Chaos

Gupta, Aman; Yadav, Chandrajeet; Dhruw, Sandeep; Mishra, Divyangi; Taori, Abhijeet

doi:10.1007/s13224-016-0910-2

Cited by 8 publications

(6 citation statements)

References 7 publications

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“…As a result, fluid is trapped in the lungs, creating internal pressure which forces the lung to grow. This idea of blocking the airway emerged from an experiment of nature in patients with congenital high airway obstruction syndrome resulting in big polyalveolar lungs [50]. 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].…”

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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Section: Treatment Of Pulmonary Vascular Defects In Cdhmentioning

confidence: 99%

Pulmonary vascular development in congenital diaphragmatic hernia

et al. 2018

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“…Extrinsic compression can be caused by lymphatic malformations, vascular rings or masses such as teratomas. Intrinsic causes are mostly secondary to laryngeal atresia or tracheal atresia [ 1 ]. Embryologically, laryngeal atresia results from failure of recanalization of the larynx, whereas tracheal atresia results from unequal partitioning of the foregut into the esophagus and trachea [ 2 ]…”

Section: Discussionmentioning

confidence: 99%

Creating Order Out of Chaos – Role of Antenatal Ultrasound in Diagnosis

et al. 2018

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SummaryBackgroundCongenital high airway obstruction syndrome (CHAOS) is a rare fetal anomaly characterized by obstruction of the higher fetal airway. This could be either complete or incomplete and is more commonly seen at the subglottic level, resulting in a spectrum of characteristic secondary features.Case ReportIn this case study, we report two cases of CHAOS with one showing laryngeal atresia and the other, tracheal atresia. Both these cases showed characteristic findings on a detailed, meticulous USG examination which led to this diagnosis.ConclusionsEarly and accurate diagnosis offers a window of opportunity for parental counseling and management using procedures such as EXIT (ex-utero intrapartum procedure). Earlier, CHAOS was thought to be incompatible with life; however, with the advent of ex-utero intrapartum procedure, a few cases of post-natal survival have been noted in the literature. In this article, we emphasize the sonographic findings found in CHAOS. Early diagnosis offers an opportunity for a intrauterine fetal intervention in potentially lethal cases.

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“…These findings are pathognomonic for complete or near-complete obstruction of the fetal upper airway and carry a poor, often fatal prognosis. Etiologies of CHAOS include laryngeal or tracheal atresia, laryngeal or tracheal webs, laryngeal or tracheal agenesis, subglottic stenosis or atresia, congenital mass, and laryngeal cyst with laryngeal atresia representing the most frequent cause [ 2 ]. Embryologically, laryngeal atresia occurs due to failed recanalization of the vestibule and subglottic regions during the development of the larynx [ 3 ].…”

Section: Introductionmentioning

confidence: 99%