Team Stress and Adverse Events during Neonatal Tracheal Intubations: A Report from NEAR4NEOS.

OBJECTIVE: This study aimed to examine the association between team stress level and adverse tracheal intubation (TI)-associated events during neonatal intubations. STUDY DESIGN: TIs from 10 academic neonatal intensive care units were analyzed. Team stress level was rated immediately after TI using a 7-point Likert scale (1 = high stress). Associations among team stress, adverse TI-associated events, and TI characteristics were evaluated. RESULT: In this study, 208 of 2,009 TIs (10%) had high stress levels (score < 4). Oxygenation failure, hemodynamic instability, and family presence were associated with high stress level. Video laryngoscopy and premedication were associated with lower stress levels. High stress level TIs were associated with adverse TI-associated event rates (31 vs. 16%, p < 0.001), which remained significant after adjusting for potential confounders including patient, provider, and practice factors associated with high stress (odds ratio: 1.90, 96% confidence interval: 1.36-2.67, p < 0.001). CONCLUSION: High team stress levels during TI were more frequently reported among TIs with adverse events.

Vascular endothelial growth factor causes pulmonary vasodilation through activation of the phosphatidylinositol-3-kinase-nitric oxide pathway in the late-gestation ovine fetus.

Vascular endothelial growth factor (VEGF) causes vasodilation in adult models of peripheral vascular disease and myocardial ischemia through the acute release of nitric oxide (NO). However, the hemodynamic effects of VEGF and its effects on NO production have not been studied in the developing lung circulation. We hypothesized that VEGF causes fetal pulmonary vasodilation, and that its actions are mediated through the release of endogenous NO. We performed surgery in 16 fetal lambs (125-135 d gestation; term = 147 d), and placed catheters in the main pulmonary artery, aorta, and left atrium to measure pressures. An ultrasonic flow transducer was placed on the left pulmonary artery (LPA) to measure blood flow, and a catheter was placed in the LPA for local drug infusion. Pulmonary vascular resistance in the left lung was calculated as pulmonary artery pressure minus left atrial pressure divided by LPA flow. Fetal lambs were treated with brief infusions of recombinant human VEGF (dose, 0.5-2.0 micro g) into the LPA. Recombinant human VEGF infusions acutely increased LPA flow by up to 3-fold (p < 0.02) and decreased pulmonary vascular resistance by 65% (p < 0.05) in a dose-related fashion, without affecting aortic pressure or heart rate. To determine the mechanism of VEGF-induced vasodilation, we studied the effects of nitro-L-arginine, an NO synthase inhibitor, and LY294002, a phosphatidylinositol-3-kinase inhibitor, on the response to VEGF. We found that pretreatment with either nitro-L-arginine or LY294002 completely inhibited the vasodilator response to recombinant human VEGF (p < 0.005). These findings suggest that recombinant human VEGF causes fetal pulmonary vasodilation, and that this response is likely mediated by the release of NO through activation of phosphatidylinositol-3-kinase.

Case report: infantile hemangioendothelioma.

During a routine physical exam, an 18-day-old male infant was noted to have persistent abdominal distention and prominent vascular markings over his abdominal wall. Laboratory studies were significant for an elevated alpha-fetoprotein level of 7051 ng/ml and mild anemia. Abdominal ultrasound and CT scan demonstrated a large, heterogeneous mass in the lateral segment of the left lobe of the liver. Although the patient did not have congestive heart failure or coagulopathy, surgical resection was performed to rule out malignancy. Histopathologic examination revealed a type I infantile hemangioendothelioma. This case report reviews the presentation and treatment of infantile hemangioendotheliomas and the differential diagnosis of neonatal hepatic neoplasms.

Intrauterine hypertension decreases lung VEGF expression and VEGF inhibition causes pulmonary hypertension in the ovine fetus.

Although vascular endothelial growth factor (VEGF) plays a vital role in lung vascular growth in the embryo, its role in maintaining endothelial function and modulating vascular structure during late fetal life has not been studied. We hypothesized that impaired lung VEGF signaling causes pulmonary hypertension, endothelial dysfunction, and structural remodeling before birth. To determine whether lung VEGF expression is decreased in an experimental model of persistent pulmonary hypertension of the newborn (PPHN), we measured lung VEGF and VEGF receptor protein content from fetal lambs 7-10 days after ductus arteriosus ligation (132-140 days gestation; term = 147 days). In contrast with the surge in lung VEGF expression during late gestation in controls, chronic intrauterine pulmonary hypertension reduced lung VEGF expression by 78%. To determine whether VEGF inhibition during late gestation causes pulmonary hypertension, we treated fetal lambs with EYE001, an aptamer that specifically inhibits VEGF(165). Compared with vehicle controls, EYE001 treatment elevated pulmonary artery pressure and pulmonary vascular resistance by 22 and 50%, respectively, caused right ventricular hypertrophy, and increased wall thickness of small pulmonary arteries. EYE001 treatment reduced lung endothelial nitric oxide synthase protein content by 50% and preferentially impaired the pulmonary vasodilator response to ACh, an endothelium-dependent agent. We conclude that chronic intrauterine pulmonary hypertension markedly decreases lung VEGF expression and that selective inhibition of VEGF(165) mimics the structural and physiological changes of experimental PPHN. We speculate that hypertension downregulates VEGF expression in the developing lung and that impaired VEGF signaling may contribute to the pathogenesis of PPHN.