Case
B/O Marianna, day 24 of life, born extreme preterm 25 weeks with
AGA weight 810gram, born via EMLSCS for Chorioamnionitis.
Issues is: 1/ Extreme preterm
2/ RDS grade II - III with evolving BPD surfactant x2 given,
ventilated since birth till now with trial extubation x3 not success.
Latest CXR good expansion 9-10 ribs with cystic changes.
3/ PDA noted at day3 of life, 1st cycle of ibuprofen given at day 6
till day8 total 3 days completed. Repeated echo PDA size 1.1mm from
1.8mm but LA:AO ratio 1.8 to 2.0mm from 1.5mm. Started 2nd cycle of
ibuprofen completed day 23 of life 3 days course.
4/ resolved Acinetobacter baumannii sepsis completed antibiotic
and repeated blood C+S x2 negative.
Case
B/O Mi, born via EMLSCS via severe IUGR with fetal bradycardia, born
late preterm, with good apgar score and symmetrical IUGR .
Issues:
1/ Premature at 32 weeks 2 days with symmetrical IUGR birth weight 1100 gram
2/ compliant chest wall with resolved RDS - no surfactant required/ on CPAP for
11 days then HFNC for 2 days with LFNC for 2 days then RA
3/ PDA hemodynamically stable
Noted murmur at day 7 of life
Received 1 course of ibuprofen day 7 of life till day 9 of life.
Initial Echo PDA size: 2.0 mm ; LA:AO: 2.7 prior start ibuprofen and CXR: cardiomegaly with
pulmonary congestion.
Repeated Echo: 1.3mm, LA/AO ratio: 1.1 mm: CXR post ibuprofen: no cardiomegaly/
congestion. Hemodynamically non significant.
Anatomy of PDA
Patent ductus arteriosus
(PDA), in which there is a
persistent communication
between the descending
thoracic aorta and the
pulmonary artery that results
from failure of normal
physiologic closure of the
fetal ductus.
In fetal life,
Gas exchange occir at the placenta not in the lungs
Only small amount of blood is need for the lung for nutritional and
metabolic requirement. this account for 5-10% of combined
ventricular output (CVO)
Whereas Right ventricle ejects about 65% of CVO, so this duct
account for divert major proportion of blood around 55% of this
CVO away from pulmonary vascular bed to low ressitance
umbilical placental circulation.
This duct is regulate to open by low partial O2 = 18 mmHg, locally
and circulation Prostaglandin E2 and fetal immature ductus
produces more prostaglandin locally to open it. Which also the
endothelial cells of the ductus produces nitric oxide which leads to
ductal patency.
After birth,
A normal term infant, - postnatally closure is in 2 phases
1. Smooth muscle constriction produces functional closure of
lumen within 18 to 24 hours after birth
Due to increase arterial pO2 + drop in circulating PGE2 + drop in pressure
within the ductus lumen as drop in pulmonary vascular resistance.
Treatment modalities
Conservative
fluid restriction 100 to 130 cc/kg/day
diuretics for congestive heart failure; - thiazide prefer than
frusemide
use of minimal supplemental oxygen
permissive hypercapnia, & avoidance or correction of
metabolic alkalosis to minimize pulmonary vasodilation
application of continuous distending airway pressure(CPAP or
PEEP - > 5mmHg) to reduce pulmonary blood flow and
increase systemic perfusion
Treatment modalities
Medical therapy - Cyclo-oxygenase inhibitors such as
indomethacin and ibuprofen remain the mainstay of
medical therapy
New emerging Paracetamol.
Hindawi Publishing Corporation BioMed Research International Volume 2013, Article ID 676192, 15 pages http://dx.doi.org/10.1155/2013/676192
S. Noori, D. Patel, P. Friedlich, B. Siassi, I. Seri, and R. Ramanathan, Effects of low oxygen
saturation limits on the ductus arteriosus in extremely low birth weight infants, Journal of
Perinatology, vol. 29, no. 8, pp. 553557, 2009.
concentration in left-to-right shunting in infants with ventricular septal defects. N Engl J Med 1982; 306:502 .
Significant PDA
the decision to intervene should be based upon a hemodynamically significant PDA, which if left
untreated leads to pulmonary overcirculation (which increases the risk of developing pulmonary
edema, pulmonary hemorrhage, and BPD), and systemic undercirculation (which increases the risk
of necrotizing enterocolitis [NEC] and systemic hypoperfusion
The size of the PDA measured by echocardiography is generally used to determine whether or not a
PDA is hemodynamically significant in preterm infants. One commonly used measure is a transductal
diameter that exceeds 1.5 mm or 1.4 mm. In one series of mechanically ventilated infants younger
than 30 weeks gestation, a ductal diameter of 1.5 mm or greater at 7 to 31 hours of life predicted a
significant PDA with 83 percent sensitivity and 90 percent specificity for a PDA that was treated.
A proposed staging system to detect clinically significant PDA uses both clinical findings (eg,
oxygenation index, degree of respiratory support, chest radiography, and end-organ function) and
echocardiographic measurements to classify the severity of PDA.
Others have used the PDA:left pulmonary artery (LPA) ratio to define large (1), moderate
(<1 but 0.5), and small (<0.5) PDAs in the first four days of postnatal life to predict which infants
would receive treatment for PDA closure. Those with large or moderate PDAs are 15 times more likely
to receive treatment, and those with small PDAs have a high likelihood of spontaneous resolution.
Sensitivity, specificity, and positive predictive value of a large or moderate PDA:LPA ratio in the first
four days were 80, 86, and 92 percent, respectively, for infants <27 weeks gestation.
There is a strong correlation between the ductal diameter and flow patterns in determining the
severity of PDA, and it is reasonable to use both methods to decide on whether to initiate intervention.
Ramos FG, Rosenfeld CR, Roy L, et al. Echocardiographic predictors of symptomatic patent ductus arteriosus in extr
emely-low-birth-weight preterm neonates. J
Perinatol 2010; 30:535.
Thankavel PP, Rosenfeld CR, Christie L, Ramaciotti
C. Early echocardiographic prediction of ductal closure in neonates 30 weeks gestation. J Perinatol 2013; 33:45.
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