Factors associated with Interhospital transfers of emergency general surgery patients from emergency departments.

BACKGROUND: Emergency general surgery (EGS) conditions account for over 3 million or 7.1% of hospitalizations per year in the US. Patients are increasingly transferred from community emergency departments (EDs) to larger centers for care, and a growing demand for treating EGS conditions mandates a better understanding of how ED clinicians transfer patients. We identify patient, clinical, and organizational characteristics associated with interhospital transfers of EGS patients originating from EDs in the United States. METHOD: We analyze data from the Agency for Healthcare Research and Quality Nationwide Emergency Department Sample (NEDS) for the years 2010-2014. Patient-level sociodemographic characteristics, clinical factors, and hospital-level factors were examined as predictors of transfer from the ED to another acute care hospital. Multivariable logistic regression analysis includes patient and hospital characteristics as predictors of transfer from an ED to another acute care hospital. RESULTS: Of 47,442,892 ED encounters (weighted) between 2008 and 2014, 1.9% resulted in a transfer. Multivariable analysis indicates that men (Odds ratio (OR) 1.18 95% Confidence Interval (95% CI) 1.16-1.21) and older patients (OR 1.02 (95% CI 1.02-1.02)) were more likely to be transferred. Relative to patients with private health insurance, patients covered by Medicare (OR 1.09 (95% CI 1.03-1.15) or other insurance (OR 1.34 (95% CI 1.07-1.66)) had a higher odds of transfer. Odds of transfer increased with a greater number of comorbid conditions compared to patients with an EGS diagnosis alone. EGS diagnoses predicting transfer included resuscitation (OR 36.72 (95% CI 30.48-44.22)), cardiothoracic conditions (OR 8.47 (95% CI 7.44-9.63)), intestinal obstruction (OR 4.49 (95% CI 4.00-5.04)), and conditions of the upper gastrointestinal tract (OR 2.82 (95% CI 2.53-3.15)). Relative to Level I or II trauma centers, hospitals with a trauma designation III or IV had a 1.81 greater odds of transfer. Transfers were most likely to originate at rural hospitals (OR 1.69 (95% CI 1.43-2.00)) relative to urban non-teaching hospitals. CONCLUSION: Medically complex and older patients who present at small, rural hospitals are more likely to be transferred. Future research on the unique needs of rural hospitals and timely transfer of EGS patients who require specialty surgical care have the potential to significantly improve outcomes and reduce costs.

Role of FOXM1 in vascular smooth muscle cell survival and neointima formation following vascular injury.

BACKGROUND: Accelerated smooth muscle cell (SMC) proliferation is the primary cause of intimal hyperplasia (IH) following vascular interventions. Forkhead Box M1 (FOXM1) is considered a proliferation-associated transcription factor. However, the presence and role of FOXM1 in IH following vascular injury have not been determined. OBJECTIVE: We examined the expression of FOXM1 in balloon-injured rat carotid arteries and investigated the effect of FOXM1 inhibition in SMCs and on the development of IH. METHODS AND RESULTS: FOXM1 was detected by immunofluorescent staining in balloon-injured rat carotid arteries where we observed an upregulation at day 7, 14, and 28 compared to uninjured controls. Immunofluorescence staining revealed FOXM1 coincided with proliferating cell nuclear antigen (PCNA). FOXM1 was also detectable in human carotid plaque samples. Western blot showed an upregulation of FOXM1 protein in serum-stimulated SMCs. Inhibition of FOXM1 using siRNA or chemical inhibition led to the induction of apoptosis as measured by flow cytometry and western blot for cleaved caspase 3. Perturbations in survival signaling were measured by western blot following FOXM1 inhibition, which showed a decrease in phosphorylated AKT and ß-catenin. The chemical inhibitor thiostrepton was delivered by intraperitoneal injection in rats that underwent balloon injury and led to reduced intimal thickening compared to DMSO controls. CONCLUSIONS: FOXM1 is an important molecular mediator of IH that contributes to the proliferation and survival of SMCs following vascular injury.