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Introduction
RDS is one of the most common causes of morbidity in preterm neonates The diagnosis can be established pathologically or by biochemical documentation of surfactant deficiency, most series refer only to a combination of clinical and radiographic features
Incidence
Risk factors
slight male predominance young gestational age and low birth weight late preterm delivery elective delivery in the absence of labor maternal diabetes and perinatal hypoxiaischemia
Pathophysiology
diffuse atelectasis eosinophilic membrane comprising of fibrinous matrix of materials derived from the blood and cellular debris derived from injured epithelium The recovery phase is characterized by regeneration of alveolar cells, including the type II cells, with a resultant increase in surfactant activity.
Clinical features
grunting respirations Tachypnea Retractions nasal flaring Cyonosis
Radiographic findings
Echocardiographic evaluation of infants with RDS may be of value in the diagnosis of a PDA to quantitate elevations in pulmonary artery pressure, to assess cardiac function, and to exclude congenital heart disease (e.g., obstructed total anomalous pulmonary venous return).
Treatment
Noninvasive ventilation Oxygen Surfactant therapy Positive pressure ventilation and Lung protective strategy Supportive measure
Do Clinical Markers of Barotrauma and Oxygen Toxicity Explain Interhospital Variation in Rates of Chronic Lung Disease?
Delivery Room Continuous Positive Airway Pressure/Positive End-Expiratory Pressure in Extremely Low Birth Weight Infants: A Feasibility Trial
Nasal CPAP or Intubation at Birth for Very Preterm Infants (COIN trial)
NIPPV vs CPAP
COMPLICATIONS
Impaired venous return CO2 retention Air leak Injury to nose
Surfactant
Synthetic Animal derived Synthetic with surfactant proteins
Effects of surfactant
Reduction in death Reduction of pneumothorax Reduction of PIE
Complications of RDS
Death IVH PH Pulm Htn BPD PDA