Respiratory distress in newborn

RDS in newborn

1. Respiratory Distress in Newborn

2. A 32 weeks preterm baby born to a GDM mother by LSCS, developed distress, grunting, cyanosis soon after birth. His SPO2 was 90%, hyperoxia test was positive. Downe’s score was 7, silverman-anderson score 8. Urgent CXR was done which showed :

3. RDS 3

4. Now what next ??? Baby shifted to NICU and put on warmer. RBS was normal, other blood samples taken. IV fluids were started, ABG was done which showed acidosis. Baby was put on nasal CPAP, meanwhile survanta was arranged. Baby then put on venti , surfactant given at 4 hours of life. Now clinically better.

5. SIGNS AND SYMPTOMS Tachypnea (RR > 60/min) Nasal flaring Retraction Grunting +/- Cyanosis +/- Desaturation D ecreased air entry

6. General Considerations

7. RD IN NB - Causes Pulmonary - Parenchymal - Extraparenchymal Non Pulmonary - Heart - Metabolic - Brain - Blood - Abdominal

8. RD in Newborn – Causes Pulmonary Parenchymal Extraparenchymal * RDS (HMD) * Upper airway obstruction * TTN (RDS II) ( Cloanal atresia , stenosis ) * Aspiration (Blood * Pneumothorax meconium ) * Pleural effusion * PPHN * Cong. Diaph . hernia * Pneumonia * Diaphragmatic paralysis * Pulm . hemorrhage * Pulm . hypoplasia

9. RD in Newborn – Causes Extrapulmonary Heart Metabolic Brain Blood Abdominal CCF - Met. Acidosis - Haemorrhage - Hypovolemia - NEC PDA - Hypoglycemia - Edema - Hyperviscosity - Pneumo CCHD - Hypothermia - Drugs - Acute blood peritonium Vascular - Sepsis - Pain loss - Large mass

10. Surgical causes of respiratory distress Tracheo-esophageal fistula Diaphragmatic hernia Lobar emphysema Pierre -Robin syndrome Choanal atresia

11. Suspect surgical cause Obvious malformation Scaphoid abdomen Frothing History of aspiration

12. A progressively increasing O2 requirement to maintain saturation is also a sensitive indicator of the severity and progress of distress >95% Term baby, pulmonary hypertension (PPHN) 88-94% 28-34 weeks preterm 85-92% Below 28 weeks gestational age Guidelines for monitoring oxygen saturation levels by pulse oximetry MJAFI, Vol. 63, No. 3, 2007 General Considerations

13. Hyperoxia test test Method result diagnosis Hyperoxia 100 % fio2 5-10 min Pao2 increases to > 100 torr Pao 2 increases by < 20 torr Parenchymal lung disease PPHN / CCHD Hyperoxia - hypervetilation MV 100 % fio2 & VR 100-150 / min Pao2 increases to > 100 torr w HV Pao2 increases at critical Pco2 No increase in Pao2 with HV Parenchymal lung disease PPHN CCHD

14. Downe’s score

15. Silverman-Andersen Retraction Scoring Interpretation Score 0-3 = Mild respiratory distress Score 4-6 = Moderate respiratory distress Score > 6 = Impending respiratory failure Score 10 = Severe Respiratory distress General Considerations

16. Investigation Complete Blood Count with a Peripheral blood smear Sepsis screen including C-reactive protein and μ ESR Arterial blood gas (ABG) analysis Blood glucose, Serum calcium Cultures: Blood , Surface swab (where indicated), maternal vaginal swab Chest radiograph with an oro -gastric tube in situ General Considerations

17. Mathai ss et al ,MJAFI 2007; 63 : 269-272

18. RR ( bpm Aspiration cong. Pneumonia, sev. HMD CDH cardiac malformation Approx. 6 Hours of age Normal 60 Course of Neonatal Tachypnoea : Etiologic possibilities Source : Baurn DJ, Birth Risks, Nastle Nutrition Workshop, 1993 TTNB HMD

19. Evaluation of RD in NB – Clinical History Antenatal History Most likely association * Prematurity, IDMs * HMD * PROM, maternal fever, * Pneumonia Unclean vaginal exams, UTI, diarrhoea * Asphyxia/MSAF * Aspiration * Caesarean delivery * TTN * Polyhydramnios * Pulm . Hypoplasia * Oligohydramnios * TE fistula, CDH * H/o receiving steroids * RDS less * Traumatic/breech delivery * ICH / Phrenic nerve paralysis

20. HMD/RDS

21. Respiratory Distress Syndrome (RDS) Also known as Hyaline Membrane Disease (HMD) Commonest cause of preterm neonatal mortality RDS occurs primarily in premature infants; its incidence is inversely related to gestational age and birth weight Nelson Textbook of Pediatrics, 18 th Ed. Gestational age Percentages Less than 28 wks 60-80% 32-36 wks 15-30% 37-39 wk 5% Term Rare Resp. Dis. Syn.

22. ETIOLOGY AND PATHOPHYSIOLOGY . Surfactant deficiency is the 1 O cause of RDS. Low levels of surfactant cause high surface tension High surface tension makes it hard to expand the alveoli. Tendency of affected lungs to become atelectatic at end-expiration when alveolar pressures are too low to maintain alveoli in expansion Leads to failure to attain an adequate lung inflation and therefore reduced gaseous exchange

23. With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells . Wk 20: start of surfactant production and storage. Does not reach lung surface until later Wk 28-32 : maximal production of surfactant and appears in amniotic fluid Wk 34-35 ; mature levels of surfactant in lungs Quality : The amounts produced or released may be insufficient to meet postnatal demands because of immaturity. Surfactant inactivating states eg maternal DM may lead to surfactant of lower quality/ immature

24. Rare genetic disorders may cause fatal respiratory distress syndrome eg . Abnormalities in surfactant protein B and C genes gene responsible for transporting surfactant across membranes (ABC transporter 3 [ABCA3] ) are associated with severe and often lethal familial respiratory disease

25. Clinical manifestation Tachypnea Nasal flaring Intercostal, sternal recession Grunting; closure of glottis during expiration Cyanosis 25

26. Risk factors Prematurity Maternal diabetes Multiple births Elective cesarean section without labor Perinatal asphyxia Cold stress Genetic disorders

27. Decreased risk Chronic intrauterine stress Prolonged rupture of membranes Antenatal steroid prophylaxis

28. Structure of lung surfactant major constituents of surfactant are dipalmitoyl phosphatidylcholine (lecithin), phosphatidylglycerol , apoproteins (surfactant proteins SP-A, -B, -C, -D), cholesterol

29. Resp. Dis. Syn.

30. Resp. Dis. Syn.

31. Normal Expiration With Surfactant Surfactant Function Abnormal Respiration Without Surfactant

32. Respiratory distress - Management Monitoring Supportive - IV fluid - Maintain vital signs - Oxygen therapy - Respiratory support Specific

33. Initial Care Maintain warmth- cold stress will mimic other causes of distress Monitor blood glucose levels- assure they are normal Provide enough oxygen to keep the baby pink

34. Is a Clinical diagnosis: respiratory distress occurring soon after birth. Pay attention to risk factors! Pulse Oximetry : aim for SPO2 >85%. ROUTINE! Full blood count and Cultures to check for sepsis: rem culture only positive 40-50% of the time!! gastic aspirates/ buffy smears for GBS Chest radiograph: air bronchogram , reticular/ ground-glass appearance after 6-12 hrs to full opacity later on. Blood gases: hypoxia, hypercapnia , acidosis. Signs of RESP FAILURE determine mgmt eg CPAP vs ventilation etc Electrolytes, glucose, renal and liver function Echocardiogram: diagnosing PDA, determine the direction and degree of shunting, making the diagnosis of pulmonary hypertension and excluding structural cyanotic heart disease

35. cxr 36 S hows air bronchograms and reticulonodular shadowing throughout the lung fields (often termed ‘ground glass’ appearance)

36. 37

37. Respiratory management Surfactant replacement therapy Ventilatory Assistance Oxygen therapy CPAP ( Nasal, ET, Face-mask ) Positive pressure ventilation High-frequency ventilation ECMO Liquid ventilation

38. Bubble CPAP

39. Avery and Mead in 1959 were the first to demonstrate that surfactant is deficient in the lungs of infants dying of HMD Fujiwara in 1980 reported the 1 st successful clinical trial of tracheal applications of surfactant in infants with RDS Commercial preparations of surfactant were subsequently approved by the FDA in the USA in 1989 Pulmonary Surfactants are phospholipids synthesized in the type II cells lining the alveoli

40. Prophylactic therapy Extremely preterm <28 wks <1000 gm Not routine in India Rescue therapy Any neonate diagnosed to have RDS Surfactant therapy - Issues Dose 100mg/kg phospholipid Intra tracheal

41. Types of Surfactant Natural Surfactants: contain appoproteins SP-B & SP-C Curosurf (extract of pig lung mince) Survanta (extract of cow lung mince) Infasurf (extract of calf lung) Synthetic Surfactants: do not contain proteins Exocerf ALEC Lucinactant (Surfaxin)

42. SURFACTANT Surfactant therapy reduces mortality rates most effectively in infants <30 weeks and those of birth weight <1250 gm 44

43. Insure technique I n tubation- sur factant- e xtubation to CPAP

44. Mode of administration of Surfactant Dosing may be divided into 2 alliquots and adminitered via a 5-Fr catheter passed in the ET

45. Management Prevention: Tocolytics to inhibit premature labor. Antenatal corticosteroid therapy: ► They induce surfactant production and accelerate fetal lung maturation. ► Are indicated in pregnant women 24-34 weeks' gestation at high risk of preterm delivery within the next 7 days. ► Optimal benefit begins 24 hrs after initiation of therapy and lasts seven days.

46. Diagnosis of lung maturity Amniotic Fluid Lecithin/Sphingomyelin Ratio ≥2 suggests lung maturity. ≤1.5 associated with HMD Phosphatidyl Glycerol estimation More specific than L/S ratio Absence is invariably associated with HMD Gastric Aspirate Shake Test Unreliable if gastric aspirate is contaminated with blood or meconium Serial tests can be done to assess maturity of lungs during course of disease Resp. Dis. Syn.

47. Shake test Take a test tube Mix 0.5 ml gastric aspirate + 0.5 ml absolute alcohol Shake for 15 seconds Allow to stand 15 minutes for interpretation of result

48. NATURAL COURSE Usually illness peaks in 3 days, then gradual improvement Improvement is often heralded by spontaneous diuresis and the ability to oxygenate the infant at lower inspired oxygen levels or lower ventilator pressures Death may occur esp from day2-3

49. MORTALITY Death is rare on the 1st day, usually occurs between days 2 and 7 causes are: alveolar air leaks (interstitial emphysema, pneumothorax ), pulmonary hemorrhage Intracranial hemorrhage Late mortality from bronchopulmonary dysplasia

50. COMLICATIONS

51. MAS

52. Meconium Aspiration Syndrome Definition MAS is defined as respiratory distress in an infant born through meconium-stained amniotic fluid (MSAF) whose symptoms cannot be otherwise explained J Perinatol . 2008 Dec Mec . Asp. Synd

53. Epidemiology Most common cause of respiratory distress in term and post-term infants . MSAF observed in 5-25% of all births out of which 10% develop MAS. One third require ventilator support 10 % develop air leaks 5-10 % of them have a fatal outcome Mec . Asp. Synd

54. What is meconium? The term was coined by Aristotle from the Greek word “ meconium arion ” meaning “ opium like ” Consists of gastrointestinal, hepatic and pancreatic secretions, cellular debris, swallowed amniotic fluid, lanugo, vernix caseosa and blood Appear in the fetal intestines by the 10th week of life gradually increasing in amount to reach 200gms at birth Mec . Asp. Synd

55. Cause of MSAF The passage of meconium from the fetus into amnion is prevented by lack of peristalsis (low motilin level) , tonic contraction of the anal sphincter , terminal cap of viscous meconium . Vagal Stimulation due to in utero hypoxia, acidosis, cord or head compression cause increased peristalsis and a relaxed anal sphincter. Fetal maturation (post term) causes high motilin level  increased peristalsis Mec . Asp. Synd

56. Risk factors for MAS Post term pregnancy Primigravida Maternal Anemia Chorioamnionitis Prolonged Labour Fetal Distress IUGR Maternal Age >30yrs Maternal DM Maternal heavy cigarette smoking Pre-eclampsia / eclampsia Oligohydramnios Antepartum Hemorrhage Mec . Asp. Synd

57. Pathophysiology Mechanical obstruction of airways Chemical Pneumonitis Surfactant Inactivation Mec . Asp. Synd

58. Mechanical obstruction of airways With onset of respiration – meconium migrates from central to peripheral airways. Thick particulate and viscous meconium lead to complete or partial airway obstruction. Complete obstruction  Atelectasis  Ventilation-Perfusion (V-Q) mismatch Partial obstruction  Ball-valve – air trapping  Obstructive Emphysema  R isk of pneumothorax (15 – 33 %) Mec . Asp. Synd

59. Chemical pneumonitis Meconium in the airways initiates an inflammatory reaction Meconium inhibits oxidative burst and phagocytosis by neutrophil  increased risk of infection Meconium induces production of inflammatory cytokines  Injury of parenchyma and vascular leakage  injury similar to ARDS Mec . Asp. Synd

60. Surfactant inactivation Bilirubin , fatty acid, triglycerides, cholesterol and proteins present in meconium alter phospholipid structure of surfactant  reduced s urfactant function Bile has cytotoxic effect on Type II Pneumocytes  Reduced surfactant production. Mec . Asp. Synd

61. Mec . Asp. Synd

62. Clinical Features History Maternal risk factors present Term or Post term Infants Meconium Stained Amniotic fluid (Thick  pea soup /Thin) IUGR. Many babies are depressed at birth.(in utero aspiration) Mec . Asp. Synd

63. Physical examination   Evidence of postmaturity : peeling skin, long fingernails, and decreased vernix . The vernix , umbilical cord, and nails may be meconium-stained, depending upon how long the infant has been exposed in utero. In general, nails will become stained after 6 hours and vernix after 12 to 14 hours of exposure . umbilical cord staining (thick-15min, thin-1hour) Mec . Asp. Synd

64. Meconium stained umbilical cord Mec . Asp. Synd

65. Meconium stained nails Mec . Asp. Synd

66. Features of respiratory distress within first few hours of birth The chest typically appears barrel-shaped, with an increased anterior-posterior diameter caused by over inflation. Auscultation reveals rales and rhonchi -immediately after birth. Some patients are asymptomatic at birth and develop worsening signs of respiratory distress as the meconium moves from the large airways into the lower tracheobronchial tree . In case of massive meconium aspiration, meconium pigments may be absorbed from lungs excreted in urine. Urine may appear dark brown in colour . Mec . Asp. Synd

67. Diagnosis MAS must be considered in any infant born through MSAF who develops symptoms of Respiratory Distress with typical chest x ray findings Mec . Asp. Synd

68. Diagnosis A chest radiographs is characterized by hyperinflation of the lung field and coarse nodular opacities due to areas of atelectasis and consolidation. There are coarse irregular patchy infiltrates A pneumothorax and pneumomediastinum may be present . Mec . Asp. Synd

69. Mec . Asp. Synd

70. Mec . Asp. Synd

71. Mec . Asp. Synd

72. Mec . Asp. Synd

73. Diagnosis Arterial blood gas measurements typically show hypoxemia and hypercarbia . Infants with pulmonary hypertension and right-to-left shunting may have a gradient in oxygenation between preductal and postductal samples. Echocardiogram for evaluation of Persistent Pulmonary Hypertension. Mec . Asp. Synd

74. Management Prenatal management: Key management lies in prevention during prenatal period. Identification of high risk pregnancies and close monitoring. Pregnancy that continue past due date, induction as early as 41 weeks may help prevent meconium aspiration. If there is sign of fetal distress corrective measure should be undertaken or infant should be delivered in timely manner. Amnioinfusion has no role . Mec . Asp. Synd

75. Delivery Room Management Baby delivered through MSAF Intrapartum Suctioning Assess the baby after 10-15 sec Vigorous HR > 100/min Spontaneous Respiration Crying Reasonable tone No intervention Non Vigorous Intubate Tracheal Suction Mec . Asp. Synd

76. When the infant is not vigorous: Place under radiant warmer but delay stimulation. Clear airways as quickly as possible. Intubation and then suction directly to the ET tube.  repeat until either ‘‘little meconium is recovered, or until the baby’s heart rate indicates that resuscitation must proceed without delay’’. May also require saline lavage to remove thick particles. After all meconium is sucked out, ventilate the baby with bag and mask. Mec . Asp. Synd

77. Postnatal Management Shift to NICU setup with respiratory support facilities available Gastric wash with normal saline to reduce gastritis and aspiration of meconium stained products. Close monitoring for Respiratory distress. Most infants who develop symptoms will do so in the first 12 hours of life. Mec . Asp. Synd

78. Management Consider CPAP, if FiO2 requirements >0.4; however CPAP mayaggravate air trapping and must be used cautiously. Mechanical ventilation: in severe cases (paCO2 >60 mmHg orpersistent hypoxemia (paO2 <50 mmHg). Correct systemic hypotension (hypovolemia, myocardial dysfunction). Manage PPHN, if present Manage seizures or renal problems, if present. Surfactant therapy in infants whose clinical status continue todeteriorate.

79. TTNB

80. Transient Tachypnea of Newborn Also called Wet Lung Syndrome or Type II Respiratory Distress Syndrome The most common cause of neonatal respiratory distress constituting more than 40 percent of cases 11 per 1,000 live births . Represents a milder form of HMD or due to failure of drainage of alveolar fluids resulting in pulmonary edema  decreased compliance and increased airway resistance  Respiratory Distress Tran. Tachy . Newborn

81. Risk Factors Term or Near Term Babies Male Child Cesarean Section Delayed cord clamping or cord milking Macrosomia Maternal Sedation Large amount of IV Fluids to mother during labor Maternal Asthma Maternal Diabetes Tran. Tachy . Newborn

82. Clinical Features Tachypnea immediately after birth or within 6hrs after delivery with mild to moderate respiratory distress. These manifestations usually persist for 12-24hrs , but can last up to 72hrs Auscultation usually reveals good air entry with or without crackles Usually maintain good color and are alert. Tran. Tachy . Newborn

83. X-Ray Chest Hyperinflation of the lungs Linear streaking at hila due to dilated lymphatics Interlobar Fluid Mild Cardiomegaly Chest x-ray usually shows evidence of clearing by 12-18 hrs with complete resolution by 48-72 hrs Tran. Tachy . Newborn

84. Tran. Tachy . Newborn

85. Fluid in the inter lobar fissure Tran. Tachy . Newborn

86. chest X-ray: Transient Tachypnea of Newborn Fluid in the fissure

87. TTN is a clinical diagnosis of exclusion Tran. Tachy . Newborn

88. General Management Provide an adequate nutrion. Infants with sustained RR >60 breaths/min should not be fed orally & should be maintained on gavage feedings for RR 60-80 breaths/min, and NPO with IV fluids or TPN for more severe tachypnea

89. Results from slow absorption of lung fluid Term born by LSCS/IDM /maternal asthma Mild respiratory distress Peaks at about 36 hours of life Resolve spontaneously SUMMARY : Transient Tachypnea of the Newborn

90. OTHERS

91. Air Leak Syndromes Risk Factors: MV,MAS, surfactant therapy without decreasing pressure support in ventilated infants vigorous resuscitation, prematurity pneumonia

92. Chest x-ray : Right-sided pneumothorax

93. Left-sided pneumothorax under tension.

94. Others Pneumomediastinum It can occur with aggressive ETT insertion, Ryle's feeding tube insertion, lung disease, MV, or chest surgery (e.g., TEF). Pneumopericardium Pneumoperitoneum Subcutaneous emphysema Systemic air embolism

95. Chest x-ray with Pneumomediastinum

96. Chest x-ray with pneumopericardium

97. Pneumopericardium 99

98. Management Conservative therapy: close observation of the degree of respiratory distress as well as oxygen saturation, without any other intervention aiming at spontaneous resolution and absorption of air. Needle aspiration should be done for suspected cases of pneumothorax with deteriorating general condition until intercostal tube is inserted. Decompression of air leak according to the type (intercostal tube insertion in case of pneumothorax).

99. Ground glass opacity

100. X-ray - RDS

101. X-ray - MAS

102. MAS 104

103. X-ray - Pneumothorax

104. Pneumothorax 106

105. Right lateral decubitus view of pneumothorax 107

106. Left Congenital Diaphragmatic Hernia 108