Improved clinical outcomes combining house staff self-assessment with an audit-based quality improvement program.

BACKGROUND: There is a focus on integrating quality improvement with medical education and advancement of the American College of Graduate Medical Education (ACGME) core competencies. OBJECTIVE: To determine if audits of patients with unexpected admission to the medical intensive care unit using a self-assessment tool and a focused Morbidity and Mortality (M&M) conference improves patient care. DESIGN: Charts from patients transferred from the general medical floor (GMF) to the medical intensive care unit (ICU) were reviewed by a multidisciplinary team. Physician and nursing self-assessment tools and a targeted monthly M&M conference were part of the educational component. PARTICIPANTS: Physicians and nurses participated in root cause analysis. MEASURES: Records of all patients transferred from a general medical floor (GMF) to the ICU were audited. One hundred ninety-four cases were reviewed over a 10-month period. RESULTS: New policies regarding vital signs and house staff escalation of care were initiated. The percentage of calls for patients who met medical emergency response team/critical care consult criteria increased from 53% to 73%, nurse notification of a change in a patient's condition increased from 65% to 100%, nursing documentation of the change in the patients condition and follow-up actions increased from 65% percent to a high of 90%, the number of cardiac arrests on a GMF decreased from 3.1/1,000 discharges to 0.6/1,000 discharges (p = 0.002), and deaths on the Medicine Service decreased from 34/1,000 discharges to 24/1,000 discharges (p = 0.024). CONCLUSION: We describe an audit-based program that involves nurses, house staff, a self-assessment tool and a focused M&M conference. The program resulted in significant policy changes, more rapid assessment of unstable patients and improved hospital outcomes.

The effect of anticoagulants and the role of thrombin on neutrophil-endothelial cell interactions in septic shock.

To examine the effects of anticoagulants and the role of thrombin on neutrophil-platelet-endothelial cell interactions in septic shock. Controlled experiments using phase-contrast microscopy to study neutrophil, platelet, and endothelial cell interactions in flowing cell suspensions under simulated physiologic conditions. University research laboratory. Adult patients with septic shock and normal volunteers. Microslides were coated with human umbilical vein endothelial cells. Neutrophils and platelets removed from control subjects were stimulated with plasma from patients in septic shock and perfused over endothelial cells. Heparin (H), argatroban (A), antithrombin III (ATIII), and recombinant human activated protein C (rhAPC) with and without thrombin were added to cells suspended in septic plasma and normal plasma. The number of neutrophils adherent to endothelial cells, neutrophil rolling velocity, and the number of neutrophils in aggregates were determined. Flow cytometric analysis of cells was used to identify cell activation and the formation of platelet-neutrophil aggregates. Heparin, A, ATIII, rhAPC all significantly decreased neutrophil adhesion and aggregation, and increased rolling velocity of neutrophils suspended in septic plasma. These results are similar to those observed with normal plasma but present greater absolute changes. Platelet-neutrophil aggregation, platelet activation, and neutrophil activation were significantly decreased by each of the anticoagulants. The addition of thrombin to cell suspensions containing anticoagulants reversed the effects of H, A, ATIII, rhAPC on neutrophil adhesion, adherence, and rolling velocity. In addition, thrombin attenuated the effects of each of these agents on platelet-neutrophil aggregation, platelet activation, and neutrophil activation. These data suggest that H, A, ATIII, and rhAPC decrease sepsis-induced neutrophil-endothelial cell interactions. The reversal of this effect by thrombin suggests that these agents alter neutrophil-endothelial interactions through their anticoagulant effects and the resulting decrease in thrombin activity.