Transcript Patent Ductus Arteriosis - Nicole Stevens

PATENT DUCTUS
ARTERIOSUS
By: Nicole Stevens
• Patent Ductus Arteriosus is a functional
connection between the pulmonary artery and
the descending aorta.
• In the fetus the DA allows blood to be diverted
away from the pulmonary artery (the high
resistance pulmonary circulation) to the
descending aorta (the low resistance systemic
circulation)
• The duct remains open due to the
prostaglandin supply coming from the placenta.
• The DA protects the lungs from circulatory
• After the birth the baby’s lungs expand as they
begin to take breaths.
• Pulmonary resistance decreases and the oxygen
levels in the blood rise causing the DA to constrict.
• Sometimes the DA doesn’t constrict and the baby
is left with a PDA.
• This can be due to lack of oxygen or an increase
in the amounts of prostaglandin.
• Sometimes the PDA will functionally close but will
• It is approximately 10mm in diameter
• Functional closure occurs between 12 hours
and 4
days of age in healthy term babies
• Structural closure takes between 2 to 6 weeks
• It is common in premature infants
• Serious concern as the pulmonary artery is not
getting enough blood for the lungs to function
effectively
• It can cause worsening RDS and an escalation
in the respiratory support that is required
• Diagnosed on ECHO
PDA in the preterm infant:
 There is nothing wrong with the heart, the PDA
just doesn’t close and usually causes a left to
right shunt
 The tissue is immature; the fetal haemoglobin
has a higher affinity for oxygen (doesn’t release
it as easily)
 The lower the gestational age the greater the
risk of PDA
 VLBW infants will have up to 50 – 60% chance
of a PDA
PDA in the term infant:
 If there is pulmonary hypertension (numerous
causes for this, eg. meconium aspiration,
infection) the blood shunts right to left through
the PDA
 Deoxygenated blood that should be going to
the lungs goes back to the body, this causes
hypoxia and acidosis, which causes vascular
smooth muscle to constrict, and the end result
can be persistent fetal circulation (without the
 When trying to determine if shunting of blood is
occuring across a PDA you may be asked to
measure pre and post ductal oxygen
saturations
 Pre ductal SaO2 are measured on the right
hand/wrist, and post ductal SaO2 can be
measured on any of the other limbs, usually a
difference of 10% or more is considered
significant and may be caused by shunting of
blood across a PDA
 The arteries that supply part of the brain, and
right arm, branch off the aorta prior to where
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Pulmonary oedema
Poor perfusion
Bounding pulses
Swinging saturations
Desaturations
Renal compromise
Heart murmur
Congestive cardiac failure
Mottled or pale
If a neonate is symptomatic of an existing PDA
they may require treatment
 Chemical treatment: Indomethacin (usually
given IV but oral route can be used, although
thought to be not as effective)
(Note: there is currently a world-wide shortage of
indomethacin as its production has stopped, in
the near future an alternate drug may be used)
 If chemical treatment fails surgical treatment
• First line treatment
• Urea & Creatinine are checked before
commencing Indomethacin to ensure
normal renal function before
commencement of the drug.
• Platelets are also checked to ensure
normal range
• 3 daily doses of 200mcg/kg at 2200hrs
• Side Effects include impairment of renal
function, reduce platelet aggregation, GI
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Monitor urine output
Daily Urinalysis
BP monitoring
Observe for bleeding and or NEC
Contraindicated in infants with recent IVH
and NEC
• Some cardiac abnormalities are considered
“duct-dependent”; these can be cyanotic or
acyanotic
• Duct-dependent defects can be related to
pulmonary flow (for example pulmonary
stenosis or pulmonary atresia); or related to
systemic flow (for example hyperplastic left
heart or transposition of the greater arteries)
• If there is a definite or suspected diagnosis of a
cardiac abnormality, that is duct dependent, a
prostaglandin infusion is the treatment of
choice (a synthetic version of the hormone that