Respiratory Distress Syndrome Year 4 Paediatrics Notes

Respiratory Distress Syndrome Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.3 / Munge / NEONATOLOGY -- Slide 1 Respiratory Distress Syndrome Dr Rose Munge Slide 2 Respiratory distress syndrome, also known as hyaline membrane disease, occurs almost exclusively in premature infants.\nThe incidence and severity of respiratory distress syndrome are related inversely to the gestational age of the newborn infant. Slide 3 Surfactant formation and physiology Surfactant is a complex lipoprotein composed of 6 phospholipids and 4 apoproteins. Surfactant recover Contains 70-80% phospholipids, 8-10% protein, and 10% neutral lipids, primarily cholesterol.\nDipalmitoyl phosphatidylcholine (DPPC), or lecithin, is functionally the principle phospholipid.\nPhosphatidylglycerol makes up 4-15% of the phospholipids; although it is a marker for lung maturity, it is not necessary for normal lung function. Slide 4 Before and After surfactant Slide 5 The components of pulmonary surfactant are synthesized in the Golgi apparatus of the endoplasmic reticulum of the type II alveolar cell. The components are packaged in multilamellar vesicles in the cytoplasm of the type II alveolar cell. Slide 6 Aetiology In premature infants, respiratory distress syndrome develops because of impaired surfactant synthesis and secretion leading to atelectasis, ventilation-perfusion (V/Q) inequality, and hypoventilation with resultant hypoxemia and hypercarbia.\nBlood gases show respiratory and metabolic acidosis that cause pulmonary vasoconstriction, resulting in impaired endothelial and epithelial integrity with leakage of proteinaceous exudate and formation of hyaline membranes (hence the name). The relative deficiency of surfactant decreases lung compliance and functional residual capacity, with increased dead space. The resulting large V/Q mismatch and right-to-left shunt may involve as much as 80% of the cardiac output. Slide 7 Hypoxia, acidosis, hypothermia, and hypotension may impair surfactant production and/or secretion.\nOxygen toxicity with barotrauma and volutrauma in their structurally immature lungs causes an influx of inflammatory cell, which exacerbates the vascular injury, leading to bronchopulmonary dysplasia (BPD).\nAntioxidant deficiency and free-radical injury worsen the injury. Slide 8 The lungs of affected newborns appear airless and ruddy (ie, liverlike).\nTherefore, the lungs require an increased critical opening pressure to inflate.\nDiffuse atelectasis of distal airspaces along with distension of distal airways and perilymphatic areas are observed microscopically.\nProgressive atelectasis, barotrauma or volutrauma, and oxygen toxicity damage endothelial and epithelial cells lining these distal airways, resulting in exudation of fibrinous matrix derived from blood. Hyaline membranes that line the alveoli may form within a half hour after birth.\nIn larger premature infants, the epithelium begins to heal at 36-72 hours after birth, and endogenous surfactant synthesis begins.\nThe recovery phase is characterized by regeneration of alveolar cells, including type II cells, with a resultant increase in surfactant activity. Slide 9 A chronic process often ensues in infants who are extremely immature and critically ill and in infants born to mothers with chorioamnionitis, resulting in BPD.\nIn extremely premature infants, an arrest in lung development often occurs during the saccular stage, resulting in chronic lung disease termed "new" BPD. Slide 10 Risk factors The greatest risk factor for respiratory distress syndrome is prematurity, although the syndrome does not occur in all premature newborns.\nOther risk factors include maternal diabetes, caesarean delivery, and asphyxia. Slide 11 Prognosis Acute complications of respiratory distress syndrome include : Alveolar rupture Infection Intracranial hemorrhage and periventricular leukomalacia Patent ductus arteriosus (PDA) with increasing left-to-right shunt Pulmonary hemorrhage Necrotizing enterocolitis (NEC) and/or gastrointestinal (GI) perforation Apnea of prematurity Chronic complications of respiratory distress syndrome include the following: Bronchopulmonary dysplasia (BPD) Retinopathy of prematurity (ROP) Neurologic impairment Slide 12 Increased risk of RDS occurs in Respiratory distress syndrome frequently occurs in the following individuals: White male infants Infants born to mothers with diabetes Infants born by means of cesarean delivery Second-born twins Infants with a family history of respiratory distress syndrome Slide 13 Secondary surfactant deficiency may occur in infants with the following: Intrapartum asphyxia Pulmonary infections (eg, group B beta-hemolytic streptococcal pneumonia) Pulmonary hemorrhage Meconium aspiration pneumonia Oxygen toxicity along with barotrauma or volutrauma to the lungs Congenital diaphragmatic hernia and pulmonary hypoplasia Slide 14 In contrast, the incidence of respiratory distress syndrome decreases with the foll