Secondary review reduced inpatient MRI orders and avoidable hospital days.

INTRODUCTION: Medical centers have dramatically increased the use of magnetic resonance imaging (MRI). At 2 large academic tertiary care centers in New York City, nearly half of inpatient MRI orders took more than 12 h to complete, delaying patient discharge and increasing avoidable hospital days. We posited that transitioning inpatient MRIs to outpatient facilities, when safe and appropriate, could reduce inpatient MRI orders and avoidable hospital days. METHODS: We manually reviewed 59 inpatient MRI orders delayed on the estimated date of discharge (EDD). These orders were often delayed due to no standard process to escalate orders for medical reasons or no system to coordinate outpatient orders. We developed a revised workflow involving an automation platform that flagged inpatient MRI orders requested within 24 h of the EDD and emailed the care team to request a second review of the order. The care team reconsidered whether the order was (1) required for discharge, (2) non-urgent and could be converted to an outpatient order, or (3) unnecessary and could be canceled. RESULTS: Over 9 months, the automation platform flagged 618 inpatient MRI orders, of which 53.9% (333/618) were reviewed by the care team. Among the orders, 24.0% (80/333) of reviewed orders and 12.9% (80/618) of all orders were transitioned to either outpatient or canceled orders. These transitioned orders were associated with 267 fewer avoidable hospital days and a cost savings of $199,194. CONCLUSION: A standardized process and second review of inpatient MRI orders on the EDD can reduce inappropriate orders and more effectively use inpatient imaging resources. PRECIS: A standardized workflow and automation platform encouraged a second review of inpatient MRI orders to reduce inappropriate orders, avoidable hospital days, and hospital costs.

Acute Kidney Injury Subsequent to Cardiac Surgery.

Acute kidney injury (AKI) after cardiac surgery is a common and underappreciated syndrome that is associated with poor shortand long-term outcomes. AKI after cardiac surgery may be epiphenomenon, a signal for adverse outcomes by virtue of other affected organ systems, and a consequence of multiple factors. Subtle increases in serum creatinine (SCr) postoperatively, once considered inconsequential, have been shown to reflect a kidney injury that likely occurred in the operating room during cardiopulmonary bypass (CPB) and more often in susceptible individuals. The postoperative elevation in SCr is a delayed signal reflecting the intraoperative injury. Preoperative checklists and the conduct of CPB represent opportunities for prevention of AKI. Newer definitions of AKI provide us with an opportunity to scrutinize perioperative processes of care and determine strategies to decrease the incidence of AKI subsequent to cardiac surgery. Recognizing and mitigating risk factors preoperatively and optimizing intraoperative practices may, in the aggregate, decrease the incidence of AKI. This review explores the pathophysiology of AKI and addresses the features of patients who are the most vulnerable to AKI. Preoperative strategies are discussed with particular attention to a readiness for surgery checklist. Intraoperative strategies include minimizing hemodilution and maximizing oxygen delivery with specific suggestions regarding fluid management and plasma preservation.

p120 regulates endothelial permeability independently of its NH2 terminus and Rho binding.

The association of p120-catenin (p120) with the juxtamembrane domain (JMD) of vascular endothelial (VE)-cadherin is required to maintain VE-cadherin levels and transendothelial resistance (TEER) of endothelial cell monolayers. To distinguish whether decreased TEER was due to a loss of p120 and not to the decrease in VE-cadherin, we established a system in which p120 was depleted by short hairpin RNA delivered by lentivirus and VE-cadherin was restored via expression of VE-cadherin fused to green fluorescent protein (GFP). Loss of p120 resulted in decreased TEER, which was associated with decreased expression of VE-cadherin, ß-catenin, plakoglobin, and α-catenin. Decreased TEER was rescued by restoration of p120 but not by the expression of VE-cadherin-GFP, despite localization of VE-cadherin-GFP at cell-cell borders. Expression of VE-cadherin-GFP restored levels of ß-catenin and α-catenin but not plakoglobin, indicating that p120 may be important for recruitment of plakoglobin to the VE-cadherin complex. To evaluate the role of p120 interaction with Rho GTPase in regulating endothelial permeability, we expressed a recombinant form of p120, lacking the NH(2) terminus and containing alanine substitutions, that eliminates binding of Rho to p120. Expression of this isoform restored expression of the adherens junction complex and rescued permeability as measured by TEER. These results demonstrate that p120 is required for maintaining VE-cadherin expression and TEER independently of its NH(2) terminus and its role in regulating Rho.