Reliability of Current Classification Systems for Periprosthetic Fractures of the Humerus.

OBJECTIVE: Numerous classification systems exist to evaluate periprosthetic humerus fractures, although most are based on limited patient numbers. The Wright and Cofield system is the most widely used classification system. We sought to evaluate the interobserver and intraobserver reliabilities of this system compared with the Unified Classification System (UCS) using the largest patient sample to date. METHODS: This retrospective study identified patients between December 2011 and January 2021 with a periprosthetic fracture of the humerus around the stem of a shoulder arthroplasty component. Three upper extremity fellowship-trained surgeons evaluated all radiographs for stem stability, evidence of preinjury stem loosening, Wright and Cofield classification, UCS classification, and recommended treatment for each case at 2 timepoints separated by 2 months. The kappa statistic for interobserver and intraobserver reliability was calculated. RESULTS: Seventy-six patients were included. There was moderate interobserver (kappa 0.53) and substantial intraobserver (kappa 0.69) agreement when classifying stem stability after fracture. There was moderate interobserver (kappa 0.48) and intraobserver (kappa 0.60) agreement when evaluating for stem loosening before fracture. There was fair interobserver (kappa 0.29) and moderate intraobserver (kappa 0.51) agreement regarding the UCS class. There was moderate interobserver (kappa 0.41) and intraobserver (kappa 0.57) agreement regarding the proposed treatment. There was slight interobserver (kappa 0.04) and moderate intraobserver (kappa 0.44) agreement regarding the Wright and Cofield classification. CONCLUSION: The Wright and Cofield system is less reliable than the UCS classification. A more reliable and clinically relevant classification system is needed to standardize discussion of periprosthetic proximal humerus fractures.

Shoulder Synovial Chondromatosis in an Adolescent Athlete: A Case Report.

Introduction: Synovial chondromatosis refers to a benign proliferative disease of the synovium. Reports in children are rare and reports involving the pediatric shoulder are even more rare. In this review of the literature and case report, we provide a summary of all published cases in children and a report of a case of shoulder synovial chondromatosis in an adolescent female athlete. Case Presentation: A 15-year-old female cheerleader presented to the clinic with gradual onset right shoulder pain with a severity of 5/10. On physician examination, the patient had tenderness over the proximal humerus, limited abduction to 160°, limited forward flexion, and a total arc of motion of <180°. Radiograph of the shoulder demonstrated multiple calcific intra-articular loose bodies consistent with synovial chondromatosis. Arthroscopic removal resulted in resolution of symptoms at the 36-week follow-up. Conclusions: Our literature search revealed only eight case reports on shoulder synovial chondromatosis in children. The location of the chondromatosis within the shoulder joint can be intra-articular, extra-articular, within the biceps sheath, or combined. In general, for chondomatoses confined to the glenohumeral joint space, open surgery is not required. Bony erosions can occur in the setting of chondromatosis though may not need to be addressed surgically. Although rare, this diagnosis should be considered when confronted with shoulder pain that is exacerbated during long athletic events with limited range of motion on physical examination in the adolescent athlete. Arthroscopic treatment in conjunction with physical therapy and early mobilization can lead to a successful outcome.

Traumatic brain injury disrupts cerebrovascular tone through endothelial inducible nitric oxide synthase expression and nitric oxide gain of function.

BACKGROUND: Traumatic brain injury (TBI) has been reported to increase the concentration of nitric oxide (NO) in the brain and can lead to loss of cerebrovascular tone; however, the sources, amounts, and consequences of excess NO on the cerebral vasculature are unknown. Our objective was to elucidate the mechanism of decreased cerebral artery tone after TBI. METHODS AND RESULTS: Cerebral arteries were isolated from rats 24 hours after moderate fluid­percussion TBI. Pressure­induced increases in vasoconstriction (myogenic tone) and smooth muscle Ca2+ were severely blunted in cerebral arteries after TBI. However, myogenic tone and smooth muscle Ca2+ were restored by inhibition of NO synthesis or endothelium removal, suggesting that TBI increased endothelial NO levels. Live native cell NO, indexed by 4,5­diaminofluorescein (DAF­2 DA) fluorescence, was increased in endothelium and smooth muscle of cerebral arteries after TBI. Clamped concentrations of 20 to 30 nmol/L NO were required to simulate the loss of myogenic tone and increased (DAF­2T) fluorescence observed following TBI. In comparison, basal NO in control arteries was estimated as 0.4 nmol/L. Consistent with TBI causing enhanced NO­mediated vasodilation, inhibitors of guanylyl cyclase, protein kinase G, and large­conductance Ca2+­activated potassium (BK) channel restored function of arteries from animals with TBI. Expression of the inducible isoform of NO synthase was upregulated in cerebral arteries isolated from animals with TBI, and the inducible isoform of NO synthase inhibitor 1400W restored myogenic responses following TBI. CONCLUSIONS: The mechanism of profound cerebral artery vasodilation after TBI is a gain of function in vascular NO production by 60­fold over controls, resulting from upregulation of the inducible isoform of NO synthase in the endothelium.