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Three skeletally immature patients with scapulothoracic dissociation were reviewed. A 5-year-old child's arm, caught in a conveyor belt, led to complete upper extremity amputation. Multiple fractures, muscular damage, and cutaneous and subcutaneous tissue disruption (degloving) were present throughout the avulsed extremity. Replantation was considered, but not carried out because of these extensive injuries. He was treated with a myoelectric prosthesis. Two older boys had scapulothoracic dissociation (one open, one closed) associated with clavicular diaphyseal fractures following blunt trauma. In each case, the clavicle was stabilized, muscular disruptions were reattached, and bleeding was controlled locally, although no specific major vascular repair was required. There was no return of neurologic function, leaving each patient with a flail upper extremity. One patient and his family eventually elected to have a shoulder disarticulation followed by fitting with a myoelectric prosthesis. The other patient still had a flail extremity at his last evaluation 17 months postinjury, but did not return for subsequent evaluation.

Recurrent posterior glenohumeral instability is uncommon and is often misdiagnosed. Damage to the posterior capsule, posteroinferior glenohumeral ligament, and posterior labrum have all been implicated as sources of traumatic posterior instability. We describe a case of traumatic recurrent posterior instability resulting from a posterior Bankart lesion accompanied by posterior humeral avulsion of the glenohumeral ligaments. The Bankart lesion was repaired using a single arthroscopic suture anchor at the glenoid articular margin. The posterior humeral avulsion of the glenohumeral ligaments was addressed with 3 suture anchors placed at the capsular origin at the posterior humeral head. Using these anchors, the posterior capsule was advanced laterally and superiorly for a secure repair. Arthroscopic anatomic reconstruction of both lesions resulted in an excellent clinical outcome.

The levels of streptococcal antibody titers in populations with or without rheumatic fever from an area with a relatively high incidence of rheumatic fever and an area with a low incidence of this disease were compared. Streptococcal antibody titers were determined for two populations, each of which included children without rheumatic fever (nonrheumatic children) and rheumatic fever patients. The two populations were derived from two separate geographic areas, one with a high incidence of rheumatic fever (Grenada) and another with a low incidence of this disease (central Florida). The results revealed an absence of consistent differences in the geometric mean antibody titers between the nonrheumatic subjects and the rheumatic fever patients from Grenada. In the population from Grenada, the mean anti-streptolysin O and anti-DNase B titers were higher in the nonrheumatic controls (P of 0.085 and 0.029, respectively). However, the mean titer of the antibody to the group A streptococcal cell wall carbohydrate was higher in the rheumatic fever patients than in the nonrheumatic controls (P = 0.047). This finding contrasted with the finding that the means of all three streptococcal antibody titers in the patients with rheumatic fever were significantly higher than those in the nonrheumatic subjects from Florida (P = 0.01-<0.001). The reason for this paradoxical finding became evident when the streptococcal antibody titers of the nonrheumatic subjects from Grenada and Florida were compared, revealing significantly higher levels of all three antibodies in the nonrheumatic subjects from Grenada than in the nonrheumatic subjects from Florida (P < 0.001). These results suggest that nonrheumatic individuals in an area with a high incidence of rheumatic fever have inordinately elevated levels of streptococcal antibodies in serum. The presence of elevated streptococcal antibody titers in such a population, which probably reflects a high background prevalence of streptococcal infections, should be taken into consideration when evaluating the role of the group A streptococcus in nonpurulent complications of infections.