Implementation of a Multimodal Hand Hygiene Intervention at a Rural Critical Access Hospital

Healthcare acquired infections are the most common complication of hospital care in the United States, with subsequent negative implications on the healthcare system. While hand hygiene has long been considered the single most important and cost-effective way of reducing healthcareacquired infections, compliance among healthcare professionals is low, and most efforts to improve it fail. When compared to single-component hand hygiene interventions, research demonstrates that tailored multimodal interventions are an effective way to improve compliance with hand hygiene practices among healthcare professionals. This Doctor of Nursing Practice project focused on implementing a multimodal hand hygiene intervention, tailored to fit the specific needs of a rural critical access hospital, to determine its effect on compliance and sustainability of hand hygiene practices among healthcare professionals. Results demonstrate an increase in organization-wide hand hygiene compliance and improved reporting from multiple departments following project implementation

Expressions 2000

https://openspace.dmacc.edu/expressions/1019/thumbnail.jp

Contribution of Hepatic Cytochrome P450 3A4 Metabolic Activity to the Phenomenon of Clopidogrel Resistance

Background— Interindividual variability of platelet inhibition after aspirin or clopidogrel administration has been described. Additionally, aspirin resistance and clopidogrel resistance occur in some individuals. Because the prodrug clopidogrel is activated by hepatic cytochrome P450 (CYP) 3A4, we hypothesized that interindividual variability in clopidogrel efficacy might be related to interindividual differences in CYP3A4 metabolic activity. Methods and Results— Platelet aggregation was measured before and after clopidogrel treatment in 32 patients undergoing coronary artery stent implantation and in 35 healthy volunteers. The erythromycin breath test was used to measure CYP3A4 activity in vivo in 25 of the healthy volunteers. Individual platelet aggregation was studied in 10 healthy volunteers after the coadministration of clopidogrel and rifampin (a CYP3A4 inducer). Clopidogrel nonresponders, low responders, and responders were defined by a relative inhibition of adenosine diphosphate (20 μmol/L)–induced platelet aggregation of less than 10%, 10% to 29%, and ≥30%, respectively. Among patients, 22% were clopidogrel nonresponders, 32% were low responders, and 47% were responders. Among volunteers, 16% were nonresponders, 12% were low responders, and 72% were responders. Percent platelet aggregation after clopidogrel inversely correlated with CYP3A4 activity (r=−0.6, P=0.003). Improved platelet inhibition in volunteers resistant to clopidogrel was observed with the coadministration of clopidogrel and rifampin. Conclusions— Clopidogrel administration results in interindividual variability in platelet inhibition, which correlates with CYP3A4 metabolic activity. Measurement of antiplatelet drug efficacy with a point-of-care device and alternative antithrombotic strategies for aspirin or clopidogrel nonresponders and low responders could reduce the incidence of thrombotic events that continue to occur despite oral antiplatelet therapy

Atorvastatin reduces the ability of clopidogrel to inhibit platelet aggregation: A new drug-drug interaction

Background— We observed that the prodrug clopidogrel was less effective in inhibiting platelet aggregation with coadministration of atorvastatin during point-of-care platelet function testing. Because atorvastatin is metabolized by cytochrome P450 (CYP) 3A4, we hypothesized that clopidogrel might be activated by CYP3A4. Methods and Results— Platelet aggregation was measured in 44 patients undergoing coronary artery stent implantation treated with clopidogrel or clopidogrel plus pravastatin or atorvastatin, and in 27 volunteers treated with clopidogrel and either erythromycin or troleandomycin, CYP3A4 inhibitors, or rifampin, a CYP3A4 inducer. Atorvastatin, but not pravastatin, attenuated the antiplatelet activity of clopidogrel in a dose-dependent manner. Percent platelet aggregation was 34±23, 58±15 (P=0.027), 74±10 (P=0.002), and 89±7 (P=0.001) in the presence of clopidogrel and 0, 10, 20, and 40 mg of atorvastatin, respectively. Erythromycin attenuated platelet aggregation inhibition (55±12 versus 42±12% platelet aggregation; P=0.002), as did troleandomycin (78±18 versus 45±18% platelet aggregation; P less than 0.0003), whereas rifampin enhanced platelet aggregation inhibition (33±18 versus 56±20% platelet aggregation, P=0.001). Conclusions— CYP3A4 activates clopidogrel. Atorvastatin, another CYP3A4 substrate, competitively inhibits this activation. Use of a statin not metabolized by CYP3A4 and point-of-care platelet function testing may be warranted in patients treated with clopidogrel

Lessons Learned from the 9/11 and WMD Commissions: IRTPA, CIA and the Intelligence Community

At the request of the CIA's Center for the Study of Intelligence, a team from the Bush School conducted an inquiry to determine how the CIA responded to the investigations of the 9/11 and WMD Commissions. The goal of the project, which involved interviews with several commissioners and numerous key staff members, was to identify what actions the D/CIA must take when confronted with future commissions to ensure that the most accurate picture of the Agency is presented, while preventing the formation of inaccurate negative impressions created by the manner in which Agency personnel interact with investigators. At the conclusion of the Capstone, the students prepared a report and orally briefed Agency supervisors on their findings and recommendations.Center for the Study of Intelligence, Central Intelligence Agenc