Patent Ductus Arteriosus

By Dr. Hanan Zekri Khaled

Lecturer of pediatrics
Pediatric cardiology
Patent Ductus Arteriosus
Patent Ductus Arteriosus
Patent Ductus Arteriosus
The ductus arteriosus in the fetus is an
important conduit that allows
deoxygenated blood to bypass the
collapsed lungs and enter the placenta
through the descending aorta and
umbilical arteries.
Patent Ductus Arteriosus
The placenta acts as an oxygenator and
returns oxygen rich blood through the
umbilical vein and ductus venosus to the
fetal heart.
Patent Ductus Arteriosus
The placenta produces prostaglandins,
which maintain prenatal patency of the
ductus and, in early gestation, inhibit the
ability of the ductus to contract in response
to oxygen.
Patent Ductus Arteriosus
The ductus arteriosus itself also produces
prostaglandins and nitric oxide-like
vasodilators.
Patent Ductus Arteriosus
During the postnatal period, final closure
of the ductus arteriosus results from
increased production of local
vasoconstrictors (like endothelin) in
response to higher arterial oxygen,
removal of placental prostaglandin and
a decrease in the number of prostaglandin
E2 receptors in the ductal wall.

Patent Ductus Arteriosus
During the first 60 hours of life,
spontaneous closure of the ductus occurs
in 55% of full-term newborn infants.
By 2-6 months of age, closure occurs in
more than 95% of healthy infants.
Patent Ductus Arteriosus
Persistent patency of the ductus arteriosus
following birth is inversely related to
gestational age.
This may be due to the smaller amount
of muscular tissue in the media with
lower intrinsic tone, and lower
responsiveness to oxygen but higher
sensitivity to the vasodilating effects of
prostaglandin E2 and nitric oxide.

Reopening of a Constricted Ductus

Before true anatomic closure occurs, the
functionally closed ductus may be dilated
by a reduced arterial Po2 or an increased
PGE2 concentration. The reopening of the
constricted ductus may occur in asphyxia
and various pulmonary diseases (as
hypoxia and acidosis relax ductal
tissues).
Patent Ductus Arteriosus
The direction of blood flow across the
PDA depends on the balance of
pulmonary and systemic vascular
resistance.

Patent Ductus Arteriosus
The most reliable non-invasive diagnostic
tool is echocardiography with Doppler
ultrasound.
In most infants, a modified parasternal
short axis view offers the best window for
PDA visualization.
This view offers the best opportunity to
directly measure the PDA.
Patent Ductus Arteriosus
Patent Ductus Arteriosus
The secondary effects of the increased
flow can estimate the volume load from
the left to right ductal shunt.
A large shunt leads to dilation of the left
atrium and left ventricle, as well as
holodiastolic reversal of blood flow distal to
the ductus in the descending aorta due to
run off into the pulmonary bed.
Patent Ductus Arteriosus
Enlargement of the left atrium reflecting
the approximate magnitude of the
shunt, can be further supported by left
atrial-to-aortic root ratio of >1.3.
In addition, continuous wave Doppler
can estimate pulmonary artery
pressures by measuring Doppler
velocities of PDA flow and tricuspid
regurgitation.
Patent Ductus Arteriosus
Patent Ductus Arteriosus
The clinical features depend on the
magnitude of left-to-right shunt through the
PDA and the ability of the infant to initiate
compensatory mechanisms to handle the
extra volume load.
Patent Ductus Arteriosus
Because many premature infants have
respiratory distress syndrome, the stage of
development of this disease and the use
of surfactant replacement therapy will
determine the pulmonary vascular
resistance and therefore the shunt.
Patent Ductus Arteriosus
The maturity of the infant and the stage of
myocardial development determine the
ability to handle the shunt.


Relationship to Systemic Organ
Perfusion with PDA
Redistribution of systemic blood flow
occurs even with moderate shunts.
Retrograde aortic flow, decreased
systemic blood flow, and moderate
hypotension are common in premature
infants with a PDA and may lead to
decreased perfusion in many organs, with
potential clinical consequences to each.
Relationship to Systemic Organ
Perfusion with PDA
Reduced cerebral blood flow or changes in
cerebral blood flow velocity patterns have
been implicated in the occurrence of
intraventricular hemorrhage.
Renal function may be compromised, and
myocardial perfusion, particularly
subendocardial blood flow, may be
reduced.

Treatment of PDA
In the premature infant an important
aspect of PDA management is fluid intake.
Early fluid restriction to allow for little more
than insensible and sensible losses will
significantly reduce the risks of PDA,
necrotizing enterocolitis, and death at the
expense of postnatal weight loss.
Treatment of PDA
Simple fluid restriction along with diuretic
use is often recommended to control the
symptoms of a PDA.
Furosemide is commonly used. Although
furosemide is a prostaglandin agonist, it
does not interfere with PDA closure.
Treatment of PDA
Furosemide merely helps the lungs clear
fluid and thereby improves the patients
ability to tolerate the PDA. Short-term use
of furosemide and fluid restriction requires
a close vigilance to prevent dehydration.

Mehta SK, Younoszai A, Pietz J, Achanti BP.
Pharmacological closure of the patent ductus arteriosus.
Images Paediatr Cardiol 2003;14:1-15

Treatment of PDA
The use of oral or, preferably, intravenous
(lyophilized) indomethacin to constrict the
ductus arteriosus has led to successful
nonsurgical closure in a large proportion of
treated infants; the effects of indomethacin
apparently are best when it is
administered before 10 days of age and
in less mature infants.
Treatment of PDA
Dose schedules vary, but commonly a first dose
of 0.2 mg/kg is given by nasogastric tube or
intravenously.
For intravenous indomethacin, subsequent
doses depend on the age at initial treatment if
<48 hours, the subsequent two doses are 0.10
mg/kg; if 2 to 7 days, 0.20 mg/kg; and if >7
days, 0.25 mg/kg. A total of three doses usually
is given 12 to 24 hours apart depending on
urinary output; if urine flow decreases, fewer
doses may be used or the time between doses
may be extended.
Treatment of PDA
If clinical signs reappear after an initially
successful course of therapy, a second
course may be considered.

Treatment of PDA
More recently, ibuprofen has also been
evaluated as a possible alternative to
indomethacin in preterm infants.
In addition, meta-analysis of the available
studies has shown a comparable rate of
ductal closure after ibuprofen treatment .
Treatment of PDA
Some evidence exists that there may be
less effect of ibuprofen on renal function
and urine output .
In addition, ibuprofen has less effect on
cerebral vasculature and cerebral blood
flow but has not shown a decreased risk
for intraventricular hemorrhage.

Treatment of PDA
Surgical ligation
In small infants that are not a candidate
for, or who have failed, medical therapy,
surgical ligation remains an effective
alternative.
Treatment of PDA
Trans-catheter closure
Although coil occlusion has been
performed in infants, a large short PDA,
which is the typical anatomy in
symptomatic newborns and premature
infants, is difficult to close.
Treatment of PDA
In addition, there is a significant risk of
obstructing the descending aorta or left
pulmonary artery, which are small caliber
vessels in neonates.
Treatment of PDA
Out of the neonatal period, cardiac
catheterization with coil occlusion of the
PDA has become the primary mode of
closure.
Newer occlusion devices similar to ones
used for ASD closure are being developed
for closure of the large PDA in older
children and adults.


Treatment of PDA
Closure of a PDA by coil
catheterization. (A)
Injection into the aorta
reveals a large PDA at
baseline. (B) Following
placement of a coil the
angiographic dye no
longer crosses into the
pulmonary artery
confirming ductal
closure. (MPA = main
pulmonary artery, PDA =
patent ductus arteriosus,
DA = descending aorta)