Congenital diaphragmatic hernia—influence of fetoscopic tracheal occlusion on outcomes and predictors of survival

Ali, Kamal; Bendapudi, Perraju; Polubothu, Satyamaanasa; Andradi, Gwendolyn; Ofuya, Mercy; Peacock, Janet L.; Hickey, Ann; Davenport, Mark; Nicolaides, Kypros H.; Greenough, Anne

doi:10.1007/s00431-016-2742-6

Cited by 30 publications

(17 citation statements)

References 18 publications

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“…King's College Hospital NHS Foundation Trust is a referral centre for fetal tracheal occlusion (FETO) and approximately one-third of the population studied had FETO. Those infants were born at an earlier gestational age (data not shown), as we have previously demonstrated 14. There was, however, no significant difference in the proportions of infants who had undergone FETO and who did and did not survive (table 1), which may reflect improvements in the lung-to-head ratio following FETO.…”

Section: Discussionsupporting

confidence: 55%

Resuscitation of infants with congenital diaphragmatic hernia

O'Rourke-Potocki

Ali

Murthy

et al. 2016

Arch Dis Child Fetal Neonatal Ed

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Objective: To determine whether the respiratory response to resuscitation in infants with congenital diaphragmatic hernia as measured by a respiratory function monitor differed between those who did and did not survive.Design: Observational study. Setting: Tertiary perinatal centre.Patients: Thirty-eight infants born at 34 weeks of gestation or greater and diagnosed antenatally with a CDH.Interventions: Expiratory tidal volume (VTe), peak inflation pressure (PIP) and end tidal carbon dioxide level (ETCO2) were simultaneously recorded during resuscitation using a respiratory function monitor. Oxygen saturation was also monitored. Main outcome measures:Mortality related to the median VTe, PIP, compliance (VTe divided by PIP) and ETCO2 levels in the first and last minute of recorded resuscitation and the maximum oxygen saturation. Results:The median gestational age, birth weight and duration of resuscitation of the eleven infants who died did not differ significantly from those who survived. During the first minute of recorded resuscitation, the VTe (median 1.89 versus 2.68 ml/kg) (p=0.009)), the ETCO2 (median 11.7 versus 41.7 mm Hg) (p=0.023)) and the compliance (0.06 versus 0.08 ml/cmH2O/kg) (p=0.018)) were lower in the non survivors. In the last minute, the PIP was higher (32.5 versus 30.3 cm H2O) (p=0.03)), the VTe (3.22 versus 4.66 ml/kg) (p=0.003)) and compliance (0.10 versus 0.15 ml/cmH2O/kg) (p=0.004)) were lower in the 3 non survivors. The maximum oxygen saturation achieved in the labour suite was lower in the non survivors (93% versus 100%) (p=0.037). Conclusions:Infants with CDH who did not survive responded less well even to initial resuscitation.4

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Section: Discussionsupporting

confidence: 55%

Resuscitation of infants with congenital diaphragmatic hernia

O'Rourke-Potocki

Ali

Murthy

et al. 2016

Arch Dis Child Fetal Neonatal Ed

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“…Previous research has shown that tracheal occlusion can indeed cause an increase in lung growth [51,52] and removing the balloon before birth has shown to be necessary for a better maturation of the lung by decreasing the apoptosis of the alveolar type 2 cells, which produce surfactant, an essential compound for lung function [53]. So far, FETO has been shown to improve survival rate in high-risk CDH patients, but at the cost of increased morbidity and premature delivery [54][55][56]. The results of the TOTAL trial will hopefully provide a more definitive answer.…”

Section: Treatment Of Pulmonary Vascular Defects In Cdhmentioning

confidence: 99%

Pulmonary vascular development in congenital diaphragmatic hernia

et al. 2018

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Congenital diaphragmatic hernia (CDH) is a rare congenital anomaly characterised by a diaphragmatic defect, persistent pulmonary hypertension (PH) and lung hypoplasia. The relative contribution of these three elements can vary considerably in individual patients. Most affected children suffer primarily from the associated PH, for which the therapeutic modalities are limited and frequently not evidence based. The vascular defects associated with PH, which is characterised by increased muscularisation of arterioles and capillaries, start to develop early in gestation. Pulmonary vascular development is integrated with the development of the airway epithelium. Although our knowledge is still incomplete, the processes involved in the growth and expansion of the vasculature are beginning to be unravelled. It is clear that early disturbances of this process lead to major pulmonary growth abnormalities, resulting in serious clinical challenges and in many cases death in the newborn. Here we provide an overview of the current molecular pathways involved in pulmonary vascular development. Moreover, we describe the abnormalities associated with CDH and the potential therapeutic approaches for this severe abnormality. Normal pulmonary vascular developmentHuman lung development can be divided into different stages based on histology, starting with the embryonic stage at 4 weeks of gestation, followed by the pseudoglandular stage in which branching of the lung buds continues. During the canalicular stage, starting at ∼16 weeks of gestation, the terminal bronchioli are formed. From 24 weeks of gestation until term, the saccular stage, airspaces widen and alveoli are formed. During the alveolar stage, which persists into the postnatal period up to 3 years of age, maturation of the airways occurs [1]. Concomitant with the expansion of the airways is the adaptation of the microvasculature to optimise the exchange of oxygen and carbon dioxide between the blood and the airways. We and others have shown that very early in lung development pulmonary vessels are present and connected to the systemic circulation. The vasculature develops in close relation with the airways and is a rate-limiting factor in branching morphogenesis [2][3][4]. This implies that the pulmonary vasculature plays an important role in lung development. The formation of new blood vessels primarily occurs through

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“…Conversely, artificially increasing luminal pressures has shown to rescue lung hypoplasia in animal models. These results have been used clinically to develop a procedure called fetal endoscopic tracheal occlusion (FETO) [78]. FETO uses a small balloon inflated within the intubated fetal trachea to block fluid efflux out of the lung and increase the fluid pressure within the developing lung.…”

Section: Examples Of Fluid Mechanical Regulation Of Organogenesismentioning

confidence: 99%

“…FETO uses a small balloon inflated within the intubated fetal trachea to block fluid efflux out of the lung and increase the fluid pressure within the developing lung. FETO and strategies used to increase transepithelial Cl− flux have been attempted in utero to increase the lumenal fluid pressure with modest success to date in humans [78–80]. As such, it is clear that the in utero mechanical environment is complex and additional study is needed to understand how pressure and/or local dynamic pressures and flows from peristaltic smooth muscle contractions spatially induce cellular mechanotransduction pathways that regulate lung morphogenesis.…”

Section: Examples Of Fluid Mechanical Regulation Of Organogenesismentioning

confidence: 99%

Fluid Mechanics as a Driver of Tissue-Scale Mechanical Signaling in Organogenesis

et al. 2016

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Purpose of Review Organogenesis is the process during development by which cells self-assemble into complex, multi-scale tissues. Whereas significant focus and research effort has demonstrated the importance of solid mechanics in organogenesis, less attention has been given to the fluid forces that provide mechanical cues over tissue length scales. Recent Findings Fluid motion and pressure is capable of creating spatial gradients of forces acting on cells, thus eliciting distinct and localized signaling patterns essential for proper organ formation. Understanding the multi-scale nature of the mechanics is critically important to decipher how mechanical signals sculpt developing organs. Summary This review outlines various mechanisms by which tissues generate, regulate, and sense fluid forces and highlights the impact of these forces and mechanisms in case studies of normal and pathological development.

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Congenital diaphragmatic hernia—influence of fetoscopic tracheal occlusion on outcomes and predictors of survival

Cited by 30 publications

References 18 publications

Resuscitation of infants with congenital diaphragmatic hernia

Resuscitation of infants with congenital diaphragmatic hernia

Pulmonary vascular development in congenital diaphragmatic hernia

Fluid Mechanics as a Driver of Tissue-Scale Mechanical Signaling in Organogenesis

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