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Abstract Introduction Physicians frequently use point-of-care ultrasound for intravenous access and bloodwork in the ED. Recently, AIUM and ACEP released recommendations on ultrasound-guided peripheral intravenous lines (USPIVs), but there are no agreed upon standardized policies. We sought to determine whether the use of sterile-covered transducers (SCT) decreases the rate of contamination when compared to uncovered transducers (UCT) after standard low-level disinfection (LLD). Methods This is a randomized control trial comparing contamination rates of US transducers between SCT and UCT after their use for USPIV by the vascular access team, also known as the “PICC” team, over a 3-month period. A sample of admitted patient with an USPIV order were included and randomized to SCT (experimental) or UCT (control) arms. Transducers were swabbed and inserted into the SystemSURE Plus Adenosine Triphosphate (ATP) Luminometer to calculate Relative Light Units (RLU). We performed a cost analysis of requiring sterile covers for USPIVs. Results The UCT and SCT arms contained 35 and 38 patients, respectively. The SCT group had a mean of 0.34 compared to the UCT group mean of 2.29. Each sterile cover costs $8.49, and over 3000 USPIVs are placed annually by the “PICC” team. Conclusion Contamination rates were similar among the UCT and SCT groups after LLD. 254 inpatient USPIVs are performed monthly, not including failed attempts or covers used in the ED where USPIV placement is an essential part of ED workflow. This study suggests that the use of SCT does not significantly affect transducer contamination rates. These findings question burdensome regulatory hospital policies that are not evidence-based.

Background/Aims: Elevated production of reactive oxygen species (ROS) is linked to endothelial dysfunction and is one of the key contributors to the pathogenesis of diabetic vascular complications. Emerging evidence has indicated that ellagic acid (EA), a polyphenol found in fruits and nuts, possesses numerous biological activities including radical scavenging. However, whether EA exerts a vasculo-protective effect via antioxidant mechanisms in blood vessels exposed to diabetic conditions remains unknown. Accordingly, the goal of this current study was to determine whether EA decreases vascular ROS production and thus ameliorates endothelial dysfunction in the diabetic milieu. Methods: Intact rat aortas and human aortic endothelial cells (HAEC) were stimulated with 30mM high glucose (HG) with and without EA co-treatment. Endothelium-dependent vasodilation was measured using a wire myograph. Gene and protein expression of non-phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidases 4 (NOX4) were detected using RT-PCR and western blotting, respectively. Oxidative stress was determined by measuring ROS levels using dihydroethidium (DHE) staining. Results: Intact aortas exposed to HG condition displayed exacerbated ROS production and impairment of endothelium-dependent vasodilation, characterizing endothelial dysfunction. These effects were markedly reduced with EA treatment. HG enhanced ROS production in HAEC, paralleled by increased ERK1/2 activation and NOX4 expression. EA treatment blunted the increase of ROS generation, ERK1/2 activation and decreased NOX4. Conclusions: EA significantly decreases endothelial ROS levels and ameliorates the impairment of vascular relaxation induced by HG. Our results suggest that EA exerts a vasculo-protective effect under diabetic conditions via an antioxidant effect that involves inhibition of ERK1/2 and downregulation of NOX4.