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 MF.et 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

9. 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

10. 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,

11. 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

14. ANC (Review by Monroe chart)
Hb,PCV (>40,<65)

15. 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.

19. 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

20. 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 et.al)
• 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)

21. 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.

22. 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.

23. 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

24. 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.

25. 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)

26. 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

27. 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.

28. 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 )

29. 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.

30. 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)

31. 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

32. 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)

33. 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.

34. 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.

35. Risk factors
• Risk factors:
1.Prematurity,
2. C-sec delivery without preceeding
labour,
3. Male baby,
4. F/H/O Asthma esp.in
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

36. 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).

37. 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 et.al,1996;Liem et
al,2007;Schaubel et al,2006)

39. 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

40. 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)

41. 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

42. 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)

43. 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.

46. • 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

47. CXR: MAS
Diffuse fluffy infiltrates.
Coarse patches of atelectasis.
HYPERINFLATED lung base.barrel shaped chest.

48. 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

49. 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.

50. 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

51. Congenital Diaphragmatic Hernia

52. 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

53. 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

54. 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/pedsinreview.aappublications.org
• Breathe March 2016

55. THANK YOU.