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Purpose The purpose of this quality improvement project was to improve consistency of discharge teaching in women who used progesterone-containing hormonal contraceptive medications and received sugammadex during general anesthesia, as there is a risk of unintended pregnancy for 1 week after administration of sugammadex. Design This project used a predesign and postdesign using two separate sample groups of patients and postanesthesia care unit (PACU) nurses. Methods The sample consisted of 31 total women of childbearing age and 59 PACU nurses. Simplification of sugammadex discharge instructions was achieved by incorporating evidence-based recommendations for electronic discharge instructions and nursing education. PACU nurses were educated and surveyed before and after regarding frequency of discharge teaching, clarity, and comprehension of the after-visit summary and knowledge of sugammadex. Patients were called via telephone postoperatively to assess recall of sugammadex discharge teaching. Findings Postoperative patient phone calls identified a small increase in patient recall of discharge instructions from 5 of 14 patients (35.7%) before implementation to 7 of 17 after implementation (41.2%). PACU nurse surveys indicated an increase in self-reported frequency of sugammadex discharge teaching (34.8% vs 64.2%, P = .024) and that new discharge instructions contained more clear, comprehensive information as compared with previous instructions (29.4% vs 75.5%, P = .001). Conclusions This quality improvement project successfully implemented more consistent and comprehensive discharge instructions for women who receive sugammadex intraoperatively. Limitations of the project included a small sample size and short implementation intervals. As a result of switching to uniform discharge instructions, more patients received important discharge teaching from PACU nurses, and the percentage of patients who recalled this information increased.

In an effort to improve pedestrian safety, several states in the United States changed their pedestrian laws by changing the requirement that drivers yield to pedestrians in crosswalks to a requirement that drivers stop for pedestrians in crosswalks. This study examined whether this change had an effect on pedestrian safety in the United States, with its focus on low-speed roads. To examine the association between changes in pedestrian laws and changes in pedestrian-involved fatal crashes, three approaches were employed: before-after analysis, time-series analysis, and cross-sectional analysis. Pedestrian-involved fatal traffic crashes on low-speed roads were extracted from the U.S. national fatal crash database, the Fatality Analysis Reporting System (FARS), from 1980 through 2005. This study found no statistically significant reduction in pedestrian-involved fatal crashes attributable to changes in the laws, yet this finding is not definitive because of study limitations such as the omission of relevant exposure data.

RASA3, a Ras GTPase activating protein, is critical to vertebrate erythropoiesis and megakaryopoiesis. The autosomal recessive mouse model scat (severe combined anemia and thrombocytopenia) carries a G125V mutation in Rasa3 that leads to profound bone marrow failure with characteristics of aplastic anemia. The phenotype is cyclic, and mice alternate between periods of crisis and remission. Our previous studies demonstrated that this mutation in Rasa3 causes defects in several aspects of erythropoiesis, including a significant delay of erythroid differentiation at the polychromatophilic stage, decreased hemoglobinization, defects in cell cycle progression past the G1 checkpoint, and increased reactive oxygen species (ROS) during terminal erythroid differentiation as well as in scat peripheral blood reticulocytes and red blood cells. We previously reported that the mislocalization of mutated RASA3 to the cytosol of reticulocytes and mature red cells plays a role in the erythropoietic defect in scat, and the observed cell cycle arrest and increased ROS likely also contribute to this unique disease phenotype. Our current efforts are focused on further elucidation of the mechanism and specific disruptions in Ras signaling that lead to anemia, membrane fragmentation, and the cyclic phenotype in scat. Interestingly, we report here that apoptosis is not increased during scat crisis, and that mitochondria, a potential source of ROS, are normally eliminated at the reticulocyte stage. The dramatic nature of remission, with complete normalization of all hematologic parameters, led us to hypothesize that a secreted factor may be mediating the cyclic phenotype of scat. Differences in the cytokine profile of the serum of scat mice compared to wild type suggest that, indeed, one or several secreted factor(s) may be influencing the occurrence of bone marrow failure. Levels of galectin-1, a known mediator of cell-cell interactions and intracellular signaling in the hematopoietic niche, are consistently decreased in scat serum according to a multispot anti-cytokine antibody array (23,326.5 ± 21,439.7 integrated density in scat vs. 31,019.6± 20,110.7 in controls, p Strengthening the notion that RASA3 has a critical conserved role in vertebrate terminal erythropoiesis, the characteristics of bone marrow failure seen in scat have been reproduced in human CD34+ cells using siRNA and shRNA knockdowns of Rasa3 . Similar to the changes seen in scat, cells with decreased RASA3 demonstrated delayed terminal erythroid differentiation and defective hemoglobinization. Finally, analysis of Ras expression and functional pull-down studies in human CD34+ cells revealed that, while K-Ras is the major active isoform expressed during terminal erythroid differentiation, H-Ras is also active during human erythropoiesis. Future studies with CD34+ Rasa3 knockdown cells will explore the influence of RASA3 on human K- and H-Ras signaling in erythropoiesis. Taken together, our studies further characterize the vital role of RASA3 in hemoglobinization, cell cycle progression, and cell survival during terminal erythroid differentiation, as well as identify novel targets for investigation of unknown mechanisms (e.g., dysregulated cytokine secretion) of bone marrow failure syndromes. Disclosures No relevant conflicts of interest to declare.