RESUMEN
BACKGROUND: High-risk therapies (HRTs), including medications and medical devices, are an important driver of preventable harm in children's hospitals. To facilitate shared situation awareness (SA) and thus targeted harm prevention, we aimed to increase the percentage of electronic health record (EHR) alerts with the correct descriptor of an HRT from 11% to 100% on a high-acuity hospital unit over a 6-month period. METHODS: The interdisciplinary team defined an HRT as a medication or device with a significant risk for harm that required heightened awareness. Our aim for interventions was to (1) educate staff on a new HRT algorithm; (2) develop a comprehensive table of HRTs, risks, and mitigation plans; (3) develop bedside signs for patients receiving HRTs; and (4) restructure unit huddles. Qualitative interviews with families, nurses, and medical teams were used to assess shared SA and inform the development and adaptation of interventions. The primary outcome metric was the percentage of EHR alerts for an HRT that contained a correct descriptor of the therapy for use by the care team and institutional safety leaders. RESULTS: The percentage of EHR alerts with a correct HRT descriptor increased from an average of 11% to 96%, with special cause variation noted on a statistical process control chart. Using qualitative interview data, we identified critical awareness gaps, including establishing a shared mental model between nursing staff and the medical team as well as engagement of families at the bedside to monitor for complications. CONCLUSIONS: Explicit, structured processes and huddles can increase HRT SA among the care team, patient, and family.
Asunto(s)
Concienciación , Niño Hospitalizado , Niño , Registros Electrónicos de Salud , Hospitales Pediátricos , HumanosRESUMEN
Previous studies show that expression of heme oxygenase-1 (HO-1) in endothelial cells results in decreased cyclooxygenase expression and prostaglandin (PG) levels through limiting heme availability. Regulation of PGs, important inflammatory mediators, may contribute to the anti-inflammatory potential of HO-1. Here we examine the effects of HO-1 expression on PG clearance via the prostaglandin transporter (PGT). Endothelial cells expressing human HO-1 via retroviral transfer exhibit approximately 7-fold higher levels of PGT RNA and equivalently elevated uptake of [(3)H]PGE(2). The pattern and extent of uptake and the substrate inhibitory constants of PGE(2), PGF(2alpha), and thromboxane B(2) are similar to those of cloned PGT. Treatment of cells with stannous chloride, an inducer of HO-1, results in increased expression of PGT while incubation of cells expressing human HO-1 with stannic mesophorphyrin, a substrate inhibitor of HO-1, decreases PG uptake. Therefore, PG clearance via PGT may contribute to the cellular regulation of PG levels by HO-1.