tissue and tumor-to-blood ratios ranged from 2.10-9.15 and 2.61-17.82, respectively, depending on the type of tumor. A scintiscan of a seminoma in a dog showed very high uptake in the viable part and lack of uptake in the necrotic mass. Toxicological studies in mice using 1000 times human tracer dose (HTD) per wk for 3 wk and in dogs using 50 times HTD per wk for 3 wk did not show any evidence of acute or chronic toxicity.