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DR.NITHU ANN GEORGE PG 1 ST YEAR PAEDIATRICS

RESPIRATORY DISTRESS SYNDROME(RDS). DR.NITHU ANN GEORGE PG 1 ST YEAR PAEDIATRICS. DR.NITHU ANN GEORGE 1 ST YR PG - PAEDIATRICS. RESPIRATORY DISTRESS. Tachypnea (RR>60/min) + Chest retractions &/ or Grunt Respiratory causes

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DR.NITHU ANN GEORGE PG 1 ST YEAR PAEDIATRICS

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  1. RESPIRATORY DISTRESS SYNDROME(RDS) DR.NITHU ANN GEORGE PG 1ST YEAR PAEDIATRICS DR.NITHU ANN GEORGE 1ST YR PG - PAEDIATRICS

  2. RESPIRATORY DISTRESS • Tachypnea (RR>60/min) + Chest retractions &/ or Grunt • Respiratory causes Non- respiratory causes

  3. Respiratory causes • RDS • MAS • Pneumonia • TTN • PPHN • Pneumothorax • Tracheoesophageal fistula • Diaphragmatic hernia • Lobar emphysema Non- respiratory causes • Cardiac CHF CHD • Metabolic Hypothermia Hypoglycemia Metabolic acidosis • CNS Asphyxia Cerebral oedema Hemorrhage • Chest wall Asphyxiating thoracic dystrophy

  4. Can occur both in preterm and term babies. • Preterm distress within 1st few hours of life mcc- RDS • Term meconium stained liquorwithin 24hr MAS • Term  uncomplicated birth 1st few hrs TTN • Suprasternal retractions with/without stridorupper airway obstruction.

  5. Respiratory distress in a neonate is recognized by the presence of varying combinations of Tachypnoea(>60/min) Chest retractions Grunting Flaring of ala nasi Cyanosis

  6. Respiratory distress syndrome(rds) • RDS or HMD (Hyaline Membrane Disease) • Common in Preterm (<34wks gestation) • Incidence – 10-15% (80% in neonates <28wks) • In addition to prematurity Maternal diabetes c/s Asphyxia Acidosis

  7. Etiopathogenesis • Abnormality – surfactant drficiency • Surfactant  lipoprotein phospholipids ( phosphatidylcholine , phosphatidylglycerol) & proteins

  8. Surfactant is produced by Type 2 alveolar cells of lungs. • Help reduce surface tension in the alveoli. • Its production starts at around 20weeks & peaks at 35wks. • So neonate <35wks prone for RDS.

  9. Absence of surfactant  surface tension increases  alveoli collapse during expiration. • Inadequate oxygenation & increased work of breathing. • Hypoxemia and acidosis  Pul. vasoconstriction & R L shunting across foramen ovale. • This worsens hypoxemia    respiratory failure • Ischemic damage to the alveoli  transudation of proteins into it forms hyaline membrane.

  10. c/f Resp distress usually within 1st 6 hrs of life • Tachypnoea • Retractions • Grunting • Cyanosis • Decreased air entry

  11. diagnosis • CXR  Reticulogranular pattern Ground glass opacity Low lung volume Air bronchogram White out lungs(severe)

  12. management • NICU care • IVF • O2 • Mild – moderate  CPAP Non invasive modality, continous distending pressure (5-7cm of water) applied at nostril level keeps the alveoli open in a spontaneously breathing baby.

  13. Minimizes lung injury and other complications (air leak and sepsis). • Preterm babies with severe RDS  Mechanical Ventillation. Lung injury by excessive pressure & high O2 High saturations of oxygen (>95%)  ROP  blindness

  14. Surfactant therapy • Exogenous surfactant  t/t of choice • Indicated in moderate to severe RDS • Route  intratracheal (InSurE) • Rescue T/t  RDS or Prophylactically (all neonates<28wks) Reduces duration & need for ventillation

  15. RDS usually good prognosis if managed well. • Survival  90% in VLBW (<1500g)

  16. prevention • Administer antenatal steroids to mothers in preterm labor (<35weeks). • It reduces RDS, intraventricularhaemorrhage and mortality in neonates.

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