Search results
Results from the WOW.Com Content Network
Infant respiratory distress syndrome (IRDS), also known as surfactant deficiency disorder (SDD), [2] and previously called hyaline membrane disease (HMD), is a syndrome in premature infants caused by developmental insufficiency of pulmonary surfactant production and structural immaturity in the lungs.
Transient tachypnea of the newborn is a respiratory problem that can be seen in the newborn shortly after delivery. It is caused by retained fetal lung fluid due to impaired clearance mechanisms. [1] It is the most common cause of respiratory distress in term neonates.
Medical diagnosis of pulmonary hypoplasia in utero may use imaging, usually ultrasound or MRI. [12] [13] The extent of hypoplasia is a very important prognostic factor. [14]One study of 147 fetuses (49 normal, 98 with abnormalities) found that a simple measurement, the ratio of chest length to trunk length, was a useful predictor of postnatal respiratory distress. [15]
Pulmonary surfactant is critical for inflation to occur, as it reduces the surface tension of the alveoli. Preterm birth around 26 weeks frequently results in severe respiratory distress, although with current medical advancements, some babies may survive. Prior to 26 weeks, sufficient pulmonary surfactant is not produced, and the surfaces for ...
Bronchopulmonary dysplasia (BPD; part of the spectrum of chronic lung disease of infancy) is a chronic lung disease which affects premature infants. Premature (preterm) infants who require treatment with supplemental oxygen or require long-term oxygen are at a higher risk. [ 1 ]
With each of the newborn's breaths, blood perfuses the pulmonary capillary beds and undergoes oxygenation before exiting the lungs via the pulmonary veins and returning to the heart. Thus, as more blood flows through the pulmonary circulation, there will be a higher volume of blood returning to the left atrium from the lungs.
The lecithin–sphingomyelin ratio is a marker of fetal lung maturity. The outward flow of pulmonary secretions from the fetal lungs into the amniotic fluid maintains the level of lecithin and sphingomyelin equally until 32–33 weeks gestation, when the lecithin concentration begins to increase significantly while sphingomyelin remains nearly the same.
ACD typically presents in newborn babies within hours of birth as rapid and labored breathing, blue-colored lips or skin, quickly leading to respiratory failure and death. Atypical forms of ACD have been reported with initially milder symptoms and survival of many months before the onset of respiratory failure or lung transplantation.