1. Respiratory distress in Newborn
Dr. Kalpana Malla
MD Pediatrics
Manipal Teaching Hospital
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2. FREQUENT CAUSES
• Medical
• TTNB – transient tachypnoea
• RDS(HMD)
• Aspiration syndromes
• Pneumonia/sepsis
• PPHN
• CCF
• Acidosis

3. FREQUENT CAUSES
• Surgical
• Pneumothorax
• Diaphragmatic hernia
• TEF
• Lobar emphysema
• Phrenic nerve paralysis

4. Resp distress – above
downwards
1) Airway obstruction
A) Nasal – choanal atresia
nasal edema
B) Oral cavity – macroglossia, micrognathia,
Glosoptosis
C) Laryngeal obstruction – laryngeal web
- Subglottic stenosis of larynx
- Laryngomalacia
- cord paralysis

5. Resp distress – above downwards
D) Neck obstruction – cystic hygroma
- cong goitre
E) Tracheal obsruction –
- Tracheomalacia
- TEF
- Tracheal stenosis

6. 2) Lung parenchyma
• Aspiration syndrome (MAS)
• Resp distress syndrome (HMD)
• TTNB
• Pneumonia
• Pleural effusion
• Pulmonary hemorrhage
• Air leak – Pneumothorax,
pneumomediastinum

7. 3) Developmental defects
• Agenesis of lung
• Hypoplasia of lung
• Diagphratic hernia
• Tracheal agenesis
• TEF

8. 4) Extrapulmonary
• B. asphyxia
• CCF
• Metabolic acidosis
• Persistent pulmonary hypertension

9. TRANSIENT TACHYPNEA OF
THE NEWBORN

10. GENERAL ASPECTS
• Occasionally called respiratory
distress syndrome type II
• Mild and self-limited
• Usually term infants, C/S and
maternal IV fluids associated
• The distinctive features of
transient tachypnea are sudden
recovery of the infant

11. Pathogenesis
• Secondary to slow absorption of
fetal lung fluid resulting in
decreased pulmonary compliance
and tidal volume and increased
dead space

12. CLINICAL MANIFESTATIONS
• Increased RR, no retractions, mild
cyanosis - relieved by minimal
oxygen (<40%)
• Expiratory grunting
• Recover rapidly within 3 days
• Lungs are generally clear
without rales or rhonchi

13. CXR
• Prominent pulmonary vascular markings
• Fluid lines in the fissures
• Over aeration
• flat diaphragms
• occasionally, pleural fluid

14. CXR
• Distinguishing from HMD may be
difficult
• Absence reticulogranular
pattern or air bronchograms in
CXR

15. TREATMENT
• Nothing to do
• General supportive measures
• Oxygen
• IVF
• Ventilation not required
• Subsides on its own

16. HYALINE MEMBRANE DISEASE

17. INCIDENCE
• Common in premature infants
• Incidence is inversely proportional to
gestational age and birth weight
• 60–80% in < 28 wk of gestational age
• 15–30% in between 32 and 36 wk
• 5% > 37 wk
• Rare at term

19. INCREASED RISK FACTORS
• Infants of diabetic mothers
• Delivery before 37 wk gestation
• Multifetal pregnancies
• Cesarean section delivery
• Precipitous delivery
• Asphyxia
• Cold stress
• History of previously affected
infants

20. DECREASED RISK FACTORS
• Chronic or pregnancy-associated
hypertension
• Maternal opiate addiction
• Prolonged rupture of membranes
• Antenatal corticosteroid use

21. PATHOPHYSIOLOGY
• Surfactant deficiency - decreased
production and secretion
• Present in amn.fluid:28-30wks, mature
levels after 35 wks
• Surfactant reduce surface tension and
prevent the collapse alveoli
• Alveolar atelectasis, hyaline
membrane formation, and interstitial
edema make the lungs less
compliant, so greater pressure is
required to expand the small alveoli

22. PATHOPHYSIOLOGY (CONTD…)
• Decreased lung compliance- insufficient
alveolar ventilation – result in hypercapnia
• Combination of hypercapnia, hypoxia, and
acidosis → pulmonary arterial
vasoconstriction → increased R → L
shunting through the foramen ovale and
ductus arteriosus → Pulmonary blood flow
is reduced → ischemic injury cap
endothelium & alveolar epithelium → leak
of plasma (proteinaceous material) into
the alveolar spaces

23. PATHOPHYSIOLOGY (CONTD…)
• leak of plasma (proteinaceous
material) into the alveolar
spaces →combine with fibrin &
necrotic alveolar pneumocytes &
form hyaline membrane
• Hyaline membranes: coagulum of
sloughed cells and
exudate, plastered against epithelial
basement membrane

24. CLINICAL MANIFESTATIONS
• Resp distress - tachypnea ,
Intercostal and subcostal retractions
Nasal flaring
• Grunting
• Cyanosis - relatively unresponsive to
oxygen
• Progressive worsening of cyanosis
and dyspnea
• Breath sounds : harsh tubular quality,
fine rales

25. PROGRESSION
• Severity peaks at 24-48 hours, resolution
by 72-96 hours (without surfactant
therap
• If not treated, BP may fall; fatigue,
cyanosis, and pallor increase, and
grunting disappears as the condition
worsens
• Apnea and irregular respirations :
ominous
• Mixed respiratory-metabolic acidosis
• Respiratory failure

26. OUTCOME
• Death is rare on the 1st day
• Death occurs at 2 -7 days
• Associated with alveolar air
leaks (interstitial
emphysema, pneumothorax) and
pulmonary hemorrhage or IVH

27. DIAGNOSIS
• CXR : fine reticular
granularity of the
parenchyma and air
bronchograms :
typical pattern
developing at 6–12hr

28. Diffused reticulogranular pattern

29. • CXR- Later:
• ground glass
opacity
• ABG : progressive
hypoxemia, hyperc
apnia, and
variable metabolic
acidosis

30. Ground glass opacity

31. DIFFERENTIAL DIAGNOSIS
• Early-onset sepsis: group B
streptococcus
• Pneumonia
• Cyanotic heart disease
• Persistent pulmonary HTN
• Transient tachypnea of newborn

32. DIFFERENTIAL DIAGNOSIS
• Spontaneous pneumothorax
• Pleural effusion
• Diaphragmatic hernia
• Lobar emphysema

33. PREVENTION
• Prevention of prematurity
• Lecithin:sphingomyelin ratio in
amniotic fluid: >2 means mature lungs
<1.5 means HMD
• Betamethasone to women 48hr before
the delivery - between 24 and 34 wk of
gestation- 6mg IM for 4 doses 12 hrs
apart or 12 mg IM for 2 doses 12 hrs
apart

34. PREVENTION (CONTD…)
• First dose of surfactant into the
trachea of symptomatic premature
baby immediately after birth
(prophylactic) or during the first
few hours of life (early rescue)

35. TREATMENT: SUPPORTIVE
• Avoid hypothermia
• IV Calories and fluids
• Warm humidified oxygen
• CPAP : prevents collapse of
surfactant-deficient alveoli
• Assisted ventilation
• High-frequency ventilation (HFV )

36. SURFACTANT THERAPY : DEFINITIVE
TREATEMENT
• Multidose endotracheal instillation :
4ml/kg
• Treatment (rescue) is initiated as soon
as possible in the 1st 24hr of life
• Dose repeated - via the ET tube 6–
12hrly for a total of 2-4 doses
• Appropriate monitoring equipment
must also be available - radiology,
blood gas laboratory, and pulse
oximetry

37. Severe (RDS) - Cystic areas in the right
lung represent dilated alveoli or early
pulmonary interstitial emphysema

38. Acute Complications
• Air Leak Syndromes
– Consider with sudden change in
condition
– More common if baby receiving
ventilatory support
– Pneumothorax most common
• Therapy
– None if stable
– Oxygen 100%
– Thorocentesis: Needle or tube

39. Complication of RDS: right tension
pneumothorax and pneumomediastinum

40. Acute Complications
• Intracranial Hemorrhage
– More common at lower gestational ages
– Rare above 33 weeks gestation
• Suspect if there is a sudden change in
condition
• May coincide with development of air
leak
• Signs: change in Fontanel, perfusion

41. MECONIUM ASPIRATION

42. GENERAL ASPECTS
• Meconium-stained amniotic fluid
is found in 10–15% of births
• Meconium aspiration pneumonia
develops in 5% of such cases
• 30% of them require mechanical
ventilation
• 3–5% expire

43. Risk Factors for Meconium Passage
• Post term pregnancy
• Pre-eclampsia - eclampsia
• Maternal hypertension
• Maternal diabetes mellitus
• Abnormal fetal heart rate
• IUGR
• Oligohydramnios

44. AETIOIOGY
• Precise mechanisms remain unclear
• Theory - to explain the passage of meconium in
utero - The fetal bowel has little peristaltic
action and the anal sphincter is contracted
• It is thought that hypoxia and academia cause
the anal sphincter to relax, whilst at the same
time increase the production of motilin, which
promotes peristalsis.

45. Meconium Aspiration Syndrome
Pathophysiology
 Airway obstruction of large and small airways
 Inflammation and edema
 Protein leak
 Inflammatory Mediators
 Direct toxicity of meconium constituents =
chemical pneumonitis
 Surfactant dysfunction or inactivation
 Effects of in utero hypoxemia and acidosis
 Altered pulmonary vasoreactivity (PPHN)

46. Meconium Aspiration Syndrome
Diagnosis
 Known exposure to meconium
stained amniotic fluid
 Respiratory symptoms not explained
by other cause
 R/O pneumonia, RDS
 Spontaneous air leak

47. CLINICAL MANIFESTATIONS
• Either in utero or with the 1st breath
meconium is aspirated into the lungs
• Tachypnea, retractions, grunting, and
cyanosis : small airway obstruction
• Partial obstruction of some airways may
lead to pneumothorax or
pneumomediastinum
• Overdistention of the chest prominent
• Tachypnea may persist for many days or
even several weeks

48. INVESTIGATIONS
 CXR - diffuse, patchy
infiltrates, consolidation,
atelectasis, air leaks,
hyperinflation
• ABG

49. Meconium in Amniotic Fluid
Intrapartum suctioning of
mouth, nose, pharynx
Infant Depressed
Infant Active
Intubate and
Observe
suction trachea
Other resuscitation as indicated

50. Meconium Aspiration Syndrome
Treatment
• Ventilation strategies
Avoid air leak, check CXR
Generous O2
Ventilator
• Steroids ( controversial)
• Antibiotics (ampicillin, gentamicin)
• Surfactant
• Inhaled Nitric Oxide

51. Other Things to Watch For
• Hypoxia
• Acidosis
• Hypoglycemia
• Hypocalcemia
• End-organ damage due to perinatal
asphyxia

52. PREVENTION
• Fetal distress - initiating prompt
delivery
• Immediate DeLee suctioning of
the oropharynx after the head is
delivered

53. PROGNOSIS
• High incidence long term
pulmonary problems include -
• At 6 months - 23% MAS with
regular bronchodilator therapy*
• symptomatic
cough, wheezing, and persistent
hyperinflation for up to 5–10 yr.

54. Meconium Aspiration Syndrome
Outcome
The ultimate prognosis depends on
the extent of CNS injury from asphyxia
- Increased risk of poor neurologic
outcome due to perinatal insult -
seizures, CP, mental retardation

55. Thank you
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Medical Post [ www.themedicalpost.net ]