• A 32weeks preterm baby born to a GDM mother by LSCS, developed
distress, grunting, cyanosis soon after birth. His SPO2 was 90%,
hyperoxia test was positive. Downe’s score was 7, silverman-anderson
score 8. Urgent CXR was done which showed :
Now what next???
• Baby shifted to NICU and put on warmer. RBS was normal, other
blood samples taken. IV fluids were started, ABG was done which
showed acidosis.
• Baby was put on nasal CPAP, meanwhile survanta was arranged.
• Baby then put on venti, surfactant given at 4 hours of life.
• Now clinically better.
Suspect surgical cause
•Obvious malformation
• Scaphoid abdomen
• Frothing
• History of aspiration
13.
A progressively increasingO2 requirement to
maintain saturation is also a sensitive indicator
of the severity and progress of distress
>95% Term baby, pulmonary hypertension (PPHN)
88-94% 28-34 weeks preterm
85-92% Below 28 weeks gestational age
Guidelines for monitoring oxygen saturation levels
by pulse oximetry
MJAFI, Vol. 63, No. 3, 2007
General
Considerations
14.
Hyperoxia test
test Methodresult diagnosis
Hyperoxia 100 % fio2 5-10
min
Pao2 increases to
> 100 torr
Pao2 increases by
< 20 torr
Parenchymal
lung disease
PPHN / CCHD
Hyperoxia-
hypervetilation
MV 100 % fio2 &
VR 100-150 /
min
Pao2 increases to
> 100 torr
w HV
Pao2 increases
at critical Pco2
No increase in
Pao2 with HV
Parenchymal
lung disease
PPHN
CCHD
Investigation
Complete Blood Countwith a Peripheral blood smear
Sepsis screen including C-reactive protein and μ ESR
Arterial blood gas (ABG) analysis
Blood glucose, Serum calcium
Cultures: Blood , Surface swab (where indicated),
maternal vaginal swab
Chest radiograph with an oro-gastric tube in situ
General
Considerations
Respiratory Distress Syndrome(RDS)
• Also known as Hyaline Membrane Disease (HMD)
• Commonest cause of preterm neonatal mortality
• RDS occurs primarily in premature infants; its incidence
is inversely related to gestational age and birth weight
Nelson Textbook of Pediatrics, 18th
Ed.
Gestational age Percentages
Less than 28 wks 60-80%
32-36 wks 15-30%
37-39 wk 5%
Term Rare
Resp.
Dis.
Syn.
23.
ETIOLOGY AND PATHOPHYSIOLOGY.
•Surfactant deficiency is the 1O
cause of RDS.
• Low levels of surfactant cause high surface tension
• High surface tension makes it hard to expand the alveoli.
• Tendency of affected lungs to become atelectatic at end-
expiration when alveolar pressures are too low to
maintain alveoli in expansion
• Leads to failure to attain an adequate lung inflation and
therefore reduced gaseous exchange
24.
• With advancinggestational 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
• Quality : The amounts produced or released may be
insufficient to meet postnatal demands because of
immaturity.
• Surfactant inactivating states eg maternal DM may
lead to surfactant of lower quality/ immature
25.
• Rare geneticdisorders may cause fatal respiratory
distress syndrome eg.
• Abnormalities in surfactant protein B and C genes
• gene responsible for transporting surfactant across
membranes (ABC transporter 3 [ABCA3]) are associated
with severe and often lethal familial respiratory disease
#16 While the Silverman Anderson Retraction Score is more suited for preterms with HMD, the Downes’ Score is more comprehensive and can be applied to any gestational age and condition.