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Sonographic Assessment of Amniotic Fluid
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Persistent oligohydramnios can lead to structural (i.e., skeletal) abnormalities and pulmonary hypoplasia [40]. The risk of pulmonary hypoplasia depends largely on gestational age at diagnosis and severity of oligohydramnios. When diagnosed after 26 weeks, the risk of pulmonary hypoplasia is less than 2%; however, if diagnosed before 24 weeks, the risk increases to 30% [41, 42]. Additionally, in patients with prolonged, severe oligohydramnios, risk of pulmonary hypoplasia is estimated to be as high as 43% [43]. The risk of skeletal deformities is over 50% with severe oligohydramnios [43]. Gestational age at diagnosis does not appear to affect risk of skeletal deformities [41, 43]. Fetal anomalies have been reported in up to 30% with oligohydramnios in the second trimester, up to 50% if severe oligohydramnios.
Prelabor rupture of the membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Lami Yeo, Francesca Gotsch, Eleazar Soto, Sonia S. Hassan, Juan Pedro Kusanovic, Ray Bahado-Singh
Three studies examined the frequency of pulmonary hypoplasia in the context of preterm PROM. Vergani et al. conducted a prospective study of patients with PROM before 28 weeks of gestation managed conservatively and found that the frequency of pulmonary hypoplasia was 28% (120). Gestational age at the time of PROM and presence of oligohydramnios, but not the latency period, were independent predictors of pulmonary hypoplasia (120).
Congenital diaphragmatic hernia
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Erin E. Perrone, George B. Mychaliska
Both lungs are involved, the ipsilateral greater than the contralateral lung. Affected infants are born with a complex combination of pulmonary hypoplasia and pulmonary hypertension. There is decreased surface area available for gas exchange, compromised bronchiolar and pulmonary vascular beds, and muscular hypertrophy of the intra-acinar arterioles. Despite significant advances in neonatal intensive care and pediatric surgical care, a cohort of affected infants does not survive. The most recent data from the Congenital Diaphragmatic Hernia Study Group (CDHSG) reports an overall survival of 71%, with survival lower in the prenatally diagnosed group (65%) when compared to the postnatally diagnosed group (83%). The CDHSG has developed a classification system based on defect size, with A being the smallest and D the largest (Figure 13.2). The system correlates with degree of pulmonary hypoplasia and severity. Mortality rate increases with defect size and is reported as 0.6%, 5.3%, 22.6%, and 45.6% in groups A, B, C, and D respectively. Pulmonary, neurologic, and gastrointestinal morbidity is also increased with defect sizes C and D.
Predicting previable preterm premature rupture of membranes (pPPROM) before 24 weeks: maternal and fetal/neonatal risk factors for survival
Published in Journal of Obstetrics and Gynaecology, 2022
Aylin Günes, Hüseyin Kiyak, Semra Yüksel, Gökhan Bolluk, Rabia Merve Erbiyik, Ali Gedikbasi
Although neonatal complications like pulmonary problems (RDS, PPH, CPD, BPD), sepsis, NEC, IVH, skeletal deformities or ROP are especially common in very early preterm neonates, only few had statistical consequences and RDS with ROP were significant for multivariate regression analysis in our study. However, RDS and other pulmonary complications were not found significant by Sim et al. (2018) with 41 early pPPROM and 89 late pPPROM cases, except pulmonary hypoplasia in early cases. Furthermore, another review written by Sim et al. (2017) mentioned that common seen neonatal morbidities were RDS, BPD and sepsis and especially draw attention for the association of neonatal deaths within 24 h and pulmonary hypoplasia. Finally, Park et al. (2019) differentiated cases with pPPROM before 25 gestational weeks after delivery into two groups as cases with and without pulmonary hypoplasia. They concluded that cases with additional findings of pulmonary hypoplasia are a significant risk factor for mortality and morbidity.
Ethics Consultations in a Fetal Health Center
Published in The American Journal of Bioethics, 2022
Brian S. Carter, Shika Kalevor
An example of the latter has been several consults around the fetal diagnosis of bilateral renal disease and associated severe oligohydramnios, or frank anhydramnios, that could present as early as 15–16 weeks of gestation. Innovative efforts to place a shunt to drain an obstructed bladder or urinary tract, or to decompress cystic renal malformations, or even perform an in-utero laser ablation of posterior urethral valves all were considered. Additionally, the question of whether serial amnioinfusion should be provided, and if so, how often, arose. Perhaps they should be done weekly. But many so affected pregnancies could not be sustained as there was chronic leakage of amniotic fluid, the development of sepsis, or fatal preterm labor and delivery in the face of severe pulmonary hypoplasia. How well were parents being informed of the long odds of adequate fetal lung development and working through or around the often life-limiting condition of pulmonary hypoplasia and neonatal respiratory failure? Did they simply hear that this was the only path forward toward a hoped for, but far from likely, course to involve neonatal and infant dialysis and a race against the clock to obtain a kidney transplant at age two years? As true informed consent requires an ability to make a free choice unencumbered by bias or coercion, could these parents give informed consent? As we all await the results of the Renal Anhydramnios Fetal Therapy (RAFT) trial uncertainty seemed to collide with desperate hope.
Managing respiratory complications in infants and newborns with congenital diaphragmatic hernia
Published in Expert Opinion on Orphan Drugs, 2020
Sandeep Shetty, Fahad M. S. Arattu Thodika, Anne Greenough
CDH survivors have reduced forced expiratory volume in one second (FEV1), FEV1/forced vital capacity (FVC) and forced expiratory flow at 25–75% of the pulmonary volume (FEF25-75) [127]. CDH survivors with a patch repair and who had their liver in their chest had reduced FEV1 and FEV1/FVC suggestive of obstructive phenotype [128]. At eight years of age, in one series CDH survivors had lower FVC, FEV1, and mean FEF25–75 [129], but this is not a universal finding [130]. At 11.9 years, lower FEV1, FVC, and FEV1/FVC results have also been reported [131]. At a mean age of 24.3 years, 12 young people had a lower FEV1, although their quality of life was comparable to the general population [132]. Lung volume abnormalities have also been demonstrated. Functional residual capacity (FRC) measured by plethysmography was increased especially in those patients who had received ECMO. In the first three years, FRC and residual volume were increased in CDH children, although total lung capacity was normal or low [133]. The degree of pulmonary function impairment correlated with markers of the initial degree of pulmonary hypoplasia and the duration of mechanical ventilation. Such abnormalities could be explained by abnormal lung development, hyperinflation, and/or abnormal diaphragm function [111].