Opioid requirements in primary versus revision reverse shoulder arthroplasty.

PURPOSE: The purpose of this study is to evaluate the inpatient pain medication use of patients who had a revision shoulder arthroplasty procedure performed and compare them to a cohort of patients who had a primary reverse total shoulder arthroplasty (rTSA) performed to determine whether revision shoulder arthroplasty requires more pain medication.. METHODS: A retrospective review was performed on patients undergoing revision arthroplasty (n = 75) and primary rTSA (n = 340). Inpatient medication records were reviewed to tabulate the visual analog pain (VAS) all narcotic medication use, and total morphine equivalent units (MEUs) were calculated for the duration of the inpatient stay. RESULTS: There was no significant difference between groups regarding age, sex, body mass index, Charlson Comorbidity Index, American Society of Anesthesiologists score, preoperative narcotic pain medication use, tobacco use, postoperative VAS scores or hospital length of stay. There were no predictors of total postoperative MEUs identified. Overall, patients in the revision arthroplasty group received significantly less total MEUs than those in the primary rTSA group, 134.96 MEUs vs. 69.79 MEUs, respectively (p < .0005). CONCLUSION: The perceived notion that revision shoulder arthroplasty is more painful may cause providers to be more inclined to increase narcotic use, or use more invasive pain control techniques. Based on these data, we found that revision shoulder arthroplasty did not require an increased opioid requirement, longer length of stay or increase VAS, suggesting that these patients can often be managed similarly to primary rTSA.

Use of the Contralateral Glenoid for Calculation of Glenoid Bone Loss: A Cadaveric Anthropometric Study.

PURPOSE: The purpose of this study was to determine if there are significant side-to-side anthropometric differences between paired glenoids. METHODS: Forty-six matched-pair cadaver glenoids were harvested, and their glenoid heights (GHs) and glenoid widths (GWs) were measured with digital calipers. The glenoid surface area was calculated using the standard assumption that the inferior two-thirds of the glenoid is a perfect circle. RESULTS: There was a statistically significant difference between matched-pair GHs of 0.96 ± 3.07 mm (P = .020) and GWs of 0.46 ± 1.64 mm (P = .033). There was a significant difference of glenoid cavity area of 20.30 ± 81.53 mm2 (P = .044), or a difference of ∼3%. A total of 4 of 46 pairs of glenoids (8.6%) showed a difference in width >3 mm. CONCLUSIONS: This study demonstrates the fallacy of use of the contralateral glenoid in measuring glenoid bone loss. Although many paired samples exhibited similar side-to-side glenoid measurements, the number of cadaveric pairs that showed differences of >3 mm was substantial. Caution should be taken when using calculation methods that include this assumption for surgical decision making, as surface area, GW, and GH were all shown to have statistically significant side-to-side differences in their measurements. CLINICAL RELEVANCE: Many methods exist for measuring glenoid bone loss after anterior shoulder dislocation, but some of the current methods may be inaccurate and lead to unreliable estimations.

Engineering Controlled Peritumoral Inflammation to Constrain Brain Tumor Growth.

Brain tumors remain a great clinical challenge, in part due to their capacity to invade into eloquent, inoperable regions of the brain. In contrast, inflammation in the central nervous system (CNS) due to injuries activates microglia and astrocytes culminating in an astroglial scar that typically "walls-off" the injury site. Here, the hypothesis is tested that targeting peritumoral cells surrounding tumors to activate them via an inflammatory stimulus that recapitulates the sequelae of a traumatic CNS injury, could generate an environment that would wall-off and contain invasive tumors in the brain. Gold nanoparticles coated with inflammatory polypeptides to target stromal cells in close vicinity to glioblastoma (GBM) tumors, in order to activate these cells and stimulate stromal CNS inflammation, are engineered. It is reported that this approach significantly contains tumors in rodent models of GBM relative to control treatments (reduction in tumor volume by over 300% in comparison to controls), by the activation of the innate and adaptive immune response, and by triggering pathways related to cell clustering. Overall, this report outlines an approach to contain invasive tumors that can complement adjuvant interventions for invasive GBM such as radiation and chemotherapy.