Collective quality improvement in the paediatric cardiology acute care unit: establishment of the Pediatric Acute Care Cardiology Collaborative (PAC3).

Collaborative quality improvement and learning networks have amended healthcare quality and value across specialities. Motivated by these successes, the Pediatric Acute Care Cardiology Collaborative (PAC3) was founded in late 2014 with an emphasis on improving outcomes of paediatric cardiology patients within cardiac acute care units; acute care encompasses all hospital-based inpatient non-intensive care. PAC3 aims to deliver higher quality and greater value care by facilitating the sharing of ideas and building alignment among its member institutions. These aims are intentionally aligned with the work of other national clinical collaborations, registries, and parent advocacy organisations. The mission and early work of PAC3 is exemplified by the formal partnership with the Pediatric Cardiac Critical Care Consortium (PC4), as well as the creation of a clinical registry, which links with the PC4 registry to track practices and outcomes across the entire inpatient encounter from admission to discharge. Capturing the full inpatient experience allows detection of outcome differences related to variation in care delivered outside the cardiac ICU and development of benchmarks for cardiac acute care. We aspire to improve patient outcomes such as morbidity, hospital length of stay, and re-admission rates, while working to advance patient and family satisfaction. We will use quality improvement methodologies consistent with the Model for Improvement to achieve these aims. Membership currently includes 36 centres across North America, out of which 26 are also members of PC4. In this report, we describe the development of PAC3, including the philosophical, organisational, and infrastructural elements that will enable a paediatric acute care cardiology learning network.

Successful Reduction of Postoperative Chest Tube Duration and Length of Stay After Congenital Heart Surgery: A Multicenter Collaborative Improvement Project.

Background Congenital heart disease practices and outcomes vary significantly across centers, including postoperative chest tube (CT) management, which may impact postoperative length of stay (LOS). We used collaborative learning methods to determine whether centers could adapt and safely implement best practices for CT management, resulting in reduced postoperative CT duration and LOS. Methods and Results Nine pediatric heart centers partnered together through 2 learning networks. Patients undergoing 1 of 9 benchmark congenital heart operations were included. Baseline data were collected from June 2017 to June 2018, and intervention-phase data were collected from July 2018 to December 2019. Collaborative learning methods included review of best practices from a model center, regular data feedback, and quality improvement coaching. Center teams adapted CT removal practices (eg, timing, volume criteria) from the model center to their local resources, practices, and setting. Postoperative CT duration in hours and LOS in days were analyzed using statistical process control methodology. Overall, 2309 patients were included. Patient characteristics did not differ between the study and intervention phases. Statistical process control analysis showed an aggregate 15.6% decrease in geometric mean CT duration (72.6 hours at baseline to 61.3 hours during intervention) and a 9.8% reduction in geometric mean LOS (9.2 days at baseline to 8.3 days during intervention). Adverse events did not increase when comparing the baseline and intervention phases: CT replacement (1.8% versus 2.0%, P=0.56) and readmission for pleural effusion (0.4% versus 0.5%, P=0.29). Conclusions We successfully lowered postoperative CT duration and observed an associated reduction in LOS across 9 centers using collaborative learning methodology.

Center Variation in Chest Tube Duration and Length of Stay After Congenital Heart Surgery.

BACKGROUND: Nearly every child undergoing congenital heart surgery has chest tubes placed intraoperatively. Center variation in removal practices and impact on outcomes has not been well described. This study evaluated variation in chest tube management practices and outcomes across centers. METHODS: The study included patients undergoing any of 10 benchmark operations from June 2017 to May 2018 at participating Pediatric Acute Care Cardiology Collaborative (PAC3) and Pediatric Cardiac Critical Care Consortium (PC4) centers. Clinical data from PC4 centers were merged with chest tube data from PAC3 centers. Practices and outcomes were compared across centers in univariate and multivariable analysis. RESULTS: The cohort included 1029 patients (N = 9 centers). Median chest tube duration varied significantly across centers for 9 of 10 benchmark operations (all P ≤ .03), with a "model" center noted to have the shortest duration for 9 of 10 operations (range, 27.9% to 87.4% shorter duration vs other centers across operations). This effect persisted in multivariable analysis (P < .0001). The model center had higher volumes of chest tube output before removal (median, 8.5 mL/kg/24 h [model] vs 2.2 mL/kg/24 h [other centers]; P < .001], but it did not have higher rates of chest tube reinsertion (model center 1.3% vs 2.1%; P = .59) or readmission for pleural effusion (model center 4.4% vs 3.0%; P = .31), and had the shortest length of stay for 7 of 10 operations. CONCLUSIONS: This study suggests significant center variation in chest tube removal practices and associated outcomes after congenital heart surgery. Best practices used at the model center have informed the design of an ongoing collaborative learning project aimed at reducing chest tube duration and length of stay.

Aortopulmonary fistula after outflow tract stent in repaired truncus.

We present a case of an iatrogenic aortopulmonary (AP) fistula in a 9-year-old patient with a history of repaired truncus arteriosus without the use of a right ventricle to pulmonary artery conduit and subsequent transcatheter placement of a right ventricular outflow tract (RVOT) stent. Redilation of the stent resulted in a defect in the aortic wall and the creation of an AP fistula with an associated hemodynamically significant left to right shunt. This case demonstrates a previously unreported adverse event of transcatheter RVOT reintervention after truncus arteriosus repair.

A unique pattern of Tie1 expression in the developing murine lung.

The molecular mechanisms responsible for organ-specific differences in vascular development are not well established. Animals lacking the receptor tyrosine kinase Tie1 die of hemorrhage and pulmonary edema. Furthermore, cells lacking Tie1 are excluded from blood vessels of the mature lung. These findings suggest the importance of Tie1 in the pulmonary vasculature. We quantified the organ-specific expression of Tie1 during embryonic and postnatal murine development using both quantitative real-time polymerase chain reaction (PCR) and chemiluminescence employing a tie1.lacZ reporter. In the lung, Tie1 expression increases markedly immediately prior to birth and rises further in the newborn animal, a pattern not found in other organs. Furthermore, expression of Tie1 in the lung is also unique by its persistent increase in the adult animal. This unique pattern of Tie1 gene expression in the embryonic and mature lung supports a distinct role for Tie1 in the development and function of the pulmonary vasculature.

Notch1 and Jagged1 expression by the developing pulmonary vasculature.

The molecular mechanisms of pulmonary vascular development are poorly understood. Cell-specific developmental pathways are influenced by cell-cell signaling. Notch signaling molecules are highly conserved receptors active in many cell-fate determination systems. Recent observations of Notch molecules and a Notch ligand, Jagged1, suggest their importance in vascular morphogenesis, and particularly pulmonary vascular development. We performed a systematic evaluation of Notch1/Jagged1 gene and protein expression in the developing mouse lung from embryonic day 11 until adulthood by using quantitative PCR, immunofluorescence, and electron microscopic analysis. mRNA transcripts for Notch1-4 and Jagged1 increased progressively from early to later lung development, accompanied by a simultaneous rise in endothelial cell-specific gene expression, a pattern not seen in other organs. Notch1 mRNA was identified on both epithelial and mesenchymal structures of the embryonic lung. Immunofluorescence staining revealed the progressive acquisition of Notch1 and Jagged1 proteins by the emerging endothelium. Notch1 and Jagged1 were seen initially on well-formed, larger vessels within the embryonic lung bud and progressively on finer vascular networks. Each was also expressed on surrounding nonvascular structures. The localization of Notch1 and Jagged1 on endothelial cell surface membranes within the alveolar microvasculature was confirmed by immuno-electron microscopy. These temporal and spatial patterns in Notch1/Jagged1 gene and protein expression suggest multiple potential paths of cell-cell signaling during lung development and vascular morphogenesis.