Improving Utilization of a Nursing-Initiated Supportive Medication Order Panel in the Inpatient Setting.

BACKGROUND: Many medications are low-risk but must undergo the same ordering process as high-risk medications in the inpatient setting. Nurses identify the need for supportive medications and notify providers. An order panel and policy were developed to allow nurses to order low-risk, supportive medications. PURPOSE: The aim of this study was to increase order panel utilization from a 6% to a goal of 15%. METHODS: This was a quality improvement study at a 1000-bed academic medical center. Five plan-do-study-act (PDSA) cycles were implemented. The primary end point was order panel utilization, and secondary end points were individual nursing unit utilization and the number of orders for each medication on the panel. RESULTS: After each PDSA cycle, order panel utilization improved to 7.8%, 13.2%, 7.5%, 10.2%, and 10.6%, respectively. The units using the order panel most often were general medicine (n = 95, 28%), medical intensive care (n = 71, 21%), and inpatient oncology (n = 40, 12%). The medication most frequently ordered was lanolin alcohols-mineral oil with petrolatum (Eucerin) cream (n = 220, 28%). CONCLUSIONS: Order panel utilization improved from a baseline of 6% to an average of 9.9%. Increasing awareness of the order panel and adding medications will contribute to improvement in order panel utilization in the long-term.

Interleukin-8 blockade prevents activated endothelial cell mediated proliferation and chemoresistance of acute myeloid leukemia.

One of the greatest challenges in treating acute myeloid leukemia (AML) is chemotherapy refractory disease. Previously, we demonstrated a novel mechanism whereby AML-induced endothelial cell (EC) activation leads to subsequent leukemia cell adherence, quiescence and chemoresistance, identifying activated ECs as potential mediators of relapse. We now show mechanistically that EC activation induces the secretion of interleukin-8 (IL-8) leading to significant expansion of non-adherent AML cells and resistance to cytarabine (Ara-C). Through crystallography and computational modeling, we identified a pocket within IL-8 responsible for receptor binding, screened for small molecules that fit within this pocket, and blocked IL-8 induced proliferation and chemo-protection of AML cells with a hit compound. Results from this study show a new therapeutic strategy for targeting the sanctuary of an activated leukemia microenvironment.