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Respiratory Distress in Newborn

Respiratory Distress in Newborn. Part 2 by Yong. Transient Tachypnea of Newborn (TTN). Most common cause of respiratory distress. 40% cases. Residual fluid in fetal lung tissues. Risk factors- maternal asthma, c- section, macrosomia , maternal diabetes.

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Respiratory Distress in Newborn

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  1. Respiratory Distress in Newborn Part 2 by Yong

  2. Transient Tachypnea of Newborn (TTN)

  3. Most common cause of respiratory distress. • 40% cases. • Residual fluid in fetal lung tissues. • Risk factors- maternal asthma, c- section, macrosomia, maternal diabetes

  4. The infant become tachypnea immediately after birth or within two hours, with other predictable signs of respiratory distress. • They are neurologically normal, symptoms can last few hours to two days. • The pathophysiological mechanism is the delayed resorption of fetal lung fluid which eventually clears over the next several hours to days.

  5. Chest radiographs • Hyperinflation with clear lung parenchyma • Perihilar linear densities • Fluid in the fissures • Laminar effusions • Fuzzy vessels • There should be no areas of consolidation .

  6. Congenital pneumonia

  7. pathophysiology • Intrauterine infection or during delivery • Most are bacterial in origin • Pneumonia that becomes clinically evident within 24 hours of birth may originate at 3 different times. • The 3 categories of congenital pneumonia are as follows: • True congenital pneumonia • Intrapartum pneumonia • Postnatal pneumonia

  8. True congenital pneumonia • True congenital pneumonia is already established at birth. • Transmission of congenital pneumonia usually occurs via 1 of 3 routes: • Hematogenous • Ascending • Aspiration

  9. Intrapartum pneumonia • Intrapartum pneumonia is acquired during passage through the birth canal. • It may be acquired via hematogenous or ascending transmission: • from aspiration of infected or contaminated maternal fluids • from mechanical or ischemic disruption of a mucosal surface that has been freshly colonized with a maternal organism

  10. Postnatal pneumonia • Postnatal pneumonia in the first 24 hours of life originates after the infant has left the birth canal. • It may result from some of the same processes described above, but infection occurs after the birth process.

  11. Etiology • Group B Streptococcus (GBS) • NontypableHaemophilusinfluenzae • cytomegalovirus, Treponemapallidum, Toxoplasmagondii, • Enterococci

  12. Clinical Findings • Afebrile • Marked respiratory distress • Tachypnea • Metabolic acidosis • Septicemia and shock

  13. Chest radiographs

  14. Meconium aspiration syndrome (MAS)

  15. Incidence- 1.5- 2 % in term or post term infants. • Meconium is locally irritative, obstructive & medium for for bacterial culture • Meconium aspiration causes significant respiratory distress. Hypoxia occurs because aspiration occurs in utero. • Thick meconium could block air passages and cause atelectasis and air leak syndromes

  16. The baby with MAS is usually post-term or small-for-date. • There may be meconium staining of the umbilical cord, nails and skin. • The chest may be hyperinflated and onset of distress is usually within the first 4-6 hours.

  17. Chest radiographs • Diffuse “ropey” densities • Patchy areas of atelectasis and emphysema from air-trapping • Hyperinflation of lungs • No air bronchograms • Clearing usually quick if mostly water; days-weeks if mostly meconium

  18. Respiratory Distress Syndrome(Hyaline Membrane Disease)(RDS)

  19. Most common cause of respiratory distress in prematurity, asphyxia and maternal diabetes infants, correlating with structural & functional lung immaturity. • Prolonged rupture of membranes and intrauterine growth retardation are believed to enhance lung maturity.

  20. Pathophysiology • Surfactant is needed to decrease alveolar surface tension and keep them open. • In a preterm baby, absence of surfactant leads to alveolar collapse during expiration. • This affects gas exchange and the baby goes into respiratory failure

  21. Clinical Findings • Diagnosis of respiratory distress should be suspected when grunting, retraction or other typical distress symtoms occur in premature infant. • Symptoms present in first 2 hours of life • Symptoms that begin > 8 hrs are not due to HMD • May turn in severity from 24 - 48 hours • Then, gradual improvement > 48-72 hours

  22. Chest radiographs • X-ray showing air bronchogram and hazy lung suggestive of HMD. • mild disease: reticulo-granular pattern • severe disease: "white out" picture • Typically, diffuse “ground-glass” or finely granular appearance • Bilateral and symmetrical distribution • Air bronchograms are common, especially extending peripherally • “Granularity” is the interplay of: • Air-distended bronchioles & ducts • Background of atelectasis of alveoli

  23. Classic respiratory distress syndrome (RDS). Bell-shaped thorax is due to generalized underaeration. Lung volume is reduced, the lung parenchyma has a diffused reticulogranular pattern, and peripherally extending air bronchograms are present.

  24. Moderately severe respiratory distress syndrome (RDS). The reticulogranular pattern is more prominent and uniformly distributed than usual. The lungs are hypoaerated. Increased air bronchograms are observed

  25. Severe respiratory distress syndrome (RDS). Reticulogranular opacities are present throughout both lungs, with prominent air bronchograms and total obscuration of the cardiac silhouette.

  26. Treatment

  27. Transient Tachypnea of Newborn • Rx is supportive because the condition is usually self limited. • Prenatal administration of steroids 48hrs before elective C- section @ 37- 39 weeks gestation reduces TTN but this has not common practice.

  28. Congenital Pneumonia in newborn • IV C Penicillin 50000unit/kg 6hly • IV Gentamycin 4mg/kg daily

  29. Respiratory distress Syndrome • General intervention for oxygenation. • Prenatal administration of corticosteroids between 24- 34 wks gestation reduces risk of respiratory distress when risk of preterm delivery is high. • Post natal steroids may decrease mortality but may increase risk of cerebral palsy.

  30. Antenatal corticosteroids • Antenatal steroids will prevent the occurrence and severity of RDS in preterm babies between 24 and 34 weeks of gestation. • Optimal effect of antenatal steroids is seen if delivery occurs after 24 hours of the initiation of therapy. Effect lasts for 7 days.

  31. If delivery is anticipated below 34 weeks of gestation. • Dose recommended is: • Inj Betamethasone 12 mg 1M every 24 hrs x 2 doses; or • Inj Dexamethasone 6 mg 1M every 12 hrs x 4 doses. • Multiple courses of antenatal steroids are not beneficial and hence are not recommended

  32. Surfactant therapy • surfactant therapy should be instituted only if there are facilities for ventilation. • The efficacy of surfactant in reducing the duration of ventilation is proven. • Prophylactic surfactant use is recommended for any neonate< 28 weeks and < 1000 gms.

  33. Choice of drugs: • Survanta • 100mg of phospholipids/kg/dose (4mL/kg) • Repeat > 6H after the previous dose if the infant remains intubated and requires at least 30% O2 to maintain PaO2 <80mmHg • BLES • 135mg phospholipids/kg/dose (5mL/kg) • Repeat up to 3 times within the 5 post natal days if difficult to maintain oxygenation

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