1. Neonatal Respiratory Distress
Priscilla Joe, MD Children’s Hospital and Research Center at Oakland

2. Neonatal Respiratory Disease
Upper airway disease
True parenchymal disease
Airleak syndromes
Disorders of development
Primary pulmonary vascular disease

3. Upper Airway Disease Choanal atresia Pierre Robin sequence
Vascular rings

4. Choanal Atresia
Pierre Robin Syndrome

5. Choanal Atresia/Upper Airway Obstruction
Cyanotic when quiet or at rest, pink with crying
Inability to pass suction catheter through nares
Stridor

6. Upper airway obstruction
Insert an oral airway
Provide oxygen
Suction secretions
May require intubation

7. Fetal Lung Characteristics
Decreased blood flow
caused by compression of the pulmonary capillaries by fetal lung fluid
Pulmonary arteries
thick muscular layer present, very reactive to hypoxemia
Lung fluid secretion
fetal lungs secrete fluid, adequate lung volume is necessary for fetal development
Fetal breathing
contributes to fetal lung development, moves fluid in and out of fetal lung
Surfactant
necessary amount to support breathing after birth, present after ~ 34 weeks gestation
Decreased blood flow: caused by compression of the pulmonary capillaries by fetal lung fluid
Pulmonary arteries: thick muscular layer present, very reactive to hypoxemia
Lung fluid: fetal lungs secrete fluid, adequate lung volume is necessary for fetal development
Fetal breathing: contributes to fetal lung development, moves fluid in and out of fetal lung
Surfactant: necessary amount to support breathing after birth, present after ~ 34 weeks gestation

8. Transition Clearance of fetal lung fluid Increased compliance
Increased pulmonary blood flow

9. Respiratory Distress Syndrome
Disease of surfactant defiency
Surfactant decreases surface tension and improves lung compliance
Surface tension: intrinsic tendency for alveoli to collapse

11. RDS: Risk Factors Secondary surfactant deficiency: Prematurity: Males
Maternal diabetes
Asphyxia
Pneumonia
Pulmonary hemorrhage
Meconium aspiration
Oxygen toxicity
Prematurity:
Males
Second born twins
C-section
Caucasian race
Develops in ~ 50% of infants born between weeks gestation
Inversely related to prematurity

12. RDS: Clinical Findings
Non-specific findings of respiratory distress
Grunting
Flaring
Retracting
O2 requirement

14. RDS: Radiography Alveolar disease:
Diffuse reticular granular or “ground glass”pattern
Air bronchograms
Underaeration

15. RDS: Treatment Maintain FRC (CPAP vs. intubation)
Surfactant replacement
Exogenous surfactants
Survanta 4cc/kg
Infasurf 3cc/kg

16. Surfactant Therapy for RDS
Decreases mortality
Greatest benefit when used with antenatal steroids
Improvement in compliance, functional residual capacity, and oxygenation
Reduces incidence of air leaks

17. Congenital Pneumonia Common organisms: Group B streptococcus
E.Coli, Klebsiella
Chlamydia, Ureaplasma, mycoplasma
Listeria
TORCH
H. Influenza (nontypeable)

18. Pneumonia: Risk Factors
Maternal chorioamnionitis
Prolonged rupture of membanes
Prematurity
Postnatal exposures: Poor hand washing, open skin lesions, contaminated blood products, infected breast milk

19. Pneumonia Inflammation and edema Bronchial plugging
Surfactant inactivation
Alveolar collapse
Ventilation/perfusion mismatch
Desaturation

20. Pneumonia: Clinical Findings
Presents with non-specific findings of respiratory distress
Grunting
Flaring
Retracting
O2 requirement

21. Pneumonia: Radiography
There are no classic x-ray findings, in fact, the X-ray in pneumonia can look like anything
Fairly normal
Classic RDS
Classic for MAS

22. RDS, H influenza pneumonia

23. Listeria, MAS

24. E coli pneumonia

25. Pneumonia: Treatment
Respiratory support as indicated with either O2 or positive pressure
Treatment with appropriate antimicrobials
Initial ampicillin/gentamicin or ampicillin/cefotaxime
Broader spectrum antibiotics for nosocomial bacteria

26. Meconium Aspiration Syndrome
Meconium contains epithelial cells and bile salts
Released with intrauterine stress or asphyxia
Present in 15% of all newborns.
Only 5-10% develop MAS
Asphyxia causes anal sphincter to relax, also leads to gasping respiratory efforts
Often ill
Be very concerned about pulmonary hypertension, as this is also a fetal response to asphyxia

27. Meconium Aspiration Airway plugging, with air trapping
Inflammation, leading to inactivation of surfactant
Surfactant inactivation leads to decreased compliance, and alveolar collapse
Alveolar collapse = loss of FRC
Loss of FRC = V/Q mismatch
V/Q mismatch = desaturation

28. Meconium aspiration: Xray
Areas of hyperexpansion mixed with patchy densities and atelectasis

29. Pneumothorax May occur spontaneously during delivery
Most common when receiving positive pressure
Space occupying lesion within the chest displacing lung, and if under tension, compromising venous return

30. Pneumothorax: Clinical Findings
Presents with non-specific signs of respiratory distress
Grunting
Flaring
Retracting
O2 requirement
Unequal, decreased breath sounds

32. Pneumothorax: Treatment
O2 as needed
Nitrogen washout (pneumo contains 21% O2, >75% nitrogen, if lung has 100% O2, nitrogen will diffuse out of pneumothorax)
Try to avoid positive pressure if able
Evacuate as needed by thoracentesis or chest tube

33. Developmental disturbances
Pulmonary hypoplasia
Congenital diaphragmatic hernia
Skeletal deformities

34. Pulmonary hypoplasia
Cannot be assessed radiographically, pulmonary hypoplasia is a pathologic diagnosis
Suspect pulmonary hypoplasia if:
Rupture of membranes with anhydramnios
Renal anomalies
Restriction of the chest wall
Congenital diaphragmatic hernia

35. Diaphragmatic Hernia Scaphoid abdomen Bowel sounds in the chest
Other associated anomalies
Decreased breath sounds
Severe hypoxemia

36. Diaphragmatic Hernia Wide range in clinical presentation
Herniation of bowel leads to altered development of the lungs bilaterally

37. Left CDH

38. Persistent Pulmonary Hypertension of the Newborn
Primary pulmonary hypertension is a pure vascular disease
More often present in a mixed picture as in the setting of meconium aspiration syndrome or asphyxia

39. PPHN
In response to an asphyxia event in utero, the fetus diverts all blood flow possible to vital organs (brain/heart/adrenals)
This leads to vasoconstriction of non-vital vascular beds, including the pulmonary bed
Remodeling of smooth muscle can occur

40. PPHN Increased PVR PDA PA Aorta RV outflow
Following delivery pulmonary vascular resistance plummets, in order to establish pulmonary blood flow
In kids with PPHN, they never drop their resistance, leading in the worst case to a right to left shunt at the ductal level PA
Aorta

41. PPHN: Clinical Findings
Respiratory distress with hypotension
Hypoxemia out of proportion to degree of distress
Difference in pre and post ductal sats
Right hand
Lower extremities
Hyperoxia test

42. PPHN Increases R L shunt: Decreases R L shunt: Increase PVR
Decrease pulmonary blood flow
Hypoxia
Hypercarbia
Acidosis
Decreases R L shunt:
Decrease PVR
Increase pulmonary blood flow
Hyperoxia
Hypocarbia
Lack of acidosis

43. PPHN: Treatment Improve pulmonary blood flow: Avoid:
Keep well saturated
Normocarbia
Avoid:
Hypoxia
Hypercarbia
Acidosis
Supportive care: temperature regulation, fluids and lytes, antibiotics

44. PPHN: Treatment Conventional ventilation or HFOV Nitric oxide
Surfactant replacement
ECMO