Debriefing after resuscitations in a pediatric emergency department

Multiple guidelines recommend debriefing of actual resuscitations to improve clinical performance. We implemented a novel standardized debriefing program using a Debriefing In Situ Conversation after Emergent Resuscitations Now (DISCERN) tool. Following the development of the evidence-based DISCERN tool, we conducted an observational study of all resuscitations (intubation, CPR, and/or defibrillation) at a pediatric emergency department (ED) over one year. Resuscitation interventions, patient survival, and physician team leader characteristics were analyzed as predictors for debriefing. Each debriefing's participants, time duration, and content were recorded. Thematic content of debriefings was categorized by framework approach into Team Emergency Assessment Measure (TEAM) elements. There were 241 resuscitations and 63 (26%) debriefings. A higher proportion of debriefings occurred after CPR (p<0.001) or ED death (p<0.001). Debriefing participants always included an attending and nurse; the median number of staff roles present was six. Median interval (from resuscitation end to start of debriefing) & debriefing durations were 33 (IQR 15,67) and 10 minutes (IQR 5,12), respectively. Common TEAM themes included co-operation/coordination (30%), communication (22%), and situational awareness (15%). Stated reasons for not debriefing included: unnecessary (78%), time constraints (19%), or other reasons (3%). Debriefings with the DISCERN tool usually involved higher acuity resuscitations, involved most of the indicated personnel, and lasted less than 10 minutes. This qualitative tool could be adapted to other settings. Future studies are needed to evaluate for potential impacts on education, quality improvement programming, and staff emotional well-being.^

Identification and characterization of cellular genes differentially expressed in a subset of tumors with non -functional WT1

Wilms tumor (WT) or nephroblastoma is a genetically heterogeneous pediatric renal tumor that accounts for 6–7% of all childhood cancers in the U.S. WT1, located at 11p13, is the sole WT gene cloned to date. Additional genomic regions containing genes that play a role in the development of Wilms tumor include 11p15, 7p, 16q, 1p, 17q and 19q. This heterogeneity has made it extremely difficult to develop an understanding of the pathways involved in the development of WT, even in the 5–20% of tumors that show mutations at the WT1 locus. My research addresses this gap in our current comprehension of the development of WT. ^ I have used two complementary approaches to extend the current understanding of molecular changes involved in the development of WT. In order to minimize complexities due to genetic heterogeneity, I confined my analysis to the WT1 pathway by assessing those genetically defined tumors that carry WT1 mutations. WT1 encodes a zinc finger transcription factor, and in vitro studies have identified many genes that are potentially regulated in vivo by WT1. However, there is very little in vivo data that suggests that they are transcriptionally regulated endogenously by WT1. In one approach I assessed the role of WT1 in the in vivo regulation of PDGFA and IGF2, two genes that are strong contenders for endogenous regulation by WT1. Using primary tissue samples, I found no correlation between the level of RNA expression of WT1 with either PDGFA or IGF2, suggesting that WT1 does not play a critical role in their expression in either normal kidney or WT. ^ In a parallel strategy, using differential display analysis I compared global gene expression in a subset of tumors with known homozygous inactivating WT1 mutations (WT1-tumors) to the gene expression in a panel of appropriate control tissues (fetal kidney, normal kidney, rhabdoid tumor and pediatric renal cell carcinoma). Transcripts that are aberrantly expressed in this subset of Wilms tumors are candidates for endogenous transcriptional regulation by WT1 as well as for potentially functioning in the development of WT. By this approach I identified several differentially expressed transcripts. I further characterized two of these transcripts, identifying a candidate WT gene in the process. I then performed a detailed analysis of this WT candidate gene, which maps to 7p. Future studies will shed more light on the role of these differentially expressed genes in WT. ^