Treatment of Facial Fractures at Safety-Net Hospitals: A National Analysis of Inpatient Burden and Cost.

PURPOSE: Safety-net hospitals (SNHs) are vital in the care of trauma populations, but little is known about the burden of facial trauma presenting to SNHs. The authors sought to characterize the presentation and treatment of facial fractures across SNHs and determine the association between SNH care and healthcare utilization in patients undergoing fracture repair. METHODS: Adult patients presenting with a facial fracture as their primary admitting diagnosis from the year 2012 to 2015 were identified in the National Inpatient Sample. The "safety-net burden" of each hospital was defined based on the proportion of Medicaid and self-pay discharges. Patient factors analyzed were sex, race, age, income level, insurance status, fracture location, and comorbidities. Hospital factors analyzed were safety-net burden, teaching status, geographic region, bed size, and ownership status. The main outcomes were length of stay (LOS), hospital costs, time to repair, and postoperative complications. RESULTS: Of 78,730 patients, 27,080 (34.4%) were treated at SNHs and 24,844 (31.6%) were treated at non-SNHs. Compared to non-SNHs, patients treated at SNHs were more likely to undergo operative repair at SNHs (65.8% versus 53.9%, P < 0.001). Overall mean LOS was comparable between non-SNH and SNH (3.43 versus 3.38 days, P = 0.611), as was mean hospital cost ($15,487 versus $15,169, P = 0.434). On multivariate linear regression, safety-net status was not a predictor of increased LOS, cost, or complications. However, safety-net status was significantly associated with lower odds of undergoing repair within 48 hours of admission (odds ratio 0.783, 95% confidence interval = 0.680-0.900, P = 0.001). CONCLUSIONS: Safety-net hospitals are able to treat facial trauma patients with greater injury burden and lower socioeconomic resources without increased healthcare utilization. Healthcare reform must address the financial challenges that endanger these institutions to ensure timely treatment of all patients.

Impact of payer status and hospital volume on outcomes after head and neck oncologic reconstruction.

BACKGROUND: High-volume centers improve outcomes in head and neck cancer (HNCA) reconstruction, yet it is unknown whether patients of all payer status benefit equally. METHODS: We identified patients undergoing HNCA surgery between 2002 and 2015 using the National Inpatient Sample. Outcomes included receipt of care at high-volume centers, receipt of reconstruction, and post-operative complications. Multivariate regression analysis was stratified by payer status. RESULTS: 37,442 patients received reconstruction out of 101,204 patients who underwent HNCA surgery (37.0%). Privately-insured and Medicaid patients had similar odds of receiving high-volume care (OR = 0.99, 95% CI = 0.87-1.11) and undergoing reconstruction (OR = 0.96, 95% CI = 0.86-1.05). Medicaid beneficiaries had higher odds of complication (OR = 1.36, 95% CI = 1.22-1.51). The discrepancy in complication odds was significant at low-volume (OR = 1.44, 95% CI = 1.12-1.84) and high-volume centers (OR = 1.30, 95% CI = 1.15-1.47). CONCLUSIONS: Medicaid beneficiaries are as likely to receive care at high-volume centers and undergo reconstruction as privately-insured individuals. However, they have poorer outcomes than privately-insured individuals at both low- and high-volume centers.

Human Haploid Cell Genetics Reveals Roles for Lipid Metabolism Genes in Nonapoptotic Cell Death.

Little is known about the regulation of nonapoptotic cell death. Using massive insertional mutagenesis of haploid KBM7 cells we identified nine genes involved in small-molecule-induced nonapoptotic cell death, including mediators of fatty acid metabolism (ACSL4) and lipid remodeling (LPCAT3) in ferroptosis. One novel compound, CIL56, triggered cell death dependent upon the rate-limiting de novo lipid synthetic enzyme ACC1. These results provide insight into the genetic regulation of cell death and highlight the central role of lipid metabolism in nonapoptotic cell death.