Elle Mizuki Fukui

All Publications

• Scaling up a diagnostic pause at the ICU-to-ward transition: an exploration of barriers and facilitators to implementation of the ICU-PAUSE handoff tool. Diagnosis (Berlin, Germany) Cornell, E. G., Harris, E., McCune, E., Fukui, E., Lyons, P. G., Rojas, J. C., Santhosh, L. 2023; 10 (4): 417-423

  Abstract

  The transition from the intensive care unit (ICU) to the medical ward is a high-risk period due to medical complexity, reduced patient monitoring, and diagnostic uncertainty. Standardized handoff practices reduce errors associated with transitions of care, but little work has been done to standardize the ICU to ward handoff. Further, tools that exist do not focus on preventing diagnostic error. Using Human-Centered Design methods we previously created a novel EHR-based ICU-ward handoff tool (ICU-PAUSE) that embeds a diagnostic pause at the time of transfer. This study aims to explore barriers and facilitators to implementing a diagnostic pause at the ICU-to-ward transition.This is a multi-center qualitative study of semi-structured interviews with intensivists from ten academic medical centers. Interviews were analyzed iteratively through a grounded theory approach. The Sittig-Singh sociotechnical model was used as a unifying conceptual framework.Across the eight domains of the model, we identified major benefits and barriers to implementation. The embedded pause to address diagnostic uncertainty was recognized as a key benefit. Participants agreed that standardization of verbal and written handoff would decrease variation in communication. The main barriers fell within the domains of workflow, institutional culture, people, and assessment.This study represents a novel application of the Sittig-Singh model in the assessment of a handoff tool. A unique feature of ICU-PAUSE is the explicit acknowledgement of diagnostic uncertainty, a practice that has been shown to reduce medical error and prevent premature closure. Results will be used to inform future multi-site implementation efforts.

  View details for DOI 10.1515/dx-2023-0046

  View details for PubMedID 37598362

• Improving Communication in Intensive Care Unit to Ward Transitions: Protocol for Multisite National Implementation of the ICU-PAUSE Handoff Tool JMIR RESEARCH PROTOCOLS Fukui, E., Lyons, P. G., Harris, E., McCune, E. K., Rojas, J. C., Santhosh, L. 2023; 12

  View details for DOI 10.2196/40918

  View details for Web of Science ID 001015247900007

• Corroborating evidence refutes batch effect as explanation for fetal bacteria. Microbiome Rackaityte, E., Halkias, J., Fukui, E. M., Mendoza, V. F., Hayzelden, C., Crawford, E. D., Fujimura, K. E., Burt, T. D., Lynch, S. V. 2021; 9 (1): 10

  View details for DOI 10.1186/s40168-020-00948-0

  View details for PubMedID 33436079

  View details for PubMedCentralID PMC7805121

• Viable bacterial colonization is highly limited in the human intestine in utero. Nature medicine Rackaityte, E., Halkias, J., Fukui, E. M., Mendoza, V. F., Hayzelden, C., Crawford, E. D., Fujimura, K. E., Burt, T. D., Lynch, S. V. 2020; 26 (4): 599-607

  Abstract

  Mucosal immunity develops in the human fetal intestine by 11-14 weeks of gestation, yet whether viable microbes exist in utero and interact with the intestinal immune system is unknown. Bacteria-like morphology was identified in pockets of human fetal meconium at mid-gestation by scanning electron microscopy (n = 4), and a sparse bacterial signal was detected by 16S rRNA sequencing (n = 40 of 50) compared to environmental controls (n = 87). Eighteen taxa were enriched in fetal meconium, with Micrococcaceae (n = 9) and Lactobacillus (n = 6) the most abundant. Fetal intestines dominated by Micrococcaceae exhibited distinct patterns of T cell composition and epithelial transcription. Fetal Micrococcus luteus, isolated only in the presence of monocytes, grew on placental hormones, remained viable within antigen presenting cells, limited inflammation ex vivo and possessed genomic features linked with survival in the fetus. Thus, viable bacteria are highly limited in the fetal intestine at mid-gestation, although strains with immunomodulatory capacity are detected in subsets of specimens.

  View details for DOI 10.1038/s41591-020-0761-3

  View details for PubMedID 32094926

  View details for PubMedCentralID PMC8110246

• Elevated faecal 12,13-diHOME concentration in neonates at high risk for asthma is produced by gut bacteria and impedes immune tolerance. Nature microbiology Levan, S. R., Stamnes, K. A., Lin, D. L., Panzer, A. R., Fukui, E., McCauley, K., Fujimura, K. E., McKean, M., Ownby, D. R., Zoratti, E. M., Boushey, H. A., Cabana, M. D., Johnson, C. C., Lynch, S. V. 2019; 4 (11): 1851-1861

  Abstract

  Neonates at risk of childhood atopy and asthma exhibit perturbation of the gut microbiome, metabolic dysfunction and increased concentrations of 12,13-diHOME in their faeces. However, the mechanism, source and contribution of this lipid to allergic inflammation remain unknown. Here, we show that intra-abdominal treatment of mice with 12,13-diHOME increased pulmonary inflammation and decreased the number of regulatory T (Treg) cells in the lungs. Treatment of human dendritic cells with 12,13-diHOME altered expression of PPARγ-regulated genes and reduced anti-inflammatory cytokine secretion and the number of Treg cells in vitro. Shotgun metagenomic sequencing of neonatal faeces indicated that bacterial epoxide hydrolase (EH) genes are more abundant in the gut microbiome of neonates who develop atopy and/or asthma during childhood. Three of these bacterial EH genes (3EH) specifically produce 12,13-diHOME, and treatment of mice with bacterial strains expressing 3EH caused a decrease in the number of lung Treg cells in an allergen challenge model. In two small birth cohorts, an increase in the copy number of 3EH or the concentration of 12,13-diHOME in the faeces of neonates was found to be associated with an increased probability of developing atopy, eczema or asthma during childhood. Our data indicate that elevated 12,13-diHOME concentrations impede immune tolerance and may be produced by bacterial EHs in the neonatal gut, offering a mechanistic link between perturbation of the gut microbiome during early life and atopy and asthma during childhood.

  View details for DOI 10.1038/s41564-019-0498-2

  View details for PubMedID 31332384

  View details for PubMedCentralID PMC6830510