Respiratory distress in the newborn

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1. Respiratory Distress in the Newborn By: Dr. Nivedita Mishra Guide: Dr. Srijana Basnet 2. OBJECTIVES ã To define and assess respiratory distress. ã To recognise the…
  • 1. Respiratory Distress in the Newborn By: Dr. Nivedita Mishra Guide: Dr. Srijana Basnet
  • 2. OBJECTIVES • To define and assess respiratory distress. • To recognise the important conditions leading to respiratory distress by clinical features, pathophysiology & radiological features. • To discuss the incidence and risk factors associated with the common conditions causing respiratory distress. • To identify the complications related to these diseases. • To discuss the management specific to different conditions causing respiratory distress.
  • 3. Definition of Respiratory Distress Presence of any 2 of the following features:* 1. R.R > 60/min 2. Subcostal/intercostal Recessions 3. Expiratory Grunt /Groaning Signs should be assessed in context of Spo2, colour, activity of the baby. * NNPD Report 2002-2003.NNPD Network,ICMR;p67
  • 4. Incidence 5.8% of live born infants have respiratory morbidities.NNPD Data 2002-03 Respiratory Distress occurs in : • 2.2% of all newborns. • 60% of infants below 1000g (ELBW): RDS(50.8%) > TTN(4.3%) >Pneumonia/Sepsis(1.9%) • In higher birth weight preterm & term babies TTN is more common.(68%) • Contributes 30-40% of admissions in NICU. Mathai SS,Raju U,Kanitkar M,et al.Management of Respiratory Distress in the Newborn.MJAFI 2007;63:269- 72r
  • 5. Causes of Respiratory Distress (Data from Rubaltelli FF,Dani C,Reali al.Acute neonatal Respiratory Distress in Italy: a one year prospective study,Acta Paediatr;1998;87:1261-68) Incidence Respiratory Distress Syndrome 46% TTN 37% Pneumonia/Sepsis 5% Meconium Aspiration Syndrome 2% Congenital Cardiac Malformation 2% Chromosomal Disorders /Multiple Congenital Anomalies 1.4% Spontaneous Pneumothorax 1.2% Perinatal Asphyxia 1.1% Pulmonary Haemorrhage 1% Persistent Pulmonary Hypertension 0.8% Diaphragmatic Hernia 0.8% Apnoea of Prematurity 0.6% Pulmonary Hypoplasia 0.3% Pulmonary Dysplasia 0.2% Hydrothorax 0.2% Post-surgical Diaphragmatic Palsy 0.2%
  • 6. Assessment of Respiratory Distress • Initial assessment: to find out life threatening conditions requiring immediate management 1. Inadequate/Obstructed Airway: Gasping ,Choking,Stridor. 2. Circulatory collapse: Bradycardia,Hypotension,poor perfusion. Intervention: Bag-Mask ventilation/intubation
  • 7. Assessment of Severity: Silverman score FEATURE 0 1 2 UPPER CHEST MOVEMENT Synchronus with abdomen Inspiratory lag See-saw respiration LOWER CHEST RETRACTIONS no minimal marked XIPHOID RETRACTIONS no minimal marked NASAL FLARING no minimal marked GRUNTING no Audible with steth Audible without steth
  • 8. Downe’s Score Downe’s score FEATURE 0 1 2 CYANOSIS No In room air/ no cyanosis with oxygen support Cyanosis inspite of oxygen support. RETRACTIONS No Mild Mod- Severe GRUNTING No Audible with steth Audible without steth AIR ENTRY Normal Decr. Barely audible RESPIRATORY RATE <60 60-80 >80 / apnoea Score > 4 = clinical respiratory distress Score > 7 = impending respiratory faliure
  • 9. Assessment of Respiratory Distress • Look for Clues to Etiology: 1. Nasal stuffiness,drooling 2. Presence of Meconium staining of nails, umbilical stump. 3. Birth trauma 4. Dysmorphic features – Pierre Robin syndrome, Beckwith- Wiedmann syndrome. 5. Anomalies-  Hydrocephalus, Arnold-Chiari malformation, MMC  Choanal atresia,  Neck masses- Cystic hygroma, congential goitre  Cleft palate, Chest wall deformities,  Scaphoid Abdomen. 6. Anaemia/Polycythemia,Hypoglycemia, Hypothermia,
  • 10. Assessment of Respiratory Distress ANTENATAL INTRANATAL POSTNATAL Diabetes mellitus, Heart disease etc. PPROM/PROM Gestational age Fever,UTI Intrapartum fever /Chorioamnionitis Appearance,activity POLY/OLIGOHYDRAMNIOS Sedative use, Onset/course of respiratory distress Antenatal steroids status Meconium stained liquor Relation to feeding/frothing from mouth, crying Rh Isoimmunisation Abnormal fetal monitoring Radiological features Antenatal scans Instrumental delivery /Birth trauma Pre and post ductal saturation. (For Cardiac cause/complication) Teratogenic drug use, Narcotic use Need for Bag-Mask ventilation
  • 11. ANC (Review by Monroe chart) Hb,PCV (>40,<65)
  • 12. BASIC MANAGEMENT • Clear airway, Ensure adequate breathing & Circulation. • Monitor SpO2. • O2 supplementation + Respiratory support. • Maintain Temperature. • Fluid and Electrolyte management. • Antibiotics if sepsis screen +ve. • SPECIFIC MANAGEMENT DEPENDS ON THE CAUSE OF DISTRESS.
  • 13. Respiratory Distress Syndrome • A Disease typical of preterm infants that arises d/t insufficient pulmonary surfactant in the alveoli. • Results in high Surface Tension and Atelectasis. • Alveolar type 2 cells do not develop until early in the third trimester. Their number & capacity to produce surfactant increases throughout third trimester. Mature levels of pulmonary surfactant after 35 wks. (normal L/S Ratio = 2:1). low risk of RDS if L/S ratio>2
  • 14. Incidence of RDS • Incidence is inversely proportional to gestational age & birth weight. Worldwide data: Indian data: • <28 WOG – 60 to 80% 58% in <30 wog • 32-36WOG- 15 TO 30% 32% b/w 30-32 wog 10% b/w 33-34 wog • 37 WOG- Term – 5% • 500-750 gm-54% (NICHD Neonatal Research Network,Fanaroff • 751-1000gm- 36% • 1251-1500gm-22% • 6.8 to 14.1% of preterm live births in India • 1.2% of all live births (NATIONAL NEONATAL PERINATAL DATA 2013 report)
  • 15. Risk factors for RDS • Prematurity- Developmental immaturity of Type II PNEUMOCYTES • Male fetus- more androgens,reduces surf.phospholipids. • Maternal diabetes- more fetal insulin,reduces surf.proteins. • Lack of labour-no endogenous maternal glucocorticoids,excess fetal lung fluid d/t delivery without labour. • No antenatal steroid administration. • Perinatal asphyxia, • Hypothermia • Pulmonary infection- inflammatory cytokines. • Mutation in surfactant protein B, ABCA3 transporter - asso.with ILD. Benefit by lung transplant.
  • 16. Pathophysiology of RDS RDS manifests histologically as HYALINE MEMBRANE DISEASE. -During breathing(spont/assisted),shear stresses in the alveoli cause damage to lung architecture : 1.Repetitive reopening of collapsed alveoli 2.Overdistension of open alveoli. -Leakage of proteinaceous debris into airways (HYALINE MEMBRANES) -Debris impairs function of surfactant. -Insufficient/Dysfunctional Surfactant -> generalised atelectasis-> V/P Mismatch-> hypoxia -> acidosis -> decr. surfactant production -Respiratory Faliure.
  • 17. Clinical signs of RDS • Tachypnoea- to increase Co2-O2 exchange • Grunting – partial closure of glottis during expiration to maintain end expiratory pressure. • Retractions- to generate high -ve intrathoracic pressure at inspiration. • Cyanosis- intrapulmonary shunting of blood past atelectatic lung tissues. • Murmur- poorly inflated lungs have widespread collapse of pulmonary vessels PAH Lt to Rt shunting across PDA. • Pallor- From acidosis d/t poor elimination of Co2 • Lethargy- D/t incr. WOB • Poor feeding • Apnoea
  • 18. Course of RDS • REPAIR PHASE: Begins during 2nd day after birth (appearance of macrophages,PMNs-> debris is phagocytosed-> epithelium regenerated) • DIURETIC PHASE: edema fluid in the interstitium mobilised to lymphatics-> High urine output. • The course of RDS is self limited. Typically improves by 3 to 4 days with onset of diuretic phase • Tends to get worse over first 1-3 days after birth before improving.
  • 19. Differential diagnosis of RDS • Extremely elevated PaCo2 within minutes of birth. = Pulmonary hypoplasia/ Tension pneumothorax/ Cong.Diaphragmatic Hernia. • Tachypnoeic, Cyanotic baby with low PaCo2 = TTN/ Cong. cyanotic Heart dis.(TAPVC) • Pneumonia/ sepsis on blood c/s • Hypoglycemia (GRBS < 40) • Symptomatic Polycythemia (PCV > 65)
  • 20. Investigations • Lab features: 1. ABG- initially only hypoxemia,later hypercarbia and then acidosis manifest. 2. GRBS 3. CBC 4. Blood c/s 5. Bedside Shake test on Gastric aspirate (-ve in RDS) 6. CXR
  • 21. HYALINE MEMBRANE DISEASE/ RDS Figure 5.Arrows on the right lung field point at the diffuse ground glass appearance. Arrows on the left demonstrate prominent air-filled bronchi, known as air bronchogram (BLACK LINES) .LOW LUNG VOLUMES-diaphragm at 8th rib or higher.
  • 22. Prevention of RDS • Antenatal steroids: causes thinning of alveolar mesenchyme for proper gas exchange. • Multiple randomized controlled trial strongly suggest use of maternal antenatal steroids • Betamethasone superior than dexamethasone European consensus guideline for respiratory disease 2010 ANC DOSES given from 24 to 34 wog : Betamethasone @ 12mg I.M/24hrly for 2 doses. Or, Dexamethasone @ 6mg I.M/12hrly for 4 doses. Benefit max. If given 24 hrs before delivery. Evidenced by significant reduction in NND by 31%,RDS by 34%,IVH by 46% (dexa),NEC by 54%. (ROBERTS & DALZIEL Meta analysis in 2006 of 21 published trials )
  • 23. Prevention of RDS • Prevention of asphyxia: delivery by C-section of at risk babies • CPAP: to prevent end expiratory alveolar collapse,reduce WOB,better match ventilation to perfusion. COIN TRIAL compared the outcomes of Early nasal CPAP vs prophylactic intubation in 25- 28 wog newborns. 46% of CPAP group eventually required intubation during first 5 days with pneumothorax in 9% compared to only 3% in intubated group.
  • 24. Prevention of RDS When to give 1st dose of surfactant ? Which populations to consider? Prophylactically, within 15 min after birth. (CUROSURF @ 200mg/kg) <26 WOG 26-30 WOG if: a. no Antenatal steroids given to mother. b. Baby needs intubation anyway. Early rescue, in 1st 60 min after birth. <30 WOG at first signs of RDS. Treatment of established RDS, within 12hrs after birth. All babies with RDS, regardless of gestational age if they need ventilator and atleast 30-40% FiO2. Repeat doses: if infant requires ventilatory support and has Fio2 req.>30%. Min 6 hrs duration is needed b/W 2 doses. Surfactant not usually contd. Beyond 3 DOL. Exogenous surfactant. Compared to 1st gen synthetic surfactants,current studies strongly support the use of natural surfactants because of reduced air leak & more rapid response to treatment.(Cochrane Review Article 2007)
  • 25. Complications of RDS • In infants < 1250 gm, larger newborns need high O2 conc. & PPV- Inflammation,inappropriate repair -> Emphysema, Fibrosis • Death is rare on 1st day of illness.Occurs by 2nd to 7th day d/t alveolar air leaks,pul.haemorrhage,IVH • Infants who do not improve after adminstration of surfactant should be evaluated for PDA or other congenital Heart disease • Neonates who initially improve with surfactant but later deteriorate are evaluated for nosocomial pneumonia
  • 26. Complications of RDS • ACUTE : 1. Air leak 2. ETT/ nasal cannulation complications 3. Infections 4. Intracranial haemorrhage 5. PDA • LONG TERM: 1. BPD,PPHN 2. ROP 3. PVL,IVH 4.AKI (d/t acidosis)
  • 27. Transient tachypnoea of Newborn • Results from delayed clearance of fetal lung fluid.(transient pulmonary oedema) • Benign,Self limited, RR=60-120/min, persisting for 12-72 hrs • Late preterm/term. • INCIDENCE: 0.3- 0.6% of term & 1% of preterm deliveries. (Pediatrics in Review Nov 2008) • TTN is a diagnosis of exclusion.
  • 28. PATHOPHYSIOLOGY OF TTN • Switch from secretory mode to absorptive mode facilitated d/t surge in glucocorticoids and catecholamines near the end of pregnancy and during spontaneous labour. • Amiloride sensitive Na+ channels on apical membrane of alveolar epithelium(ENaC activated by Na+/K+ATPase) • ALVEOLI- TYPE 2 PNEUMOCYTES- INTERSTITIUM-LYMPHATIC • Accumulation of fluid in the interstitium ->airway compression- >air trapping,V/Q mismatch,reduced FRC.
  • 29. Risk factors • Risk factors: 1.Prematurity, 2. C-sec delivery without preceeding labour, 3. Male baby, 4. F/H/O Asthma mother(altered sensitivity of beta-adrenergic Rs to catecholamines), 5. Macrosomia, 6. Maternal diabetes, 7. Multiple gestations, 8. Excessive maternal sedation, 9. Vol.of Maternal i.v fluids 10. Milking of the cord before cord clamping
  • 30. CXR: TTN Normal / High lung vol.+ prominent interstitial fluid pattern.(coarse white lines radiating from the hilum. Perihilar markings(sunburst pattern),Fluid in fissure, Hyperinflation(palpable liver & spleen), Cardiomegaly (distinguishes it from TAPVR).
  • 31. MANAGEMENT OF TTN • Avoiding elective cesarean section before onset of labor • Antenatal corticosteroids have a PROTECTIVE EFFECT. Single Course at least 48 hour before CS decreases the reparatory morbidity. (Pediatrics in review October 2014) • Supportive t/t: Delay oral feeding till tachypnoea settles. Supplemental O2. Requires FiO2 <0.40 • Rapid resolution distinguishes it from Pneumonia, MAS. • Newborns with TTN are at mildly increased risk for later development of Asthma (Birnkrant,1996;Liem et al,2007;Schaubel et al,2006)
  • 32. Pneumonia/Sepsis • INCIDENCE: 5% overall • Birth wt. 1500-2500gm =0.28%, <1000gm = 1.9% Causative organisms: 1. E.coli (44%), 2. Grp.B Streptococcus (11%), 3. CONS (11%), 4. H.Influenzae, 5. S.viridans (8%), 6. Listeria,Citrobacter,Candida (2%) May acquire transplacentally through infected amniotic fluid or nosocomially
  • 33. Risk factors Multiple/single unclean vaginal exams,  GBS carrier mother  History of GBS bacteriuria  Delivered before 37 weeks  PROM > 18 Hours or more  Mother having Intrapartum Fever (100.4 F)  Preterm birth following spontaneous labor  Suspected or confirmed infection in another baby in multiple pregnancy. (Common respiratory conditions of newborn, Breathe, March 2016)
  • 34. MANAGEMENT Presents before 72hol as EONNS as Newborns are unable to localise Pul. Infections. Depressed baby with prolonged CRT. • LAB Dx: Marked by Leucopenia, incr.CRP • T/t: supportive care. Empirically Ampicillin + Gentamycin for 48 hrs while awaiting blood c/s reports. If blood c/s –ve, mother has been on Abx give for 5- 7 days
  • 35. Meconium Aspiration Syndrome Incidence: 10-15% overall.Low incidence in preterms.High incidence in post mature & SGA babies. • >37 wog = 0.4% to 1.8% (Dargaville & Copnell,2006;Singh et al,2009), >39wog =50% (Gouyon et al,2008) • Approx 3-4% of infants born through MSAF develop MAS (meconium found below vocal cords) • 30-50% of MAS cases require mech.ventilation/CPAP. • Mortality b/w 4-12% (Gordon & Avery,2009)
  • 36. PATHOPHYSIOLOGY • MSAF results from : 1. a post-term fetus with rising motilin levels & normal G.I function, 2. vagal stimulation d/t cord or head compression or in-utero fetal stress, 3. Decr. Anal sphincter tone. • FETAL ACIDEMIA-> Incr. PERISTALSIS-> passage of meconium-> fetal gasping-> meconium inhaled->chemical pneumonitis, ball- valve obstruction-> Hypoxia + Air Trapping + Air Leak. • Meconium inactivates surfactants. Leads to PPHN. • Thin meconium is more notorius.
  • 37. • Clinical signs of MAS vary with timing,volume,consistency of aspirated meconium. • S/s develop by 12 HOL. 1. Tachypnoea,cyanosis,WOB 2. Metabolic acidosis 3. Hypotension, 4. Postductal desaturation (Rt-Lt shunt via PDA) indicating PPHN 5. Pneumothorax
  • 38. CXR: MAS Diffuse fluffy infiltrates. Coarse patches of atelectasis. HYPERINFLATED lung base.barrel shaped chest.
  • 39. Prevention • C-sec for Utero-placental insufficiency d/t: 1. Chr. respiratory ds./cvd 2. Heavy smokers 3. Pre eclampsia/HTN 4. IUGR 5. Big baby 6. Post term baby • Fetal heart rate monitoring
  • 40. Management • SUCTIONING: 80-100 mmHg • Surfactants • Corticosteroids • GASTRIC WASH with N.S to reduce Meconium induced gastritis. • No2 improves oxygenation in PPHTN • Mech.ventilation: High freq.device-> high risk of hyperinflation- > PPHTN Slower rate better gas exchange. • Antioxidants: vit.E • ECMO if respiratory faliure: 94-97% survival range • ANTIBIOTICS : Intrauterine infection may be the Cause of initial passage of meconium. Meconium may itself promote the growth of bacteria in the lungs.
  • 41. Cyanotic Heart Disease Vs Pulmonary Disease Variables Cyanotic Heart Disease Pulmonary Disease History Previous sibling with congenital heart disease, Diagnosis of congenital heart disease by prenatal usg or echo Maternal fever, MSAF, Preterm Delivery Physical Examination Cyanosis , Gallop rhythm, or murmur, single second heart sound, Large liver, Mild respiratory distress Cyanosis , severe retraction, Split second heart sound Chest Radiograph Cardiomegaly, Decrease pulmonary vascularity Normal heart size, abnormal pulmonary parenchyma like total white lung, consolidation, prominent fissures, Ground glass apperance ABG Normal or Decreased PaCO2, Decreased PaO2 Increased PaCO2 ,Decreased Pao2 ECHO Abnormal Heart Or Vessels Normal Heart or vessels
  • 42. Congenital Diaphragmatic Hernia
  • 43. Approach to Respiratory Distress Is it Severe or Mild Respiratory Distress?? What is the Gestational Age of the baby?? Are there any known Congenital Anomalies? Review antenatal scan for CDH, TEF What was the Delivery Method? Are there any risk Factor for sepsis??  Is it a Respiratory or Cardiac Problem? Is there is poor improvement with increasing oxygen flow? Consider Persistent pulmonary hypertension or cyanotic heart disease if cyanosis and hypoxia are persistent. Is anything else causing Respiratory distress? Consider Metabolic ,Renal or Neurological cause
  • 44. Summary • Respiratory Distress Present as Tachypnea, nasal flaring, grunting and may proceed to respiratory failure if not recognized and managed • Cause of respiratory distress vary and not only lies in lung • If respiratory distress not improving , other causes of respiratory distress must be ruled out including congenital anomalies
  • 45. References • Avery’s Diseases of the Newborn. 9TH EDN. Chap.42,43,44,46. • Cloherty and Stark’ Manual of Neonatal care. 8TH EDN. Chap 32,33,35. • AIIMS Protocols in Neonatology. • OP Ghai, Textbook of Pediatrics, 8th edition • Respiratory Distress Syndrome – Dilemmas in management; Journal of neonatology;P.N Rao.2007;21(2):92-8 • Surfactant replacement therapy. Journal of neonatology;S.Kalra,D.Singh 23(2):163-8 • Respiratory Distress in Newborn/ • Breathe March 2016
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