approach to respiratory distress in neonates - dr amar naik

1. Respiratory distress in a
newborn baby

2. CASE 1
•B/O A
•1st issue
•Antenatal history -uneventful
•Term, Born by LSCS , meconium stained
liquor, CIAB ,shifted mother side
•12 hrs later developed tachypnea, so
shifted to NICU ,Required ventilation
•Spo2 rt upper limb 96, rt lower limb 89

3. ABG- Ph 7.12, PCO2-12, HCO3- 11
CXR-

5. CASE 2
Primi, Full term, 2.9 kg, Male child,
delivered by vaginal route
Cried immediately
Had respiratory distress & grunt
since birth
registered pregnancy
H/O poly-hydroamnios
No any drug history or any other
illness

6. On admission:
HR 168/min,RR 58/min,SPO2 92%
on room air,CRT 4sec
R/S:
shape:asymmetrical,
hyperinflsted
Air entry diminshed on Lt side,
Mediastinum shifted on Rt side
P/A: scaphoid

7. X-ray chest

8. CASE 3
33 wks,2.2 kg, male child deliverd by
LSCS(ivo dimished fetal activity and
fetal bradycardia)
Cried immediately
Had respiratory distress and grunt

9. On examination……
HR 165/min
RR 60/min
CRT 3sec
spo2 85% with NPO2 2 ltr/min
PP well felt
R/S: b/L air entry diminished
Grunting +nt, subcostal
retraction +nt
CVS :normal
CNS: normal

10. Rx:
non invasive ventilation given but
grunt & tachypnoea persist,so x ray
chest done

12. Inubated, required high pressure
surfactant given
Post surfactant FiO2 & pressure
requirement decreases

13. 6 hours Post surfactant x ray

14. CASE 4
Primi,Full term, 2.3 kg, Male
child,delivered by vaginal route in
Govt. hospital
Cried immediately
Had respiratory distress & grunt after
30 minutes of life

15. Unregistered pregnancy
H/O polyhydroamnios on 3rd trimester
scan 1 month back
No any drug history or any other
illness

16. On Examination…….
HR 175/min
RR 60/min
CRT 3sec
spo2 90% with NPO2 2 ltr/min
PP low volume,+nt on all 4 limbs
Fine white froathy bubbles of mucus
present(+nt) in mouth

17. R/S:
B/L air entry diminshed
B/L crepitation +nt,grunting +nt
subcostal retraction +nt
CVS:
S1 S2 heard,no murmer
P/A:
soft,but no gastric sounds on
auscultation

18. X-ray

19. CASE 5
•antenatal history uneventful
•Born by lscs
•Did not cry after birth
•Required suction stimulation, bag and
mask ventilation for 1.30 min, then
improved.
•Shifted to nicu
•o/e : HR- 100/min, RR-80/min, grunting
present, air entry normal
•Inv – ph-7.12, pco2- 20, Pa02-130,
hco3- 10

20. Respiratory distress
• Cause of significant morbidity and
mortality
• Incidence 4 to 6% of live births
• Many are preventable
• Early recognition, timely referral,
appropriate treatment essential

21. • RR > 60/ min*
• Retractions
• Grunt
• + Cyanosis
Respiratory distress

22. Pathophysiology considerations
unique to the newborn
Prolonged and unattended distress
leads to hypoxemia, hypercarbia and
acidosis. This leads to pulmonary
vasoconstriction and persistence of
fetal circulation with right to left
shunting through the ductus and
foramen ovale , thereby aggravating
hypoxemia.

23. Causes of respiratory distress -
Medical
• Respiratory distress syndrome (RDS)
• Meconium aspiration syndrome (MAS)
• Transient tachypnoea of newborn (TTNB)
• Asphyxial lung disease
• Pneumonia- Congenital, aspiration, nosocomial
• Persistent pulmonary hypertension (PPHN)
• Cardiac: Congenital heart disease, Ductus dependant
lesions, PDA of prematurity,
• Metabolic: Acidosis, hypoglycemia, polycythemia, anemia
• Shock due to any cause

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

25. Approach to respiratory distress
History
• Onset of distress
• Gestation
• Predisposing factors- PROM, fever
• Meconium stained amniotic fluid
• Asphyxia

26. Approach to respiratory distress
Examination
• Severity of respiratory
distress
• Neurological status
• Blood pressure, CFT
• Hepatomegaly
• Cyanosis
• Features of sepsis
• Look for malformations

27. Approach to respiratory distress
Chest examination
• Air entry
• Mediastinal shift
• Adventitious sounds
• Hyperinflation
• Heart sounds

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

29. Were there any risk factors in the antepartum
period or evidence of foetal distress prior to
delivery? (Birth asphyxia or PPHN)
Did the mother receive antenatal steroids if it
was a preterm delivery? (Antenatal steroids
decrease the incidence of HMD by 50%)
Was there a history of premature rupture of
membranes and fever? (congenital pneumonia
or sepsis)
Was there meconium stained amniotic fluid?
(MAS is a possibility)

30. A look at the antenatal ultrasonography (USG) for
the amount of amniotic fluid would tell us the status
of the foetal lung. (congenital anomalies of lung)
Was resuscitation required at birth? (resuscitation
trauma/PPHN/ acidosis)
Did the distress appear immediately or a few hours
after birth? (HMD appears earlier than pneumonia)
Was it related to feeding or frothing at the mouth?
(tracheo-esophageal fistula or aspiration)
Does the distress decrease with crying? (choanal
atresia).

31. For babies presenting later with distress we
have to ask a few other questions :-
Is the distress associated with feed refusal
and lethargy? (sepsis, pneumonia)
Did the distress appear slowly after starting
feeds? (IEM).
Is there a family history of early neonatal
deaths? (CHD, IEM).

32. Clinical Examination
A preterm baby weighing <1500 gms with retractions and
grunt is likely to have HMD.
A term baby born through meconium stained amniotic fluid
with an increase in the anterior- posterior diameter of the
chest (full chest) is likely to be suffering from MAS.
A depressed baby with poor circulation is likely to have
neonatal sepsis with or without congenital pneumonia.
A near term baby with no risk factors and mild distress may
have TTNB

33. An asphyxiated baby may have PPHN.
A growth retarded baby with a plethoric look may have
polycythaemia.
A baby with respiratory distress should be checked for
an air leak by placing a cold light source over the chest
wall in a darkened room.
A baby presenting with tachypnoea and a cardiac
murmur - congenital heart disease.
Inability to pass an 5F catheter through the nostril --
choanal atresia.

34. Congenital Pneumonia

36. Assessment of respiratory
distress
Score
*
0 1 2
1. Resp. rate
2. Central
<60
None
60-80
None with
>80
Needs
cyanosis 40% FiO2 >40% FiO2
3. Retractions None Mild Severe
4. Grunting None Minimal Obvious
5. Air entry Good Decreased Very poor
* Score > 6 indicates severe
distress

37. Silverman Andersons scoring
Score > 6 indicates severe distress

38. Investigations
• Gastric aspirate
• Polymorph count
• Sepsis screen
• Chest X-ray
• Blood gas analysis

39. Pulse oximetry
• Effective non invasive monitoring of
oxygen therapy
• Ideally must for all sick neonates and
those requiring oxygen therapy
• Maintain SaO2 between 90 – 95 %

40. 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

41. Arterial blood gas (ABG) analysis:
Blood gas is essential because with clinical
assessment and pulse oximetry alone, one
would not be able to assess PaO2, PCO2
and pH.
Normal & abnormal values:
PaO2: Pre-ductal PaO2 50–70 mmHg with an
O2 saturation of 87-93%. A PaO2 up to 80
mmHg is acceptable in term infants

42. PaO2:
Hypoxemia: PaO2<50 mmHg
Low normal oxygenation: PaO2 - 50-
60mmHg
Hyperoxemia: >80 mmHg in preterm
and >90 in term.
Hyperoxia is associated with adverse
effects like ROP and BPD due to
increase in the reactive oxygen
species (ROS).

43. PaCO2:
Normal PaCO2 is 35-45 mmHg
Acceptable upper limit: 45-50mmHg,
There is increasing evidence that the strategy of
permissive hypercapnia reduces the duration of
ventilation and decreases the severity of
bronchopulmonary dysplasia (BPD) .
Hypocarbia: <35 mmHg.
Hypocarbia with PaCO2<30 mmHg increases the
risk of periventricular leucomalacia (PVL) in
preterm neonates

44. Assessment of gas exchange
1)Alveolar-arterial Oxygen
gradient (A-aDO2)
2)a/A ratio
3)Oxygenation Index (OI)

45. A-aDO2 (alveolar arterial oxygen diffusion
gradient):
This is to be calculated as shown below.
A-a DO2 =PAO2 – PaO2
= [(PB-PW) × FiO2 – PaCO2/RQ] – PaO2
= [(760-47) × FiO2 – PaCO2/.8] – PaO2
Normally it ranges between 5-15, if breathing room
air.
A-aDO2 is considered to be abnormal if more than
40.

46. 2) a /A ratio:
Ratio of PaO2 to PAO2.
It is considered to be a better indicator of gas
exchange as the ratio is usually not affected by
changes in FiO2
Interpretation:
a) Greater than 0.8: Normal
b) Less than 0.6: indicates need for O2 therapy
c) Less than 0.15: severe hypoxemia

47. 3)Oxygenation Index (OI):
Recommended in babies
who are mechanically ventilated as this index
includes mean airway pressure (MAP).
OI = (MAP × FiO2 ×100) / PaO2
Interpretation:
a) OI 25 – 40: severe respiratory failure;
mortality risk is 50 – 60%
b) OI > 40: Mortality risk is >80%

48. A comparison of indices of respiratory failure in ventilated
preterm infants
N V Subhedar, A T Tan, E M Sweeney, N J Shaw
There was no evidence of a Significant
difference between the performance of the a/A
ratio, A-aDO2, and OI in predicting adverse
respiratory outcomes.
use of the OI is recommended because of its
ease of calculation.

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

50. Oxygen therapy*
Indications
• All babies with distress
• Cyanosis
• Pulse oximetry SaO2 <90%
Method
• Flow rate 2-5 L/ min
• Humidified oxygen by hood or nasal prongs
* Cautious administration in pre-term

53. [*Failure of CPAP (): Even on a CPAP of
7cmH2O and 70% FiO2if the neonate has
excessive work of breathing (or)
PCO2>60mmHg with pH <7.2 (or)
recurrent apnea or hypoxemia (PaO2 <50
mmHg), this should be considered as
failure of CPAP].

54. Respiratory distress syndrome
(RDS)
• Pre-term baby
• Early onset within 6 hours
• Supportive evidence: Negative shake test
• Radiological evidence

55. X-ray - RDS

56. Pathogenesis of RDS
• Decreased or abnormal surfactant
• Alveolar collapse
• Impaired gas exchange
• Respiratory failure

57. RDS - Predisposing factors
• Prematurity
• Cesarean born
• Asphyxia
• Maternal diabetes
RDS - Protective factors
• PROM
• IUGR
• Steroids

58. Antenatal corticosteroid
- Simple therapy that saves neonatal lives
• Preterm labor 24-34 weeks of gestation
irrespective of PROM, hypertension and
diabetes
• Dose:
Inj Betamethasone 12mg IM every 24 hrs X
2 doses; or Inj Dexamethasone 6 mg IM
every 12 hrs X 4 doses
• Multiple doses not beneficial

59. Surfactant therapy - Issues
• Should be used only if facilities for
ventilation available
• Cost
• Prophylactic Vs rescue

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

61. Meconium aspiration syndrome
(MAS)
• Meconium staining
- Antepartum, intrapartum
• Thin
- Chemical pneumonitis
• Thick
- Atelectasis, airway blockage,
air leak syndrome

62. Meconium aspiration syndrome
• Post term/SFD
• Meconium staining – cord, nails, skin
• Onset within 4 to 6 hours
• Hyperinflated chest

63. X-ray - MAS

64. MAS - Prevention
• Oropharyngeal suction before delivery of
shoulder for all neonates born through
MSAF
• Endotracheal suction for non vigorous*
neonates born through MSAF
*Avoid bag & mask ventilation till trachea
is cleared

65. Transient tachypnoea of newborn
(TTNB)
• Cesarean born, term baby
• Delayed clearance of lung fluid
• Diagnosis by exclusion
• Management: supportive
• Prognosis - good

66. X-ray- TTNB

67. Congenital pneumonia
Predisposing factors
PROM >24 hours, foul smelling liquor,
Peripartal fever, unclean or multiple
per vaginal
Treatment
Thermoneutral environment, NPO, IV
fluids, Oxygen, antibiotics-
(Amp+Gentamicin)

68. X-ray – Congenital pneumonia

69. Nosocomial pneumonia
Risk
Factor
: Ventilated neonates
: Preterm neonates
Prevention : Handwash
: Use of disposables
: Infection control measures
Antibiotic
s
: Usually require
higher antibiotics

70. Respiratory distress in a neonate with
asphyxia
• Myocardial dysfunction
• Cerebral edema
• Asphyxial lung injury
• Metabolic acidosis
• Persistent pulmonary hypertension

71. Pneumothorax
Etiology
Spontaneous, MAS, Positive pressure
ventilation (PPV)
Clinical features
Sudden distress, indistinct heart sounds
Management
Needle aspiration, chest tube

72. X-ray - Pneumothorax

73. Persistent pulmonary
hypertension (PPHN)
Causes
• Primary
• Secondary: MAS, asphyxia, sepsis
Management
• Severe respiratory distress needing
ventilatory support, pulmonary
vasodilators
• Poor prognosis