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Respiratory Distress Syndrome - Yale University:呼吸窘迫综合征-耶鲁大学
* - Surfactant deficiency - Inflammation and Lung injury - Pulmonary edema - Surfactant inactivation - Pulmonary function and gas exchange Impaired surfactant synthesis and secretion ? atelectasis, V/Q inequality, hypoventilation ? hypoxemia and hypercarbia Respiratory / metabolic acidosis ? pulmonary vasoconstriction ? impaired endothelial and epithelial integrity ? leakage of proteinaceous exudate and formation of hyaline membranes Deficiency of surfactant ? decreases lung compliance and FRC, with increased dead space Impair surfactant production and/or secretion Hypoxia, acidosis, hypothermia, hypotension Oxygen toxicity ? influx of inflammatory cell ? exacerbates vascular injury ? BPD Antioxidant deficiency and free-radical injury worsen injury * Lungs with HMD require far more pressure than to achieve a given volume of inflation than do lungs obtained from an infant dying of a nonrespiratory cause. Arrows indicate inspiratory and expiratory limbs of the pressure-volume curves. Note the decreased lung compliance and increased critical opening and closing pressures, respectively, in the premature infant with HMD * line the alveoli (see the image below) may form within a half hour after birth. In larger premature infants, the epithelium begins to heal at 36-72 hours after birth, and endogenous surfactant synthesis begins. The recovery phase is characterized by regeneration of alveolar cells, including type II cells, with a resultant increase in surfactant activity. * low lung volume and the classic diffuse reticulogranular ground-glass appearance with air bronchograms * two doses of betamethasone administered 24 hours apart is currently the recommended steroid for antenatal use Antenatal steroid administration has been shown to be beneficial if provided fewer than 24 hours before delivery Furthermore, a reduction in RDS has been seen in infants born up to 7 days after the first dose of antenatal steroids was administered. (1) No benefit is seen in in
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