The document discusses respiratory distress in neonates. It describes the clinical presentation of respiratory distress and various scoring systems used to assess severity. It then covers the major causes of respiratory distress including transient tachypnea of the newborn, respiratory distress syndrome, meconium aspiration syndrome, pneumonia and others. For each cause, it discusses risk factors, clinical features, investigations and management. The management sections provide details on oxygen therapy, CPAP, surfactant administration and mechanical ventilation.

1. Respiratory distress in neonates
Presenter- Dr. Aftab Ahmad Siddiqui
Moderators- Prof. S M Ali, Prof. F. K Beig, Dr. K Afzal, Dr. Kashif Ali,
Dr. Shaukat, Dr. Iraj Alam

2. Presence of at least 2 of the fallowing features are essential
1)Tachypnea (RR>60 PER MIN..)
2)Retractions (intercostal retractions and /or sub costal)
3) Expiratory grunt
Introduction

3. Clinical presentation of respiratory
distress in the newborn includes;
 cyanosis,
 grunting,
 inspiratory stridor,
 nasal flaring,
 poor feeding,
 tachypnea (more than
60 breaths per minute),
 Lethargy.
 retractions in the:
 intercostal,
 subcostal, or
 suprasternal spaces.

4. Perinatal history
h/o of polyhydramnios -- congenital diaphragmatic hernia/TEF
h/o of oligohydramnios -- pulmonary hypoplasia
h/o of PROM -- congenital pneumonia
h/o of pretem delivery -- respiratory distress syndrome
h/o of MSAF -- meconium aspiration syndrome

5. Perinatal history
 IUGR with Resp. distress -- Congenital infection/MAS
 LGA with Resp. distress -- Decreased surfactant/
Polycythemia/CHD
 Well baby for 1-2 days then resp. distress -- Sepsis/IEM

6. Obstruction of the airway Lung parenchymal disease
1- Choanal atresia
2- Congenital stridor
3- Tracheal or bronchial stenosis
1- Meconium aspiration
2- Respiratory distress syndrome
3- Pneumonia
4- Transient tachypnea of the newborn
(retained lung fluid)
5- Pneumothorax
6- Atelectasis
7- Congenital lobar emphysema
Non-pulmonary causes Miscellaneous
1- Heart failure
2- Intracranial lesions
3- Metabolic acidosis
1- Disorders of the diaphragm e.g.
(diaphragmatic hernia)
2- Pulmonary haemorrhage
3- Pulmonary hypoplasia
CAUSES OF RESPIRATORY DISTRESS

8. 0 1 2
Cyanosis None In room air In 40% FIO2
Retractions None Mild Severe
Grunting None
Audible with
stethoscope
Audible without
stethoscope
Air entry Clear
Decreased or
delayed
Barely audible
Respiratory
rate
Under 60 60-80 Over 80 or apnea
Score:
> 4 = Clinical respiratory distress; monitor arterial blood gases
> 8 = Impending respiratory failure
DOWNE’s SCORING OF RESPIRATORY DISTRESS

9. SILVERMAN- ANDERSON RETRACTION
SCORE FOR PRETERMS

10. SILVERMAN-ANDERSON
RETRACTIONSCOREFORPRETERMS
 A score of 7 or more is indicative of impending resp. failure.

11.  SOME IMPORTANT CAUSES OF RESPIRATORY DISTRESS ARE DESCRIBED IN
SOME DETAIL
 Choanal Atresia
 Tracheoesophageal fistula
 Transient tachypnea of newborn
 Hyaline Membrane disease (RDS)
 Meconium Aspiration Syndrome
 Congenital pneumonia
 Pneumothorax

12. Choanal Atresia
 The back of the nasal passage (choana) is blocked, usually by
abnormal bony or soft tissue (membranous).
 Bilateral choanal atresia is a serious life-threatening condition as babies
are obligate nasal breathers.
 The distress may improve when the baby cries.

13. Choanal Atresia
 Choanal atresia. Rhinogram
demonstrating blockage of
radiopaque dye at the posterior
choanae.
 Oral airway which is the initial
treatment of choice can also be
seen.

14. Tracheo-esophageal fistula
 A tracheoesophageal fistula (TEF) is a congenital communication between the
trachea and esophagus.

15. Tracheo-esophageal fistula
 Clinical features-
 Maternal polyhydramnios and absence of stomach gas on prenatal
ultrasound.
 Copious, fine white frothy bubbles of mucus in the mouth and nose.
Secretions recur despite suctioning.
 Episodes of coughing and choking in association with cyanosis esp. during
feeding.
 Inability to pass a NG/OG tube.

16. Tracheo-esophageal fistula

17. TRANSIENT TACHYPNEA OF THE
NEWBORN (TTN)
 A very common cause of neonatal respiratory distress,
constituting about 40 percent of cases.
 Infants are usually full term/late preterm.
 They are not at risk for other illnesses.

18.  It occurs due to delayed clearance of fetal lung fluid.
 Change in hormonal milieu (surge in glucocorticoids and
catecholamines) near end of pregnancy and labor facilitates
fetal lung fluid clearance.
 Risk for TTN increases if normal labor is bypassed
(Caessarian/Precipitate labor).

19.  RISK FACTORS:
 cesarean delivery
 Precipitous labor
 Preterm birth
 Male sex
 Macrosomia,
 Maternal diabetes
 Maternal Asthma
 Multiple gestation

20. CLINICAL PICTURE- TTN
 Tachypnea immediately after birth or within 6 hours with mild
respiratory distress.
 A-P diameter of chest may be increased (barrel shape).
 Usually responds to supplemental Oxygen @ FiO2 <40 %.
 Respiratory failure and mechanical ventilation are rare.
 Symptoms usually last 12 to 24 hrs but in severe cases it can last till
72 hours.

21. TTN
Radiological features of TTN-
 Retained lung fluid with characteristic
prominent perihilar streaking (sun-burst
pattern)
 Coarse fluffy densities may reflect
alveolar edema
 Hyperinflation with widening of
intercostal spaces.
 Fluid filled interlobar fissure.

22. TREATMENT- TTN
 It is supportive with close observation because the condition is
usually self limited.
 Low flow supplemental oxygen may be necessary for several
hours.
 More severe cases- CPAP.
 Oral furosemide (Lasix) has not been shown to significantly
improve status and should not be given

23. 23
Respiratory distress
syndrome
- RDS
(hyaline membrane
disease)

24. • Inadequate pulmonary surfactant due to preterm birth.
• Alveoli with low surfactant tend to collapse, leading to atelectasis,
VQ mismatching, hypoxemia and respiratory acidosis.
•Repetitive reopening & collapse of alveoli can damage the fragile
lung architecture leakage of protein-debris into the airways
(hyaline membranes).
•These debris impair the function of what little surfactant is present.
RDS- Introduction

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

28. RDS- Introduction
 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

29. Incidence of respiratory problems in preterms

30. RISK FACTORS-RDS
 Prematurity
 Maternal diabetes
 Caesarean delivery without preceding labor
 Precipitous labor
 Foetal asphyxia
 Genetic factors (white race, history of RDS in siblings, male
sex).
 Thoracic malformations that cause lung hypoplasia, such as
diaphragmatic hernia

31. Secondary surfactant deficiency may occur in infants with the
following:
 Pulmonary infections (eg, group B beta-hemolytic streptococcal
pneumonia)
 Pulmonary hemorrhage
 Meconium aspiration pneumonia
 Oxygen toxicity along with barotrauma or volutrauma to the lungs

32. Prenatal Prediction-RDS
 Assessment of fetal lung maturity (FLM)- testing amniotic fluid obtained by
amniocentesis.
 Lecithin/Sphingomylin ratio- Risk is very low if the L/S ratio is >2
 The TDx-FLM II- measures the surfactant-albumin ratio, >55mg
surfactant/gm albumin correlates with lung maturity.
 Lamellar body counts- >50,000 lamellar bodies/microliter predicted lung
maturity.
 Presence of Phosphatidyglycerol (PG)
 Foam stability index (FSI)- stability foam when amniotic fluid is shaken
with ethanol.

33. CLINICAL COURSE-RDS
 Signs of RDS start in minutes to hours after birth
 Tachypnea, prominent (often audible) Grunting, Flaring, Retractions,
and Cyanosis relatively unresponsive to oxygen
 Breath sounds normal or harsh bronchial
 Crepitations esp over posterior lung bases
 RDS tends to get worse over the first 1 to 3 days after birth, and then
usually improves gradually over a few days

34.  Tachypnoea and grunting may decreases or disappear with fatigue and
apnoea may occur.
 Initially, ABG or SpO2 may show only hypoxemia or desaturation. The
PaCO2 may be normal because of tachypnea.
 Later, with fatigue, the PaCO2 will rise - respiratory acidosis. With
imminent respiratory failure, there may be metabolic acidosis due to
inadequate oxygen delivery to tissues. (Mixed acidosis)
 If inadequately treated, hypotension, fatigue, cyanosis, and pallor
increase- MODS.
CLINICAL COURSE-RDS

35. Investigations-RDS
 ABG/Capillary blood gas – low PaO2, high PaCO2, respiratory/mixed
acidosis.
 Chest X-ray (AP&Lat) – Reticulogranular (ground-glass) pattern and air
bronchograms, lungs are diffusely and homogeneously dense due to
widespread collapse of alveoli with low lung volume.
 Blood glucose, Electrolytes, RFT
 Complete blood count
 Blood culture

36. X-Ray RDS

37. Management-RDS
1. Warmth - radiant warmer/ incubator
2. Maintain Hydration
3. Nutrition
a) Initially D5W or D10W (with protein, if
possible)
b) NPO if RR > 60 or moderate/severe
work of breathing
c) Gavage feeds if stable
d) Consider parenteral nutrition if
enteral feeds are delayed
4. Antibiotics if at risk for pneumonia/sepsis
5. Supplemental oxygen
6. SpO2 monitoring, with appropriate target
for infants at risk for ROP.
7. Exogenous surfactant
8. CPAP or mechanical ventilation, as
needed.

38. Management-RDS
 Oxygen Therapy
 Target SpO2
 <30 weeks or wt< 1.250gm – 88 to 92 %
 >30 weeks or wt > 1.250gm- 88 to 95%
 Blood gas monitoring- Frequent measurements during acute
stage, do ABG after 30 min of changes in FiO2/ventilator setting.

39. Management-RDS
 CPAP
 Indication- In infants with RDS start CPAP as soon as possible.
 The most common cause of failed CPAP is ???
 Starting pressure 5 to 7 cm H2O, at flow of 5 to 10 L/min, FiO2
titrated to target SpO2.
 Use OG tube to decompress swallowed air.
 As the infant improves, start tapering FiO2, when FiO2 requirement
is 0.3 bring CPAP to 5 cm H2O.
 Discontinue CPAP if no distress and FiO2 remains <0.3.

40. Bubble CPAP

41. Management-RDS
 Problem encountered with CPAP
 Decreased venous return.
 Raised pulmonary vascular resistance – increased Rt to Lt. shunt.
 Hypercarbia- if CPAP is too high with low tidal volumes.
 Nasal prongs may fail to generate pressure if crying or mouth
opening.
 Pulmonary air leak syndromes
 Damage to nasal septum

42. Management-RDS
 Surfactant Therapy
 Indicated for all diagnosed cases of RDS.
 “Early rescue” (before 2 hours of age) is preferable to delayed
treatment.
 Prophylactic surfactant can be given in very premature (<27
weeks) neonates.
 Repeated doses (upto 4) can be given, most infants require only
one or two doses.

43. Management-RDS
Administration of Surfactant –
 Given through endotracheal tube – If not on ventilator use ‘INSURE’
technique (INtubate SURfactant Extubate).
 Given as bolus through ET tube as rapidly as tolerated.
 Neonates posture can be changed to allow better distribution of
Surfactant (though no evidence supports this practice).
 If intubation is difficult/risky LMA can be used.

44. Surfactant Preparations and their sources
Doses (*use package insert)
Curosurf - 2.5 mL/kg (200 mg/kg
phospholipid)
Infasurf - 3 mL/kg (105 mg/kg
phospholipid)
Survanta - 4 mL/kg (100/kg mg
phospholipid)
Exosurf - 5 ml/kg

45. SURFACTANT
Surfactant therapy reduces mortality rates most effectively in infants
<30 weeks and those of birth weight <1250 gm
45

46. Management-RDS
 Mechanical Ventilation
 Indications-
 Respiratory acidosis with a
PaCO2 >55 mm Hg or rapidly
rising,
 PaO2 <50 mm Hg or SPO2 <90%
with an Fio2 above 0.50.
 Severe Apnoea
 Ventilator settings-
 Rapid rates
 Moderate Peep (4-6 cm H2O)
 Low PIP
 Short Ti 0.24-0.4 sec
 Low tidal volume 3-6 ml/kg
 Early extubation to nasal CPAP

47. Congenital pneumonia
 Pneumonia that presents within the first 24 hours after birth.
 The 3 categories of congenital pneumonia are as follows:
 True congenital pneumonia - already established at birth, infection occurs
by Hematogenous, Ascending or Aspiration.
 Intrapartum pneumonia - acquired during passage through the birth
canal.
 Postnatal pneumonia - originates after the infant has left the birth canal
*Pneumonia in association with sepsis presenting beyond 24 hrs is well known
and not discussed here.

48. Congenital pneumonia
 Etiology
 Group B Streptococcus (GBS)
 Escherichia coli
 Haemophilus influenza
 Other gram-negative bacilli
 Listeria monocytogenes
 Enterococci
 Occasionally, Staphylococcus aureus
 Rarely, Mycoplasma pneumonia/Ureaplasma urealyticum

49. Congenital pneumonia
 Etiology- Atypical organisms
 Cytomegalovirus
 Treponema pallidum
 Toxoplasma gondii
 Rubella
 Neisseria gonorrhoeae
 Congenital tuberculosis
 Congenital candidiasis

50. Congenital pneumonia
 Etiology – Developing countries
 Escherichia coli
 Enterobacter aerogenes
 Group B streptococci
 Klebsiella
 Pseudomonas
 Staphylococcus

51. AP X ray in an infant born at 28 weeks‘ was performed following apnea and
profound birth depression. Subtle reticulogranularity and prominent distal air
bronchograms were consistent with respiratory distress syndrome, prompting
exogenous surfactant and antimicrobial therapy. Initial smear of endotracheal
aspirate revealed few neutrophils but numerous, small, gram-negative
coccobacilli. Culture of blood and tracheal aspirate yielded florid growth of
nontypeable Haemophilus influenzae.
Case 1

52. Full-term infant with progressive respiratory distress from birth following delivery to a
febrile mother through thick, particulate, meconium-containing fluid and recovery
of copious meconium from the trachea. Right clavicle is fractured without
displacement. Note the coarse dense infiltrates obscuring the cardiothymic
silhouette bilaterally with superimposed prominent air bronchograms. Listeria
monocytogeneswas recovered from the initial blood culture.
Case 2

53. Congenital pneumonia
 Work up-
 CBC, CRP
 Blood gases, B. Glucose, Electrolytes, RFT, Blood culture
 Imaging- X-ray, USG, CT
 Tracheal aspirate
 Bronchoscopy

54. Congenital pneumonia
 Treatment
 Supportive measures (oxygen, warmth, hydration, nutrition
etc)
 Antimicrobial therapy
 Respiratory support ( airway patency, CPAP, Ventilation)
 Maintain optimal hemoglobin (13-16 g/dL)

55. Meconium aspiration syndrome(MAS)
 Acute or chronic hypoxia and/or infection can result in the passage of
meconium in utero.
 5% of neonates born through MSAF develop meconium aspiration
syndrome (MAS).
 Meconium itself, or the resultant chemical pneumonitis, mechanically
obstructs small airways, causes atelectasis and a “ball-valve” effect.

56. Meconium aspiration syndrome
 MAS classification-
 Mild MAS- requiring <40% oxygen for <48 hours.
 Moderate MAS- requiring >40% oxygen for >48 hours without air leak.
 Severe MAS- requiring assisted ventilation for >48 hours, often
associated with PPHN.

57. There are bilateral course interstitial markings and widespread
alveolar opacification.

58. MAS- Treatment
 Supportive measures, Oxygen, Antibiotics
 Respiratory Support
 CPAP- consider CPAP if FiO2 requirement is > 0.40
 Mechanical ventilation- if excessive carbon dioxide retention (Paco2 >60
mm Hg) or persistent hypoxemia (Pao2 <50 mm Hg).
PIP requirement is high (30-35 cm H2O), PEEP selected 3-6 cm H2O,
Adequate expiratory time should be permitted (I:E=1:2 or 1:3).

59. MAS- Treatment
 Surfactant –
 Endogenous surfactant activity may be inhibited by meconium.
 Used in infants with deteriorating course and who require escalating
support.
 Washing meconium from the lungs with bronchioalveolar surfactant
lavage is not recommended.

60. Pneumothorax
 Spontaneous pneumothorax occurs in 0.07% of otherwise healthy
appearing neonates.
 One in ten of these infants is symptomatic.
 More common in newborns treated with mechanical ventilation.

61. There is a large right pneumothorax demonstrated on AP and lateral films
with a pig-tail catheter in situ with its tip at the apex.

62. Pneumothorax
 Treatment-
 Conservative therapy – if no underlying lung disease or complicating therapy
(ventilator), no significant respiratory distress, and have no continuous air leak.
The extrapulmonary air will usually resolve in 24 to 48 hours.
 Needle aspiration- Thoracentesis with a “butterfly” needle or intravenous
catheter. Needle aspiration may be curative in infants not receiving
mechanical ventilation.
 Chest tube drainage- needed esp. in those on ventilator. These air leaks are
continuous and will result in severe hemodynamic compromise if left untreated

63. Thank you