2. Common cause of respiratory distress in
newborn
Transient
tachypnea in
newborn
Congenital
pneumonia
Respiratory
distress
syndrome
Meconium
aspiration
syndrome
Pneumothorax
3. Signs of respiratory distress in newborn
• Nasal flaring
• Grunting
• Forced inspiration against a partially closed glottis
• Stridor
• Harsh sound caused by partially obstructed extra-thoracic airway- more commonly
heard on inspiration
• Wheezing
• Produced by partial obstruction of the lower airways more commonly heard during
exhalation
• Rhonchi
• Crackles
4. Grunting
• It generally occurs throughout the expiratory phase of breathing, and
represents breath against a partially closed glottis
• It may be considered a self administered form of peak end expiratory
pressure; by maintaining a high pressure more oxygen diffuses into
the blood in the lungs.
6. Transient tachypnea in newborn
• TTN is caused by retained lung fluid or slow resorption of the lung
fluids (impaired clearance of lung fluids right after delivery)
• It usually resolves within 48-72 hours of life
• Risk factors
• Infants born via caesarean section without precipitation of labor
• Can occur in any gestational age infants
• Infants of mother with gestational diabetes mellitus
• infants with poor respiratory effort (as a result of placental passage of
analgesics drugs)
• Maternal asthma
7. • Signs and symptoms
• Tachypnea (>60 breaths per minute)
• Nasal flaring
• Grunting
• Retractions
• On auscultation: clear lung fields/ crackles
• Cyanosis (usually requiring FiO2 not more than 40%)
8. • Radiography
• Fluid in interlobar fissure
• Hyperinflated lungs
• Falattened diaphragms
• Prominent vasculature in a sunburst
pattern
• Fluffy densities –alveolar edema
• Air bronchograms and reticulogranular
pattern are not seen (if these are
present, it suggest another pulmonary
pathology such as RDS or pneumonia
10. Congenital pneumonia
• Acquired through the transplacental/ transcervical route during or
after birth
• Ascending infection through the cervix, with or without rupture of the
amniotic fluid membranes may results in multiple infection including
congenital pneumonia
• Common organisms of the maternal genitourinary tract that are
causing these infections are
• Group B streptococcus, E.coli, hemophilus influenza klebsiella and herpes
simplex virus
11. • Risk factors
• Low birth weight infant
• preterm (as maternal humoral immunity may protect the fetus against some
neonatal pathogens, nonetheless various deficiencies of the neonatal
antimicrobial defense are probably > important than maternal immune
status)
• Maternal choriamnionitis
• PROM >18H
12. • Signs and symptoms
• Respiratory distress
• Poor feeding
• Apnea
• Tachycardia
• Poor perfusion
• Blood investigation
• Raised in TWC suggesting infection
• Radiographs
• Bilateral alveolar opacities with air
bronchograms
13. • Management
• Mainstay of treatment is antibiotic therapy – combination of IV c- penicillin
and gentamicin for atleast 5-10 days is effective treatment for most organisms
responsible / ampicillin and cefotaxime is an alternative choice of treatment
• Supportive measures (assisted ventilation and cardiovascular support)
14. Neonatal respiratory distress syndrome
• Occurs after the onset of breathing and associated with on
insufficiency of pulmonary surfactant
• Symptoms onset immediately after birth
• Symptoms
• Tachypnea
• Nasal flaring
• Grunting (generally grunt to produce positive pressure to keep alveoli open)
• Retractiosn
• Cyanosis
15. • Risk factors
• Premature (with immature
lung/surfactant ratio)
• Delivery of previous preterm infant with
RDS
• Maternal diabetes
• Hypothermia
• Fetal distress/ asphyxia
• Male infants
• White race
• Radiography
• Low lung volume
• Diffused ground glass appearance with
air bronchograms
16. • Management
• Giving antenatal corticosteroids between 24-34 weeks of gestation can
decrease the risk of RDS (single dose of antenatal corticosteroid is beneficial if
given >24H before delivery and provides coverage for 7 days)
• Respiratory support that reduced the risk of atelectasis (eg: CPAP, BiPAP)
• Persistent respiratory distress – intubate
• Surfactant can also be given
17. Meconium aspiration syndrome
• Meconium stained should be considered as a sign of fetal distress in all
infants (presence of meconium in the amniotic fluid suggest in utero
distress with asphyxia, hypoxia and acidosis)
• Release of inflammatory factors following the aspiration of the meconium
(which causes airway obstruction gas trapping alveolar rupture)
• Deactivation and decrease production of surfactant
• Signs and symptoms
• Tachypnea
• Retractions
• Grunting
• Nasal flaring
• Cyanosis
Developed right after delivery
19. • Treatment
• Primarily respiratory support
• General supportive care and assisted ventilation
• Since PPHN is often accompanied by meconium aspiration, infants with
PPHN-like presentation should be treated for PPHN
• Conventional or high frequency ventilation, surfactant therapy,and inhaled
nitric oxide can be given in severe hypoxia
• Extracorporeal membrane oxygenation (ECMO) may be beneficial if the
hypoxia does not subside with other therapy
20. Pneumothorax
• Accumulation of air in the pleural space
• Result from the external trauma or from leakage of air from lungs or
airways
• Risk factors of pneumothorax: premature infants, RDS, infant
delivered via caesarean section
• Signs and symptoms
• Cyanosis, bradycardia
• Reduced breaths sound over the affected area, positive transillumination test
(affected side is brighter than the other), mediastinal shift from the affected
side
21. • Radiography
• Hyperlucent hemithorax sign is seen
as unilateral or bilateral areas of
increased lucency confirmed
pmeumothorax
• Reduced marking over affected side
22. Treatment
• Types of intervention depends on the size of pneumothorax and
nature of underlying disease
• Small pneumothoraces (<20%of thorax that is filled with pleural air)
may not require intervention as they often resolves spontaneously
• Inhalation if high concentration O2 may enhanced reabsorption of
pleural air by washing out nitrogen from the blood
• Larger pneumothorax and tension pneumothorax may require
immediate drainage of the air via chest tube of in acute cases of
pneumothorax for immediate release (but usually will be needing
chest tube insertion as definite treatment)
23. Other causes of respiratory distress in
newborn
• PPHN
• Seen in severe hypoxemia, without any evidence of parenchymal lung, or structural cardiac disease
• Characteristics: significant left to right shunt through patent foramen ovale, through PDA and through
intrapulmonary channels
• Often seen with asphyxia or meconium stained fluid
• CXR: severe pulmonary venous engorgement and small heart
• Confirm by echocardiography or cardiac catheterization – elevated pulmonary artery pressure
• Congenital heart disease
• PDA – closes spontaneously 24-48 hours of life
• Usually seen in preterm infants- failure to close (less responsive to vasoconstrictive stimuli)
• Acute RDS hypoxia, hypercapnia pulmonary arterial vasoconstriction equalize the pulmonary and
systemic pressure small flow of through the PDA may be small or bidirectional
• RDS improves pulmonary artery resistance declines left to right flow through PDA increases heart
failure and pulmonary edema
• Clinical signs usually at 2-4 days of life (widens pulse pressure, bounding pulse, systolic murmur,
hepatomegaly, rales)
24. • Congenital diaphragmatic hernia
• Condition resulting from a developmental defect in the diaphragm leading to
protrusion of abdominal contents into the thoracic cavity.
• Disturbance in the formation of the pleuroperitoneal membranesresult in
diaphragmatic discontinuity and congenital diaphragmatic hernia
• Can cause lung hypoplasia and abnormal pulmonary vascular development
• Signs and symptoms: retractions, cyanosis, grunting, barrelled chest, scaphoid
abdomen
• Eryhtoblastosis
• Pulmonary hypoplasia
• Congenital emphysema
• Apnea in prematurity
25. Thus, the importance of asking relevant
history in resuscitating newborn
• Gestational age
• Mode of delivery
• Preterm, term, or post term
• Risk factors of sepsis
• Helps in determining cause of respiratory distress in newborn and
assist in further management in infants
26. Referances
• Kliegman, R., & Nelson, W. E. (2007). Nelson Textbook of Pediatrics.
Saunders.
• L. HERMANSEN, MD, MBA, C.H.R.I.S.T.I.A.N. and MAHAJAN, MD,
A.N.A.N.D. (2015) Newborn Respiratory Distress, pp. Volume 92,
Number 11.
• Lissauer, T. and Carroll, W. (2018) Illustrated textbook of paediatrics. S.
l.: Elsevier.
Editor's Notes
Infants below 32 weeks:
have not received full complements of maternal antibodies (IgG) that crosses the placenta by active transportation [redominantly in the latter phase of 3rd trimester.
They may have igM, but the IgG response to infection is reduced
Newborn infants
Shows deficit in phagocytic migration to the site of infection
Presence of suboptimal complement, neonatal neutrophils ingest and and kills bacteria less effectively than adult neutrophils do
C penicillin
Covers for many infections encounter in early few days of life
Group B strep and other streptococci, some strains of Ecoli, enterococci and influenza
Gentamicin
Used for gram negative coverage
Typically used with gram positive agents
Covers for ecoli, klebsiella, H influenza, including some gram positive S aureaus, enterococci and L monocytogens
It does not cross the BBB well
Less expensive compared to cefotaxime (crosses the BB and less renal toxixity and ototoxicity
Less rapid emergence or resistance organisms
Covers broader range of gram negative organisms
Surfactant
prevents atelectasis by reducing surface tension (helps with lung expansion)
Timing of surfactant production is between 32 and 34 weeks of gestation
Premature infants are at higher risk of developing pneumothorax due to absent of surfactant that expands the lungs and prevent it from lung collapse
Protrusion of the bowel content into the mediastinum can hinder the delepment ot the lungs structure, causing lung hypoplasia