Patent Ductus Arteriosus,pathophysiology and diagnosis

Patent ductus arteriosus

1. NICU seminar

2. OBJECTIVES
INCIDENCE
PHYSIOLOGY OF FETAL CIRCULATION
DUCTUS ARTERIOSUS IN FETUS
DUCTUS CLOSURE AFTER BIRTH
TRANSITIONAL CIRCULATION
FAILURE OF TRANSITION
CLINICAL FEATURES
DIAGNOSIS
MANAGEMENT

3. INTRODUCTION
An essential muscular contractile
structure in fetal life
Derivative of the Lt 6th aortic arch
Ductus is responsible for most of the
right ventricular outflow
Normally closes within hours of birth
Patent ductus after birth leading to Left
to Right shunt has adverse effect on
multiple organ perfusion

4. INCIDENCE
Directly related to the degree of
prematurity and the presence/severity of
respiratory distress.
Preterm infants of <30 weeks gestation with
severe respiratory distress have a high
incidence of PDA – ranging from 15 to 35%.
Isolated cardiac anomaly in 1:2000-2500
live births
In term infants,mostly associated with
other cardiac lesions

5. PHYSIOLOGY-FETAL
CIRCULATION
Parallel circulation
Intracardiac & venous
streaming of blood
Single ventricle can
maintain circulation
Right ventricle output
almost 62% of combined
cardiac output
Slide courtesy: Dr.Kotari

6. DUCTUS ARTERIOSUS IN
FETUS
Before birth
Patency of ductus - maintained by balance between
dilating and constricting factors
Premature closure of ductus in utero leads to right
ventricular failure
A basal tone of ductus exists – mediated by
endothelin 1
Factors that oppose ductus constriction are
 elevated pressure in the ductus due to high
PVR
vasodilators –PGE
2,
NO , CO

7. PGE 2 is the most potent PG produced by the
ductus & placenta
PGE receptors EP 2 , EP 3 , and EP 4
intracellular concentrations of cAMP
relaxes the ductus smooth muscle by
opening KATPchannels which hyperpolarize
the muscle
Inhibit sensitivity of the ductus’ contractile
proteins tocalcium

8. TRANSITIONAL CIRCULATION
Change in source of
oxygenated blood &
First few breaths
1.Fall in PVR
2.Closure of ductus
3.Increase in LA
pressures due to
increased blood flow
4.Flap closure of foramen
ovale
Slide Courtesy: Dr.Kotari

9. TRANSITIONAL CIRCULATION
Three critical adaptation occur
1.Increase in Pulmonary blood flow
2.Altered Central blood flow patterns
3.Increase in Combined ventricular output

10. Pulmonary blood flow
In fetus- high PVR, due to
Fluid filled atelectatic alveoli – mechanical
compression
During early gestation – limited no of
pulmonary blood vessels
Lack of rhythmic distention
Low oxygen tension

11. PVR-after birth
 PBF increases 8-10 fold and PVR decreases by
50% with in first 24hrs.
This fall in PVR is brought about by 3 main factors.
Ventilation of the lungs(negative dilating
pressure on the small pulmonary arteries and
veins)
Increased oxygenation
Hemodynamic forces like shear stress.

12. FACTORS CAUSING DUCT
CLOSURE
Increase in PaO
2

Decrease in blood pressure within
the ductal lumen
A decrease in circulating PGE
2 due to
loss of placental source and
increased removal by the lungs.
Decrease in the no. of PGE receptors
in the ductal wall

13. Increase in oxygen saturation at birth is
the most inportant factor
Oxygen inhibits K + channels
1. membrane depolarization
2.increase in smooth muscle
intracellular calcium
3.formation of endothelin-1

14. FUNCTIONAL DUCT CLOSURE
Closure by 24-72 hrs of life
Constriction of ductus-smooth muscle
contraction increased wall
thickness & shortening with protrusion
of intimal cushions & mucoid lakes
Depends on
1.Partial pressure of oxygen in blood
2.Prostaglandins
3.Muscle mass of ductus

15. PERMANENT CLOSURE OF
DUCTUS
Anatomical closure by
remodelling & apoptosis
Progressive intimal thickening
and fragmentation of the
internal elastic lamina
Migration of smooth muscle
from the media to intima
Proliferation of luminal
endothelial cells & infolding
 Forms mounds that
ultimately occlude lumen

16. DUCTUS CLOSURE IN TERM &
PRETERM
 Term babies- ischemic hypoxia of
the vessel wall occurs due to
constriction, but it does not require
elimination of flow in ductus.
Preterm require complete cessation
of blood flow across ductus for
permanent anatomic closure.

17. WHY MORE COMMON IN
PRETERM
Intrinsic tone is less due to weak
contractile capacity of smooth muscle
myosin
Potassium channel in preterm are of K
ca
which are unresponsive to oxygen levels
( in term – K
DR)
Preterm infants require greater degree of
ductal constriction
Absence of vasa vasorum.
Continue to produce PGE
2 ,NO after birth

18. Endogenous factors that alter the ability of
the preterm ductus to constrict with
advancing gestation not clearly known
Elevated cortisol concentrations in the
fetus have been found to decrease the
sensitivity of the ductus to the vasodilating
effects of PGE 2
Prenatal vitamin A increase both the
intracellular calcium responseand the
contractile response of the preterm ductus
to oxygen

19. RISK FACTORS FOR PDA
Prematurity
Presence/ severity of Respiratory
distress
Surfactant therapy
Excess fluid administration in 1
st
week
Infants born at high altitude
Congenital rubella syndrome

20. Significance of PDA

21. COMORBIDITIES OF sPDA
NEC
Intracranial hemorrhage
Pulmonary edema/Hge
Retinopathy
Increased risk of CLD

22. DIAGNOSIS
Clinical features
ECHO
Chest Xray
ECG
Brain natriuretic peptide

23. CLINICAL FEATURES
Typically appear by 72 to 96 hours of life
SYMPTOMS-nonspecific
 SIGNS- prolonged systolic (rarely
continuous) murmur at the left upper
sternal edge
Hyperdynamic precordium
Bounding peripheral pulses
Widened pulse pressure (Rule of thumb:
pulse pressure > half of systolic pressure

24. INVESTIGATIONS
Chest Xray- cardiomegaly
pulmonary plethora
prominent main
pulmonary artery
leftatrial enlargment
ECG- Left ventricular or atrial
hypertrophy
ST-T changes in failure

25. ECHOCARDIOGRAPHIC
FINDINGS
Direct visualization of the ductus (2D echo –
parasternal view)
Turbulent flow in the main pulmonary
artery (Pulsed wave Doppler)
Continuous flare in the main pulmonary
artery from arterial duct (Color Doppler)
Raised LV stroke volume
Bowing of interatrial septum to the right
with enlarged LA and LV (2D – four chamber
view)

26. DIASTOLIC FLOW IN DESC
AORTA

27. Hemodynamically
significant shunt
Transductal diameter >1.5 mm (by
measuring the width of the color
Doppler jet )
A low velocity pulsatile flow pattern
through the ductus (‘Unrestrictive PDA’)
LA: Ao >1.4:1
Retrograde diastolic flow in descending
aorta, superior mesenteric, middle
cerebral, and renal arteries

28. Newer investigations
Brain natriuretic peptide
Plasma NT-proBNP level on day 3 is a good
marker for hsPDA in preterm infants.
Serial measurements of NT-proBNP may be
useful in assessing the clinical course of PDA.
 I Farombi-Oghuvbu et al Arch. Dis. Child.
Fetal Neonatal Ed. 2008;93;F257-F260;

29. MANAGEMENT
MEDICAL
indomethacin
ibuprofen
SURGICAL LIGATION- If
failure/contraindication to medical
therapy
PROPHYLAXIS-not recommended

30. Controversies on
management
Medical or surgical
Ibuprofen or Indomethacin
adverse effects such as oliguria,
reduction in glomerular filtration rate,
reduced cerebral and mesenteric
perfusion
Early vs Late- early indomethacin (day
1-3) is better than late (day 7-12)
therapy in ELBW infants

31. PROTOCOL ON PDA
MANAGEMENT
Confirm PDA by ECHO

if hemodynamically significant/
symptomatic
no yes
birth weight >1000 gm <1000 gm

Conservative medical therapy if no
contraindication