AimTo evaluate the accuracy of lung ultrasound in diagnosing and differentiating transient tachypnea of the newborn and respiratory distress syndrome in preterm neonates.Material and methodsThis was a single-center study. From January 2020 to June 2021. A total of 100 preterm neonates, admitted to the neonatal intensive care unit with symptoms of respiratory distress within six hours of birth, including 50 diagnosed with transient tachypnea of the newborn and 50 with respiratory distress syndrome on the basis of clinical examination, laboratory testing, chest X-rays, were recruited in the study. Lung ultrasound was performed in each neonate by a senior radiologist who was blinded to the clinical diagnosis. Lung ultrasound findings in both conditions were analyzed and compared.ResultsPulmonary edema manifesting as alveolar-interstitial syndrome, double lung point sign and less commonly as white out lungs in the absence of consolidation has 100% sensitivity and specificity in diagnosing transient tachypnea of the newborn. A combination of three signs of consolidation with air or fluid bronchograms, white out lungs and absent spared areas has 100% sensitivity and specificity for diagnosing respiratory distress syndrome. Double lung point sign was seen only in infants suffering from transient tachypnea of the newborn and consolidation with air or fluid bronchograms only in cases of respiratory distress syndrome.ConclusionLung ultrasound can accurately diagnose and reliably differentiate transient tachypnea of the newborn and respiratory distress syndrome in preterm neonates. It has advantages that cannot be replicated by chest radiography. Lung ultrasound may be used as an initial screening tool.

Neonatal respiratory distress syndrome (RDS) usually occurs in very low or ultra-low birth weight infants with small gestational age, mainly due to low synthesis of pulmonary substances and immature lung development. At present, the substitution therapy of exogenous pulmonary surfactant is the main method to prevent and treat premature infants with RDS. In addition, prenatal prevention, resuscitation strategy and early postnatal respiratory support therapy also play an important role in the prevention and treatment of the disease. This paper reviews the prevention and treatment of respiratory distress syndrome in premature infants. Key words: Respiratory distress syndrome, newborn; Infant, premature; Respiration, artificial; Glucocorticoids

Acute respiratory distress syndrome is an acute,progressive and inflammatory process of lung injury.The disease is very serious with the neonatal mortality as high as 30％-60％.In recent years,with the development of the study on the mechanisms of newborns with acute respiratory distress syndrome,a lot of new viewpoints on diagnosis and treatments have been explored.This review focuses on the recent advances on new mechanisms,diagnosis and therapy strategies of acute respiratory distress syndrome. Key words: Newborn; Acute respiratory distress syndrome; Mechanical ventilation

Objective To study the value of lung ultrasonography in the diagnosis of neonatal respiratory distress syndrome (RDS). Methods From April 2015 to September 2016, 50 newborn infants with RDS and 50 neonates without lung disease were enrolled into this study. Lung ultrasonography was performed at bedside by a single expert physician in the first 24 h of life before exogenous pulmonary surfactant administration. The transthoracic approach was performed with longitudinal SCABS of the anterior, 1ateral, and posterior chest walls. A conventional anteroposterior chest X rag was performed at bedside in the patients immediately when lung ultrasonography was finished. Results The ultrasound signs of lung consolidation, pleural line abnormalities, alveolar interstitial syndrome were seen in 100% of RDS patients, while they were not found in any of the controls (P<0.05). A-1ine disappearance and lung pulse were seen in 86% and 52% of RDS patients and in 0% of controls respectively (P<0.05). Conclusions The main ultrasound imaging features of neonatal RDS include lung consolidation, pleural line abnormalities, and alveolar interstitial syndrome. And the lung consolidation is the essential ultrasound imaging feature. It is accurate and reliable that using ultrasound to diagnose neonatal RDS, which also has many other advantages including non-ionizing, can be performed at bedside, easy-operating, can be repeated several times in a day without hazards to the operators and the patients. Therefore, it deserves to be carried out in the neonatal ward. Key words: Lung ultrasonography; Respiratory distress syndrome; Newborn

The utility of a lung ultrasound score (LUS) has been described in the early phases of neonatal respiratory distress syndrome (RDS). We investigated lung ultrasound as a tool to monitor respiratory status in preterm neonates throughout the course of RDS. Preterm neonates, stratified in 3 gestational age cohorts (25-27, 28-30, and 31-33 weeks), underwent lung ultrasound at weekly intervals from birth. Clinical data, respiratory support variables, and major complications (sepsis, patent ductus arteriosus, pneumothorax, and persistent pulmonary hypertension of the neonate) were also recorded. We enrolled 240 infants in total. The 3 gestational age intervals had significantly different LUS patterns. There was a significant correlation between LUS and the ratio of oxygen saturation to inspired oxygen throughout the admission, increasing with gestational age (b = -0.002 [P < .001] at 25-27 weeks; b = -0.006 [P < .001] at 28-30 weeks; b = -0.012 [P < .001] at 31-33 weeks). Infants with complications had a higher LUS already at birth (12 interquartile range 13-8 vs 8 interquartile range 12-4 control group; P = .001). In infants 25 to 30 weeks' gestation, the LUS at 7 days of life predicted bronchopulmonary dysplasia with an area under the curve of 0.82 (95% confidence interval 0.71 to 93). In preterm neonates affected by RDS, the LUS trajectory is gestational age dependent, significantly correlates with the oxygenation status, and predicts bronchopulmonary dysplasia. In this population, LUS is a useful, bedside, noninvasive tool to monitor the respiratory status.

Background:Respiratory distress syndrome (RDS) is one of the most common causes of neonatal respiratory failure and mortality. The risk of developing RDS decreases with both increasing gestational age and birth weight.Objectives:The aim of this study was to evaluate the value of lung ultrasound in the diagnosis of respiratory distress syndrome (RDS) in newborn infants.Materials and Methods:From March 2012 to May 2013, 100 newborn infants were divided into two groups: RDS group (50 cases) and control group (50 cases). According to the findings of chest x-ray, there were 10 cases of grade II RDS, 15 grade III cases, and 25 grade IV cases in RDS group. Lung ultrasound was performed at bedside by a single expert. The ultrasound indexes observed in this study included pleural line, A-line, B-line, lung consolidation, air bronchograms, bilateral white lung, interstitial syndrome, lung sliding, lung pulse etc.Results:In all of the infants with RDS, lung ultrasound consistently showed generalized consolidation with air bronchograms, bilateral white lung or alveolar-interstitial syndrome, pleural line abnormalities, A-line disappearance, pleural effusion, lung pulse, etc. The simultaneous demonstration of lung consolidation, pleural line abnormalities and bilateral white lung, or lung consolidation, pleural line abnormalities and A-line disappearance co-exists with a sensitivity and specificity of 100%. Besides, the sensitivity was 80% and specificity 100% of lung pulse for the diagnosis of neonatal RDS.Conclusions:This study indicates that using an ultrasound to diagnose neonatal RDS is accurate and reliable too. A lung ultrasound has many advantages over other techniques. Ultrasound is non-ionizing, low-cost, easy to operate, and can be performed at bedside, making this technique ideal for use in NICU.

Perinatal glucocorticoid therapy has been proved to be effective on promoting fetal/neonatal lung maturity and has contributed to a dramatic improvement in the mortality and morbidity associated with neonatal respiratory distress syndrome.The underlying mechanisms studies are aimed primarily at accelerating the development of alveoli and pulmonary surfactant system.Meanwhile, a growing number of investigations focus on the side effects of perinatal glucocorticoid therapy on fetal/neonatal.Whether the repeat antenatal glucocorticoid and early postnatal glucocorticoid by intravenous injection is safe remains unclear.More studies are needed on the different route of giving glucocorticoid, the effect of different doses and their machanisms.This review presents the relevant information surrounding perinatal glucocorticoid therapy to enhance fetal/neonatal lung maturity, including clinical and animal studies over the last decades. Key words: Glucocorticoid; Promoting fetal/neonatal lung maturity; Pulmonary surfactant; Premature infant; Neonatal respiratory distress syndrome

Surfactant substitution has been a major breakthrough in the treatment of neonatal respiratory distress syndrome (RDS), primarily caused by a lack of pulmonary surfactant; it has significantly reduced mortality and acute pulmonary morbidity in preterm infants. Some very immature infants, however, have a poor response to surfactant replacement or an early relapse. This brief article is based on the hypothesis that neonatal RDS has a complex and multifactorial pathogenesis characterized by an injurious inflammatory sequence in the immature lung. Fetal exposure to chorioamnionitis has been shown to initiate an inflammatory reaction beginning in utero. A ‘low-grade’ inflammatory stimulus in utero may ‘prime’ the fetal lung for accelerated maturation of the surfactant system, especially in conjunction with prenatal steroids, and may protect the preterm infant from developing moderate to severe RDS. Depending on the severity of inflammatory injury to the alveolar-capillary unit, however, serum proteins will leak into the airways and induce surfactant inactivation. Following this intrauterine ‘first hit’, the immature infant may develop severe RDS and have a poor response to surfactant substitution. Secondary insults such as traumatic stabilization techniques, oxygen toxicity, initiation of mechanical ventilation and others injure the immature lung immediately after birth and perpetuate and may aggravate the inflammatory process. Observational studies in preterm infants and animal experiments support this concept. Whenever surfactant inactivation is suspected, higher or repetitive doses of natural surfactant may help to overcome surfactant inactivation and to restore lung function.

BackgroundAlveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV) is a lethal neonatal lung disorder characterized by the decrease of the alveolar units, abnormalities in the air–blood barrier of the lung, and impaired gas exchange. Typically, it affects a full-term newborn; the symptoms usually start within a few hours after birth, resulting in severe respiratory distress and pulmonary hypertension. In most of the cases, this disorder is refractory to conventional pulmonary support.Case presentationWe report a case of a newborn male of 29 weeks gestational age, with birth weight of 850 g and intrauterine growth restriction. Severe respiratory distress appeared a few minutes after birth; non-invasive ventilatory support was provided in the delivery room and, as a consequence of persistent respiratory failure, he was admitted to the neonatal intensive care unit (NICU) where mechanical ventilation was required.Due to the symptoms and pulmonary ultrasound pattern suggestive of respiratory distress syndrome, surfactant treatment was administered. Lung ultrasound (LU) was used for monitoring the responsiveness to surfactant; severe pulmonary hypertension ensued, followed by respiratory failure, refractory shock, and death within 48 h.Owing to the poor response to the established therapy, ACD/MPV was suspected. The diagnosis was confirmed through autopsy. The main goal of this case report is to show the role of LU for monitoring the evolution of this disorder.ConclusionLU could provide essential information to help diagnose and follow-up the underlying cause of persistent pulmonary hypertension of the newborn in an earlier and more effective way than chest X-ray. LU is suitable for routine monitoring of lung disease in the NICU.

Pulmonary surfactant is required for lung function at birth and throughout postnatal life. Defects in the surfactant system are associated with common pulmonary disorders including neonatal respiratory distress syndrome and acute respiratory distress syndrome in children and adults. Lipogenesis is essential for the synthesis of pulmonary surfactant by type II epithelial cells lining the alveoli. This study sought to identify the role of pulmonary epithelial SREBP, a transcriptional regulator of cellular lipid homeostasis, during a critical time period of perinatal lung maturation in the mouse. Genome wide mRNA expression profiling of lung tissue from transgenic mice with epithelial-specific deletions of Scap (ScapΔ/Δ, resulting in inactivation of SREBP signaling) or Insig1 and Insig2 (Insig1/2 Δ/Δ, resulting in activation of SREBP signaling) was assessed. Differentially expressed genes responding to SREBP perturbations were identified and subjected to functional enrichment analysis, pathway mapping and literature mining to predict upstream regulators and transcriptional networks regulating surfactant lipid homeostasis. Through comprehensive data analysis and integration, time dependent effects of epithelial SCAP/INSIG/SREBP deletion and defined SCAP/INSIG/SREBP-associated genes, bioprocesses and downstream pathways were identified. SREBP signaling influences epithelial development, cell death and cell proliferation at E17.5, while primarily influencing surfactant physiology, lipid/sterol synthesis, and phospholipid transport after birth. SREBP signaling integrated with the Wnt/β-catenin and glucocorticoid receptor signaling pathways during perinatal lung maturation. SREBP regulates perinatal lung lipogenesis and maturation through multiple mechanisms by interactions with distinct sets of regulatory partners.