Aurora, CO, United States
Aurora, CO, United States

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Baker C.D.,Pediatric Heart Lung Center | Martin S.,Childrens Hospital Colorado | Thrasher J.,Childrens Hospital Colorado | Moore H.M.,Pediatric Heart Lung Center | And 4 more authors.
Pediatrics | Year: 2016

Objective: Children who require chronic mechanical ventilation via tracheostomy are medically complex and require prolonged hospitalization, placing a heavy burden on caregivers and hospital systems. We developed an interdisciplinary Ventilator Care Program to relieve this burden, through improved communication and standardized care. We hypothesized that a standardized team approach to the discharge of tracheostomy-and ventilator-dependent children would decrease length of stay (LOS), reduce patient costs, and improve safety. METHODS: We used process mapping to standardize the discharge process for children requiring chronic ventilation. Interventions included developing education materials, a Chronic Ventilation Road Map for caregivers, utilization of the electronic medical record to track discharge readiness, team-based care coordination, and timely case management to arrange home nursing. We aimed to decrease overall and pediatric respiratory care unit LOS as the primary outcomes. We also analyzed secondary outcomes (mortality, emergency department visits, unplanned readmissions), and per-patient hospital costs during 2-year "preintervention" and "postintervention" periods (n = 18 and 30, respectively). RESULTS: Patient demographics were not different between groups. As compared with the preintervention cohort, the overall LOS decreased 42% (P =.002). Pediatric respiratory care unit LOS decreased 56% (P =.001). As a result, unplanned readmissions, emergency department visits, and mortality were not increased. Direct costs per hospitalization were decreased by an average of 43% (P =.01). CONCLUSIONS: Although LOS remained high, a standardized discharge process for chronically ventilated children by an interdisciplinary Ventilator Care Program team resulted in decreased LOS and costs without a negative impact on patient safety. © 2016 by the American Academy of Pediatrics.


Galambos C.,Aurora University | Galambos C.,Pediatric Heart Lung Center | Sims-Lucas S.,University of Pittsburgh | Abman S.H.,Pediatric Heart Lung Center | Abman S.H.,Aurora University
Annals of the American Thoracic Society | Year: 2013

Rationale: Bronchopulmonary dysplasia (BPD) is the chronic lung disease of infancy that occurs in premature infants after oxygen and ventilator therapy for acute respiratory disease at birth. Despite improvement in current therapies, the clinical course of infants with BPD is often characterized by marked hypoxemia that can become refractory to therapy. Preacinar anatomic and functional communications between systemic and pulmonary vascular systems has been established in fetal lungs, but whether increased intrapulmonary anastomotic vessels or their failure to regress after birth contributes to hypoxemia in preterm infants with BPD is unknown. Objectives:Wesought tofind histologic evidence of intrapulmonary anastomotic vessels in lungs of patients who died of severe BPD. Methods: We collected lung tissues from fatal BPD cases and performed histology, immunohistochemistry, and high-precision three-dimensional reconstruction techniques. Measurements and Main Results: We report histologic evidence of intrapulmonary vessels that bridge pulmonary arteries and veins in the distal lungs of infants dying with severe BPD. These prominent vessels appear similar to "misaligned pulmonary veins" described in the lethal form of congenital lung disorder, alveolar capillary dysplasia. Conclusions: We found striking histological evidence of precapillary arteriovenous anastomotic vessels in the lungs of infants with severe bronchopulmonary dysplasia.We propose that persistence or expansion of these vessels after premature birth provides the anatomic basis for intrapulmonary shunt and hypoxemia in neonates with severe bronchopulmonary dysplasia and may play a significant role in the morbidity and mortality of BPD. Copyright © 2013 by the American Thoracic Society.


PubMed | Pediatric Heart Lung Center
Type: Journal Article | Journal: American journal of physiology. Lung cellular and molecular physiology | Year: 2011

Maternal use of selective serotonin (5-HT) reuptake inhibitors (SSRIs) is associated with an increased risk for persistent pulmonary hypertension of the newborn (PPHN), but little is known about 5-HT signaling in the developing lung. We hypothesize that 5-HT plays a key role in maintaining high pulmonary vascular resistance (PVR) in the fetus and that fetal exposure to SSRIs increases 5-HT activity and causes pulmonary hypertension. We studied the hemodynamic effects of 5-HT, 5-HT receptor antagonists, and SSRIs in chronically prepared fetal sheep. Brief infusions of 5-HT (3-20 g) increased PVR in a dose-related fashion. Ketanserin, a 5-HT 2A receptor antagonist, caused pulmonary vasodilation and inhibited 5-HT-induced pulmonary vasoconstriction. In contrast, intrapulmonary infusions of GR127945 and SB206553, 5-HT 1B and 5-HT 2B receptor antagonists, respectively, had no effect on basal PVR or 5-HT-induced vasoconstriction. Pretreatment with fasudil, a Rho kinase inhibitor, blunted the effects of 5-HT infusion. Brief infusions of the SSRIs, sertraline and fluoxetine, caused potent and sustained elevations of PVR, which was sustained for over 60 min after the infusion. SSRI-induced pulmonary vasoconstriction was reversed by infusion of ketanserin and did not affect the acute vasodilator effects of acetylcholine. We conclude that 5-HT causes pulmonary vasoconstriction, contributes to maintenance of high PVR in the normal fetus through stimulation of 5-HT 2A receptors and Rho kinase activation, and mediates the hypertensive effects of SSRIs. We speculate that prolonged exposure to SSRIs can induce PPHN through direct effects on the fetal pulmonary circulation.

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