Respiratory Distress in Newborns


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Respiratory Distress in Newborns

  1. 1. Respiratory distress in Newborn Dr. Kalpana Malla MD Pediatrics Manipal Teaching HospitalDownload more documents and slide shows on The Medical Post [ ]
  2. 2. FREQUENT CAUSES• Medical• TTNB – transient tachypnoea• RDS(HMD)• Aspiration syndromes• Pneumonia/sepsis• PPHN• CCF• Acidosis
  3. 3. FREQUENT CAUSES• Surgical• Pneumothorax• Diaphragmatic hernia• TEF• Lobar emphysema• Phrenic nerve paralysis
  4. 4. Resp distress – above downwards1) Airway obstructionA) Nasal – choanal atresia nasal edemaB) Oral cavity – macroglossia, micrognathia, GlosoptosisC) Laryngeal obstruction – laryngeal web - Subglottic stenosis of larynx - Laryngomalacia - cord paralysis
  5. 5. Resp distress – above downwards D) Neck obstruction – cystic hygroma - cong goitre E) Tracheal obsruction – - Tracheomalacia - TEF - Tracheal stenosis
  6. 6. 2) Lung parenchyma• Aspiration syndrome (MAS)• Resp distress syndrome (HMD)• TTNB• Pneumonia• Pleural effusion• Pulmonary hemorrhage• Air leak – Pneumothorax, pneumomediastinum
  7. 7. 3) Developmental defects• Agenesis of lung• Hypoplasia of lung• Diagphratic hernia• Tracheal agenesis• TEF
  8. 8. 4) Extrapulmonary• B. asphyxia• CCF• Metabolic acidosis• Persistent pulmonary hypertension
  10. 10. GENERAL ASPECTS• Occasionally called respiratory distress syndrome type II• Mild and self-limited• Usually term infants, C/S and maternal IV fluids associated• The distinctive features of transient tachypnea are sudden recovery of the infant
  11. 11. Pathogenesis• Secondary to slow absorption of fetal lung fluid resulting in decreased pulmonary compliance and tidal volume and increased dead space
  12. 12. CLINICAL MANIFESTATIONS • Increased RR, no retractions, mild cyanosis - relieved by minimal oxygen (<40%) • Expiratory grunting • Recover rapidly within 3 days • Lungs are generally clear without rales or rhonchi
  13. 13. CXR• Prominent pulmonary vascular markings• Fluid lines in the fissures• Over aeration• flat diaphragms• occasionally, pleural fluid
  14. 14. CXR• Distinguishing from HMD may be difficult• Absence reticulogranular pattern or air bronchograms in CXR
  15. 15. TREATMENT• Nothing to do• General supportive measures• Oxygen• IVF• Ventilation not required• Subsides on its own
  17. 17. INCIDENCE• Common in premature infants• Incidence is inversely proportional to gestational age and birth weight• 60–80% in < 28 wk of gestational age• 15–30% in between 32 and 36 wk• 5% > 37 wk• Rare at term
  18. 18. INCREASED RISK FACTORS • Infants of diabetic mothers • Delivery before 37 wk gestation • Multifetal pregnancies • Cesarean section delivery • Precipitous delivery • Asphyxia • Cold stress • History of previously affected infants
  19. 19. DECREASED RISK FACTORS • Chronic or pregnancy-associated hypertension • Maternal opiate addiction • Prolonged rupture of membranes • Antenatal corticosteroid use
  20. 20. PATHOPHYSIOLOGY• Surfactant deficiency - decreased production and secretion• Present in amn.fluid:28-30wks, mature levels after 35 wks• Surfactant reduce surface tension and prevent the collapse alveoli• Alveolar atelectasis, hyaline membrane formation, and interstitial edema make the lungs less compliant, so greater pressure is required to expand the small alveoli
  21. 21. PATHOPHYSIOLOGY (CONTD…) • Decreased lung compliance- insufficient alveolar ventilation – result in hypercapnia • Combination of hypercapnia, hypoxia, and acidosis → pulmonary arterial vasoconstriction → increased R → L shunting through the foramen ovale and ductus arteriosus → Pulmonary blood flow is reduced → ischemic injury cap endothelium & alveolar epithelium → leak of plasma (proteinaceous material) into the alveolar spaces
  22. 22. PATHOPHYSIOLOGY (CONTD…) • leak of plasma (proteinaceous material) into the alveolar spaces →combine with fibrin & necrotic alveolar pneumocytes & form hyaline membrane • Hyaline membranes: coagulum of sloughed cells and exudate, plastered against epithelial basement membrane
  23. 23. CLINICAL MANIFESTATIONS • Resp distress - tachypnea , Intercostal and subcostal retractions Nasal flaring • Grunting • Cyanosis - relatively unresponsive to oxygen • Progressive worsening of cyanosis and dyspnea • Breath sounds : harsh tubular quality, fine rales
  24. 24. PROGRESSION• Severity peaks at 24-48 hours, resolution by 72-96 hours (without surfactant therap• If not treated, BP may fall; fatigue, cyanosis, and pallor increase, and grunting disappears as the condition worsens• Apnea and irregular respirations : ominous• Mixed respiratory-metabolic acidosis• Respiratory failure
  25. 25. OUTCOME• Death is rare on the 1st day• Death occurs at 2 -7 days• Associated with alveolar air leaks (interstitial emphysema, pneumothorax) and pulmonary hemorrhage or IVH
  26. 26. DIAGNOSIS• CXR : fine reticular granularity of the parenchyma and air bronchograms : typical pattern developing at 6–12hr
  27. 27. Diffused reticulogranular pattern
  28. 28. • CXR- Later:• ground glass opacity• ABG : progressive hypoxemia, hyperc apnia, and variable metabolic acidosis
  29. 29. Ground glass opacity
  30. 30. DIFFERENTIAL DIAGNOSIS • Early-onset sepsis: group B streptococcus • Pneumonia • Cyanotic heart disease • Persistent pulmonary HTN • Transient tachypnea of newborn
  31. 31. DIFFERENTIAL DIAGNOSIS • Spontaneous pneumothorax • Pleural effusion • Diaphragmatic hernia • Lobar emphysema
  32. 32. PREVENTION• Prevention of prematurity• Lecithin:sphingomyelin ratio in amniotic fluid: >2 means mature lungs <1.5 means HMD• Betamethasone to women 48hr before the delivery - between 24 and 34 wk of gestation- 6mg IM for 4 doses 12 hrs apart or 12 mg IM for 2 doses 12 hrs apart
  33. 33. PREVENTION (CONTD…)• First dose of surfactant into the trachea of symptomatic premature baby immediately after birth (prophylactic) or during the first few hours of life (early rescue)
  34. 34. TREATMENT: SUPPORTIVE • Avoid hypothermia • IV Calories and fluids • Warm humidified oxygen • CPAP : prevents collapse of surfactant-deficient alveoli • Assisted ventilation • High-frequency ventilation (HFV )
  35. 35. SURFACTANT THERAPY : DEFINITIVE TREATEMENT • Multidose endotracheal instillation : 4ml/kg • Treatment (rescue) is initiated as soon as possible in the 1st 24hr of life • Dose repeated - via the ET tube 6– 12hrly for a total of 2-4 doses • Appropriate monitoring equipment must also be available - radiology, blood gas laboratory, and pulse oximetry
  36. 36. Severe (RDS) - Cystic areas in the rightlung represent dilated alveoli or early pulmonary interstitial emphysema
  37. 37. Acute Complications• Air Leak Syndromes – Consider with sudden change in condition – More common if baby receiving ventilatory support – Pneumothorax most common• Therapy – None if stable – Oxygen 100% – Thorocentesis: Needle or tube
  38. 38. Complication of RDS: right tensionpneumothorax and pneumomediastinum
  39. 39. Acute Complications• Intracranial Hemorrhage – More common at lower gestational ages – Rare above 33 weeks gestation• Suspect if there is a sudden change in condition• May coincide with development of air leak• Signs: change in Fontanel, perfusion
  41. 41. GENERAL ASPECTS• Meconium-stained amniotic fluid is found in 10–15% of births• Meconium aspiration pneumonia develops in 5% of such cases• 30% of them require mechanical ventilation• 3–5% expire
  42. 42. Risk Factors for Meconium Passage • Post term pregnancy • Pre-eclampsia - eclampsia • Maternal hypertension • Maternal diabetes mellitus • Abnormal fetal heart rate • IUGR • Oligohydramnios
  43. 43. AETIOIOGY• Precise mechanisms remain unclear• Theory - to explain the passage of meconium in utero - The fetal bowel has little peristaltic action and the anal sphincter is contracted• It is thought that hypoxia and academia cause the anal sphincter to relax, whilst at the same time increase the production of motilin, which promotes peristalsis.
  44. 44. Meconium Aspiration Syndrome Pathophysiology Airway obstruction of large and small airways Inflammation and edema  Protein leak  Inflammatory Mediators  Direct toxicity of meconium constituents = chemical pneumonitis Surfactant dysfunction or inactivation Effects of in utero hypoxemia and acidosis Altered pulmonary vasoreactivity (PPHN)
  45. 45. Meconium Aspiration Syndrome Diagnosis  Known exposure to meconium stained amniotic fluid  Respiratory symptoms not explained by other cause  R/O pneumonia, RDS  Spontaneous air leak
  46. 46. CLINICAL MANIFESTATIONS • Either in utero or with the 1st breath meconium is aspirated into the lungs • Tachypnea, retractions, grunting, and cyanosis : small airway obstruction • Partial obstruction of some airways may lead to pneumothorax or pneumomediastinum • Overdistention of the chest prominent • Tachypnea may persist for many days or even several weeks
  47. 47. INVESTIGATIONS CXR - diffuse, patchy infiltrates, consolidation, atelectasis, air leaks, hyperinflation• ABG
  48. 48. Meconium in Amniotic Fluid Intrapartum suctioning of mouth, nose, pharynx Infant DepressedInfant Active Intubate andObserve suction trachea Other resuscitation as indicated
  49. 49. Meconium Aspiration Syndrome Treatment • Ventilation strategies Avoid air leak, check CXR Generous O2 Ventilator • Steroids ( controversial) • Antibiotics (ampicillin, gentamicin) • Surfactant • Inhaled Nitric Oxide
  50. 50. Other Things to Watch For• Hypoxia• Acidosis• Hypoglycemia• Hypocalcemia• End-organ damage due to perinatal asphyxia
  51. 51. PREVENTION• Fetal distress - initiating prompt delivery• Immediate DeLee suctioning of the oropharynx after the head is delivered
  52. 52. PROGNOSIS• High incidence long term pulmonary problems include -• At 6 months - 23% MAS with regular bronchodilator therapy*• symptomatic cough, wheezing, and persistent hyperinflation for up to 5–10 yr.
  53. 53. Meconium Aspiration Syndrome Outcome The ultimate prognosis depends on the extent of CNS injury from asphyxia - Increased risk of poor neurologic outcome due to perinatal insult - seizures, CP, mental retardation
  54. 54. Thank youDownload more documents and slide shows on The Medical Post [ ]