Hemiarthroplasty for Femoral Neck Fractures: Does Surgeon Subspecialty Affect Perioperative Outcomes?

OBJECTIVES: To determine if surgeon subspecialty training affects perioperative outcomes for displaced femoral neck fractures treated with hemiarthroplasty. DESIGN: Retrospective comparative study. SETTING: One health system with 2 hospitals (Level I and Level III trauma centers). PATIENT AND PARTICIPANTS: Patients who were treated with hemiarthroplasty for displaced femoral neck fractures between October 2012 and September 2017. OUTCOME MEASURES: Leg length discrepancy, femoral offset, estimated blood loss (EBL), incidence of blood transfusion, time to surgery, operative time, and length of stay. Data were analyzed based on the treating surgeon's subspecialty training [arthroplasty (A), trauma (T), other (O)]. Hierarchical regression was used to compare the groups and control for confounding variables. RESULTS: A total of 292 patients who received hemiarthroplasty for displaced femoral neck fractures were included (A = 158; T = 73; O = 61). Surgeon subspecialty had a statistically significant effect on operative time, with arthroplasty surgeons completing the procedure 9.6 minutes faster than trauma surgeons and 17.7 minutes faster than other surgeons (P < 0.01; ΔR = 0.03). Surgeon subspecialty did not significantly affect other outcomes, including leg length discrepancy (P = 0.26), femoral offset (P = 0.37), EBL (P = 0.10), incidence of transfusion (P = 0.67), time to surgery (P = 0.10), or length of stay (P = 0.67). CONCLUSIONS: This study demonstrates that arthroplasty-trained surgeons perform hemiarthroplasty slightly faster than other subspecialists, but subspecialty training does not affect other perioperative outcomes, including leg length discrepancy, femoral offset, EBL, transfusion rate, time to surgery, or length of stay. This suggests that hemiarthroplasty can be adequately performed by various subspecialists, and deferring treatment to an arthroplasty surgeon might not have a clinically significant benefit in the perioperative period. LEVEL OF EVIDENCE: Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.

Gene expression changes in the MAPK pathway in both Fragile X and Down syndrome human neural progenitor cells.

The two most common genetic developmental disorders that cause intellectual disability are Down syndrome (DS) and Fragile X syndrome (FXS). Although the genetics and behavioral hallmarks of these two disorders are distinct, common underlying defects in neural development may lead to the cognitive impairment characteristic of both. Human neural progenitor cells (hNPCs) enable the study of prenatal human brain development in these developmental disorders. We therefore tested whether there are common affected molecular pathways in FXS and DS hNPCs that may be indicators of the fundamental developmental causes of intellectual disability. Comparison of gene expression data from FXS and DS (disorder group) hNPCs to unaffected hNPCs indicated genes in specific signal transduction cascades are dysregulated. Importantly, altered expression of genes in these signaling pathways did not emerge when the two disorder hNPCs were analyzed separately. Specifically, genes in the mitogen-activated protein kinases (MAPK/ERK) and calcium signaling pathways are mis-expressed in disorder hNPCs. These results suggest that DS and FXS hNPCs do not communicate or respond appropriately to extracellular cues during neural development. These results validate the use of hNPCs as a tool to assess complex cell functions during neural development and suggest that defects in the pathways identified could have profound effects on how neural progenitor cells survive, proliferate and differentiate, thereby leading to intellectual disability.