Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Respiratory distress of the newborn

7,491 views

Published on

RDS, TTN, MAS etc

Published in: Health & Medicine
  • Be the first to comment

Respiratory distress of the newborn

  1. 1. RESPIRATORY DISEASES OF THE NEWBORN By: dr Ismah, Paeds department 1
  2. 2. 2 Respiratory diseases of the newborn Respiratory distress syndrome - RDS (hyaline membrane disease) Transient tachypnea of the newborn (TTN) Meconium aspiration syndrome (MAS) Primary pulmonary hypertension of the newborn (PPHN) Apnea of prematurity Congenital pneumonia
  3. 3. 3 Preterm infant Term infant Both • RDS • Erythroblastosis fetalis • Nonimmune hydrops • Pulmonary hemorrhage • PPHN • MAS • Polycythemia • Amniotic fluid aspiration • Bacterial sepsis e.g. GBS • TTN • Spontaneous pneumothorax • Congenital anomalies e.g. congenital lobar emphysema, diaphragmatic hernia • Congenital heart disease • Pulmonary hypoplasia • Viral infection e.g. CMV, herpes • Inborn metabolic errors
  4. 4. 4 1. Respiratory distress syndrome - RDS (hyaline membrane disease)
  5. 5. Occurred after the onset of breathing and is associated with an insufficiency of pulmonary surfactant  Incidence of RDS increase with decrease gestational age  RDS develops in 30-60% in infant 28-32 W  Others risk factors: delivery of previous preterm infant with RDS, maternal DM, male sex, 2nd born of twins, c sec not in labor  May develop immediately in extremely immature infant or 3-4 hrs after birth in 34W infant 5
  6. 6. LUNG DEVELOPMENT  Lining of alveolus consists 90% type 1 and 10% types II cells  The surfactant production depends on the fetal cortisol, begins between 32-34 W of gestation  Surfactant produced by type II cells sufficiently by 34- 36 W 6
  7. 7.  Contents of surfactant are 90% lipids (lecithin, phosphatidylglycerol) and proteins SP-A, SP-B, SP-C and SP-D  Surfactant prevents atelectasis and contributes to the lung recoil by manipulates the surface tension of the lungs  Lecithin/Sphingomyelin ratio 2:1 in amniotic fluid usually indicate fetal lung maturity or the presence of minor phospholipids e.g. phosphatidylglycerol 7
  8. 8. CLINICAL MANIFESTATION  Tachypnea  Nasal flaring  Intercostal, sternal recession  Grunting; closure of glottis during expiration  Cyanosis 8
  9. 9. CXR Shows air bronchograms and reticulonodular shadowing throughout the lung fields (often termed ‘ground glass’ appearance) 9
  10. 10. 10
  11. 11. PREVENTION AND TREATMENT  Prevent preterm birth; treatment of infections, cervical cerclage  Prevention of neonatal cold stress, birth asphyxia, hypovolemia reduces risk of RDS  Administration of corticosteroid before delivery for lung maturity  Surfactant usage  Aim SPO2 ≥ 90%, PaO2 60-70 mmHg, pH> 7.25  Start antibiotic for 48-72 hrs (difficult to differentiate sepsis, pneumonia from RDS) 11
  12. 12. SURFACTANT Surfactant therapy reduces mortality rates most effectively in infants <30 weeks and those of birth weight <1250 gm 12
  13. 13. WHO TO GIVE?  Depressed preterm infants who have no spontaneous respiration after 30 seconds of ventilation that require positive pressure ventilation (PPV)  Preterm infants below 28 weeks gestation who are given only CPAP from birth in delivery room, i.e. the infant has spontaneous respiration and good tone at birth. Surfactant to be given within 30 minutes after birth  Preterm infants between 28-32 weeks – to have CPAP from birth in delivery room. To assess requirement for surfactant in NICU based on oxygen requirement of FiO2 > 30% and respiratory distress  More mature or larger infants should also be given surfactant if the RDS is severe 13
  14. 14. TIMING OF SURFACTANT THERAPY  The first dose has to be given as early as possible to the preterm infants requiring mechanical ventilation for RDS but not in 1st minute OL  The repeat dose is given 4-6 hours later if FiO2 is still > 0.30 with optimal tidal volume settings for those below 32 weeks;  And if FiO2 > 0.40 and CXR still shows moderate to severe RDS (“white” CXR) for those infants > 32 weeks gestational age. 14
  15. 15. TYPES OF SURFACTANT  Survanta , a natural surfactant, bovine derived Dose : 4 ml/kg per dose.  Curosurf , a natural surfactant, porcine derived Dose: 1.25 mls/kg per dose. 15
  16. 16. COMPLICATIONS PDA Pulmonary air leaks Bronchopulmonary dysplasia (chronic lung disease) ROP 16 RDS  increased pulmonary pressure  prevent closure of ductus arteriosus Associated with ventilation that may lead to ruptured alveolar O2 dependent ≥ CGA 36W Excessive O2  developing blood vessels of premature infant retina  blindness
  17. 17.  Tachypnea, mild retraction, hypoxia, occasional grunting, rarely cyanosis  which may persist for up to 48 hrs  Caused by retained lung fluid or slow resorption of lung fluid  Associated in larger premature infant or term infant in precipitate delivery (not in labor), infant DM mother or use of analgesia intrapartum 17 2. TTN
  18. 18. PATHOPHYSIOLOGY The lungs in utero are constantly secreting fluid to aid lung growth and development However the rate of lung fluid production and volume of foetal lung lumen decreases before birth, most during labour The mechanism for fluid absorption is triggered by neuroendocrine hormones, which cause lymphatic vessel dilatation As the lung pulmonary circulation increases following the first breath, the fluid in the lungs is cleared thus interruption of this process of clearing fluid from the lungs may result in respiratory distress. 18
  19. 19. 19
  20. 20. MANAGEMENT  It is often managed conservatively by a period of close observation on the postnatal ward or in the neonatal unit but must be weighed against other differential diagnoses including RDS and pneumonia which may progress rapidly in newborn infants  Oxygen therapy  Antibiotics may be used if persistent (consider other associated condition e.g. sepsis) 20
  21. 21. 3. MAS  Term and post term delivery  Tachypnea, hypoxia, hypercapnia, small airway obstruction, air trapping, overdistention and extra alveolar air leaks  Meconium stained liquor suggest utero distress with asphyxia, hypoxia and acidosis 21
  22. 22.  The inhaled meconium can cause: • Mechanical obstruction of the airways leading to mismatched ventilation/ perfusion • Chemical pneumonitis (in 24-48 hrs) • Infection which inhibit surfactant function and leads to inflammation and swelling, which also can obstruct small airways • The combination of ventilation/perfusion mismatch and pulmonary inflammatory can trigger vasoconstriction of the pulmonary vasculature leading to PPHN 22
  23. 23. MANAGEMENT  Mostly supportive therapy  Most cases of MAS will recover within 2–3 days  However, some infants will progress to develop severe MAS requiring intubation and ventilation  Start on antibiotic in view of distinguishing MAS from pneumonia can be difficult • The initial chest radiograph is often similar to findings associated with pneumonia with bilateral patchy infiltrates and possible pleural effusion 23
  24. 24. CXR 24 Bilateral diffuse grossly patchy opacities
  25. 25. 4. PPHN  Term, post term  Defined as a failure of normal pulmonary vasculature relaxation at or shortly after birth, resulting in impedance to pulmonary blood flow which exceeds systemic vascular resistance, such that unoxygenated blood is shunted to the systemic circulation 25
  26. 26.  PPHN can be: • Idiopathic - 20% • Associated with a variety of lung diseases: Meconium aspiration syndrome (50%) Pneumonia/sepsis (20%) RDS (5%) Congenital diaphragmatic hernia (CDH) Others: Asphyxia, Maternal diabetes, Polycythemia 26
  27. 27. DIAGNOSIS  History - Precipitating factors during antenatal, intrapartum, postnatal periods  Respiratory signs - Signs of respiratory distress - Onset at birth or within the first 4 to 8 hours of life - Marked lability in pulse oximetry  Cardiac signs - Central cyanosis - Prominent precordial impulse - Murmur 27
  28. 28.  Radiography - Lung fields: normal, parenchymal lesions if lung disease is present, or oligaemia - Cardiac shadow: normal sized-heart, or cardiomegaly (usually right atrial or ventricular enlargement)  Echocardiography - Exclude congenital heart disease - To look for pulmonary artery pressure - Define the presence, degree, direction of shunt through the duct / foramen ovale - Define the ventricular output. 28
  29. 29. Differentiate PPHN from Congenital Cyanotic Cardiac diseases. Differentiating points between the two are: • Infants with PPHN usually had some perinatal hypoxia • Bradycardia is almost always due to hypoxia, not a primary cardiac problem • Babies with congenital cyanotic heart diseases are seldom critically ill at delivery • Infants with cyanotic lesions usually do not have respiratory distress • The cyanosed cardiac baby is usually pretty happy, but blue 29
  30. 30. MANAGEMENT 30 • Preventing and treating; hypothermia, hypoglycaemia, hypocalcaemia, hypovolemia, anaemia General measures • Morphine, midazolamSedation Ventilation
  31. 31. 31 • Aim MAP>50 mmHg • Inotropes to increase CO Circulatory • Inhaled NOVasodilators • Extracorporeal membrane oxygenationECMO
  32. 32. 5. APNEA OF PREMATURITY  Defined as sudden cessation of breathing that lasts for at least 20 seconds or is accompanied by bradycardia or oxygen desaturation (cyanosis) in an infant less than 37 weeks’ gestational age  Incidence increase with decrease gestational age 32
  33. 33. CLASSIFICATION  Central Complete cessation of airflow and respiratory efforts with no chest wall movement with no evidence of obstruction  Obstructive Absence of noticeable airflow but with continuation of chest wall movement  Mixed apnea – most common 33
  34. 34. ETIOLOGY  Symptomatic of underlying problems, commoner ones of which are: • Respiratory conditions (RDS, pulmonary haemorrhage, pneumothorax, upper airway obstruction, respiratory depression due to drugs). • Sepsis • Hypoxemia • Hypothermia • CNS abnormality (e.g. IVH, asphyxia, increased ICP, seizures) • Metabolic disturbances (hypoglycaemia, hyponatraemia, hypocalcaemia) • Cardiac failure, congenital heart disease, anaemia • Aspiration/ Gastro-oesophageal reflux • Vagal reflex: Nasogastric tube insertion, suctioning, feeding 34
  35. 35. Differentiate from Periodic breathing  Regular sequence of respiratory pauses of 10-20 sec interspersed with periods of hyperventilation (4-15 sec) and occurring at least 3x/ minute, not associated with cyanosis or bradycardia  Benign respiratory pattern for which no treatment is required  Respiratory pauses appear self-limited, and ventilation continues cyclically  Periodic breathing typically does not occur in neonates in 35
  36. 36. MANAGEMENT  Immediate resuscitation. 36 Pediatrics Protocol 3rd ed
  37. 37. Review possible underlying causes and institute specific therapy, e.g. septic workup if sepsis suspected and commence antibiotics Remember to check blood glucose via glucometer Management to prevent recurrence - Nurse baby in thermoneutral environment - Nursing prone can improve thoraco-abdominal wall synchrony and reduce apnoea Monitoring: - Pulse Oximeter, cardio-respiratory monitor 37
  38. 38.  Drug therapy - Methylxanthine compounds: Caffeine citrate (preferred if available) IV Aminophylline or Theophylline • Start methylxanthines prophylactically for babies < 32 weeks gestation • For those > 32 weeks of gestation, give methylxanthines if babies have apnoea • To stop methylxanthines if - Gestation > 34 weeks - Apnoea free for 1 week when the patient is no longer on CPAP - Monitor for at least 1 week once the methylxanthines are stopped 38
  39. 39.  After discharge, parents should be given advice - Supine sleep position - Elimination of exposure to tobacco smoke 39
  40. 40. 6. CONGENITAL PNEUMONIA  Acquired through the birth passages especially after prolonged rupture of membranes  Pneumonia in newborn infants is often difficult to diagnose and often difficult to distinguish from other causes of respiratory distress including RDS and TTN  Investigations including blood white cell counts, blood cultures, C-reactive protein, CXR 40
  41. 41. PATHOPHYSIOLOGY Pneumonia may be acquired due to ascending infection especially when chorioamnionitis is present Common pathogens include • Bacteria, such as group B Streptococci (GBS), Streptococcus pneumonia, Staphylococcus aureus, Listeria and gram- negative enteric rods (e.g. E.Coli) • Viruses, such as Herpes simplex virus, Respiratory syncytial virus and Influenza A & B viruses • Atypical organisms such as chlamydia • Fungi such as Candida albicans. 41
  42. 42. RISK FACTORS Prolonged rupture of membranes (PROM) Prematurity Maternal infection (maternal fever or raised white cell count) e.g. GBS 42
  43. 43. MANAGEMENT  Blood gases and pulse oximetry monitoring will guide the respiratory support required by the infant  Antibiotic; Penicillin and gentamicin  Supportive care such as oxygen, thermoregulation, prevention of hypoglycaemia and parenteral nutrition or nasogastric tube feeding 43
  44. 44. CXR A chest radiograph may show bilateral patchy shadowing with or without pleural effusion. 44
  45. 45. TAKE HOME MESSAGE Gestation age Risk factors Recognize signs of respiratory distress Early intervention, consultation and close monitoring 45
  46. 46. THANK YOU Ref: 1. Nelson Essential of Pediatrics 6th ed 2. Pediatrics Protocol 3rd ed 3. http://www.learningradiology.com 46

×