Application of the Plan-Do-Study-Act method to optimize the ordering and administration of dexmedetomidine for sleep hygiene in the intensive care unit.

PURPOSE: To describe the Plan-Do-Study-Act (PDSA) methodology utilized by a multidisciplinary team to address the discordance between ordering and administration of dexmedetomidine for sleep hygiene in the intensive care unit (ICU). SUMMARY: The addition of sleep hygiene as an indication for the use of dexmedetomidine at University of Virginia (UVA) Health led to discordance between the medication orders in the electronic medical record and the subsequent administration of dexmedetomidine. A multidisciplinary team implemented interventions that included modifying the order panel, streamlining the institutional formulary, developing institutional practice guidelines, and providing education to healthcare team members. After completion of the first PDSA cycle, the mean number of discordant order elements decreased to 1.96 out of 5 possible order elements from an initial 2.5 out of 5 elements before the interventions, meeting the aim to reduce the mean to less than 2. There was a significant decrease in the discordance in the duration of infusion (discordant for 14 of 30 orders before the interventions vs 1 of 28 orders after the interventions, P = 0.0002) but a significant increase in the discordance in the titration dose (discordant for 13 of 30 orders before the interventions vs 24 of 28 orders after the interventions, P < 0.0001). Other discordant order elements including the starting dose, maximum rate, and titration interval time decreased in frequency after the interventions, although the differences were not statistically significant. The interventions made during the first PDSA cycle are anticipated to lead to an estimated cost savings of up to $180,000 per year within the UVA Health system. CONCLUSION: The multidisciplinary team utilizing a PDSA method to modify the order panel, streamline the institutional formulary, develop institutional practice guidelines, and provide education to healthcare team members was effective at reducing overall discordance between order intent and administration of dexmedetomidine for sleep hygiene in the ICU.

Copper is taken up efficiently from albumin and alpha2-macroglobulin by cultured human cells by more than one mechanism.

Ionic copper entering blood plasma binds tightly to albumin and the macroglobulin transcuprein. It then goes primarily to the liver and kidney except in lactation, where a large portion goes directly to the mammary gland. Little is known about how this copper is taken up from these plasma proteins. To examine this, the kinetics of uptake from purified human albumin and alpha(2)-macroglobulin, and the effects of inhibitors, were measured using human hepatic (HepG2) and mammary epithelial (PMC42) cell lines. At physiological concentrations (3-6 muM), both cell types took up copper from these proteins independently and at rates similar to each other and to those for Cu-dihistidine or Cu-nitrilotriacetate (NTA). Uptakes from alpha(2)-macroglobulin indicated a single saturable system in each cell type, but with different kinetics, and 65-80% inhibition by Ag(I) in HepG2 cells but not PMC42 cells. Uptake kinetics for Cu-albumin were more complex and also differed with cell type (as was the case for Cu-histidine and NTA), and there was little or no inhibition by Ag(I). High Fe(II) concentrations (100-500 microM) inhibited copper uptake from albumin by 20-30% in both cell types and that from alpha(2)-macroglobulin by 0-30%, and there was no inhibition of the latter by Mn(II) or Zn(II). We conclude that the proteins mainly responsible for the plasma-exchangeable copper pool deliver the metal to mammalian cells efficiently and by several different mechanisms. alpha(2)-Macroglobulin delivers it primarily to copper transporter 1 in hepatic cells but not mammary epithelial cells, and additional as-yet-unidentified copper transporters or systems for uptake from these proteins remain to be identified.