Patent ductus arteriosus (PDA) is a congenital disorder in the heart wherein a neonate's ductus arteriosus fails to close after birth. Early symptoms are uncommon, but in the first year of life include increased work of breathing and poor weight gain. With age, the PDA may lead to congestive heart failure if left uncorrected. The ductus arteriosus is a normal fetal blood vessel that closes soon after birth. In a patent ductus arteriosus (PDA) the vessel does not close and remains "patent" (open) resulting in irregular transmission of blood between two of the most important arteries close to the heart, the aorta and the pulmonary artery. PDA is common in neonates with persistent respiratory problems such as hypoxia, and has a high occurrence in premature children. In hypoxic newborns, too little oxygen reaches the lungs to produce sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have PDA because of their underdeveloped heart and lungs. A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure. In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open

1. The bottle neck of large PDA:Occasional missed large PDAs with or without
Eisenmenger syndrome by even renowned cardiologist.
Patent Ductus Arteriosus
Ramachandra

2. Time line
1939:Surgical ligation by Gross and Hubbard
1980:Maturation stages of ductus by
Gittenberger-De Groot AC et.al
1989: Krichenko A, Benson LN, Burrows P, et al:
classification
1967:First transcatheter closure by Portsmann
and coworkers
1979:doubleumbrella device by Rashkind
2003:Amplatzer device

3. Define
If ductus remains patent beyond 3 months of
life in full-term infants and beyond 1 year in
premature infants, it is termed persistent
PDA

4. Signature of PDA
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Most of them small
Seesaw murmur
TTE is enough for Dx and Rx
PDA with noise needs closure
Percutaneus closure is Rx-98% success
No IE prophylaxis

5. Foetal Life
PDA is life thread in normal developing heart
like
part of series connection in electrical circuit
shunting 60-70% oxygenated umbilical venous
return to aorta

6. Post natal
After birth the duct closes functionally in 12 to
18 hours and anatomically in 2 to 3 weeks.

7. Embryology
 day 29 6th aortic /pulmonary arch develops
 8th week of gestation, the ventral portions of the RT
and LT 6th AA form the proximal part of the RPA and
the proximal part of LT MPA ,respectively. The dorsal
portion of the right sixth arch is obliterated along with
the right dorsal aorta. Sometimes the dorsal portion
of the left 6th arch persists as a vascular conduit
called PDA arising from the roof of the junction
between the main and LPA and joining the left dorsal
aorta just distal to the LSCA in normal left-sided aorta

8. Anatomy
• Usually LPDA
• PDA and DTA angle at junction is 30 degree
• Angiographic class: A to E (90 degree LL) by
Krichenko & colleagues®
• 80% of PDA : A or B, Rx=Percutaneus closure
• Siblings: Reverse , Rt AA,aneurysm
•

9. Krichencko et.al:1989
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Angiography
Dead left lateral
Left angiograms
Types
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A:conical
B:window(L< 2 to 3 mm)
C:Tubular(both ends narrowing)
D:complex(multiple narrowing)
E :Elongated=a beaklike constriction at the
pulmonary end

10. Hemodynamic classification
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Small PDA :QP:QS <1.5 to 1
moderate PDA: QP:QS :1.5 and 2.2 to 1
large PDA:QP:QS >2.2 to 1.43
silent PDA :shunt is minimal/no murmur
detected on echocardiography

11. Reverse PDA
• Pulmonary atresia
• Tricuspid atresia
• Inferior angle near 90 degree OK but if <60
deree ,needs ductal stenting

12. Ductal aneurysm
 90% spontaneous closure except large size
causing pressure effect
Up to 8% reported of all PDA

13. Phenotypes
 Rt-sided PDA X RPA to the RT DTA
 LPDA X RT Brachiocephalic A.
 LSCA X LPA
 Dual PDA
 LPDA from LSCA
 Vascular ring: SCA from RT DTA and runs behind
the trachea and esophagus, forming a around
them by the right aortic arch anteriorly, and to
the RT,the LSCA at the back and the PDA to the
left.

14. Histology
• Mature:SMC are arranged longitudinally and
circularly helping close by spasm

15. Physiology in foetus
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Life thread
Tunnels 70% saturate blood into DA
Only 7% of volume enters unexpanded lungs
Patency:Immature duct,low O2 ,high O2/PGE-2
from placenta
• Functional closure:15th day
• Anatomical closure:21st day=placenta turn off,
high O2 stops Ik ,intracellular ca2+ increase add
to spasm in mature duct

16. Incidence
 1/2000 births
 5% to 10% of CHD
 With silent PDA ,Incidence is 1:500
 F>M(2:1)

17. Etiologic factors
• Sporadic
• Multifocal(genetic+environmental+ low
O2(Asphyxia),rubella(First 4 weeks)/chemicals

18. Genetics
 Chromosomal aberrations:Trisomy 21
 Single-gene mutations:Holt-Oram syndrome/
Char syndrome(TFAP2B mutations )
 X-linked mutations

19. Pathophysiology
 Small PDA :asymptomatic throughout life.Accidental detection by ECHO
for murmur
 Moderate PDA:compensate well throughout childhood and may
remain completely asymptomatic in early adulthood but will eventually
present with exercise intolerance and symptoms related to left ventricular
failure, usually starting in the third decade.
 Moderate to large:Large volume of blood leads to the very early
development of pulmonary congestion,decreased lung compliance, and
failure of the left ventricle, often presenting within weeks after birth with
failure to thrive, recurrent pulmonary infections, and even death.
Pulmonary overcirculation remains uncorrected,the arteriolar medial
hypertrophy, intimal proliferation,and eventual obliteration of pulmonary
arterioles and capillaries will lead to an irreversible marked increase in
pulmonary arterial pressure. When pulmonary vascular resistance
exceeds the systemic vascular resistance, ductal shunting is reversed and
becomes right to left (Eisenmenger syndrome)

20. Natural History
• Spontaneous closure may be delayed until 3
months of life, after which the closure rate is
less than 0.6%/Yr
• Silent PDA remain undetected for life
• premature :Closure could be delayed up to
1 year and more PDA
• Sibling :1% and 5%
• Parents:3%

21. Physical Examination
• Small PDA:Gr-II/III continuous murmur engulfing
and peaking around S2
• Thrill :moderate to large PDA
• S1 normal,S2 usual split with P2 accentuated
• S3 and diastolic rumble : moderate/ large PDA
• Eisenmenger syndrome:P2 loud/PSL/Graham
Still’s murmur
• wide pulse :large shunt
• Cyanosis/clubbing: Eisenmenger

22. ECG
• LAE
• LVH
• RVH

23. Chest Radiograph
• Small PDA: normal
• moderate to large: increased pulmonary
vascular markings with prominent ascending
aorta, and enlarged cardiac silhouette with
prominence of the left atrium, left Ventricle
and peripheral pruning
• Calcification

24. ECHO
• TTE allows the assessment of ductal
size,geometry, the degree of shunt, and
pulmonary artery pressures
• A left atrium/aorta ratio greater than 1.3/1 is
considered to be a reliable marker of a
hemodynamically significant ductal shunt
• Shunt ratio: continuity equation

25. Catheterization
• PDA closure
• Hypertensive PDA

26. Management
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Ignore
Follow
Transcathetor closure
Surgical closure
IE prophylaxis

27. Class I closure
Evidence of volume overload on the left
atrium or left ventricle (LAE/LVH)
 Development of PAH but the pressure and
the resistance still remain less than two-thirds
of the systemic levels
Endarteritis

28. Class IIa closure
Small PDAs with normal PA pressures and
normal heart size with a shunt ratio less than
1.5/1 or followed with repeat evaluations
every 3 to 5 year

29. Class III closure
Silent PDA
PDA with net right-to-left shunting

30. Closure method
• Cox inhibitors has no role in grown up
• Percutaneus Methods: Coil and device
• Surgical

31. Transcathetor
• Coils :<3 mm
• Device:3-12mm

32. Post closure follow up
Six months with IE prophylaxis

33. The basic of transcathetor technique
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Coils :Retrograde aortic
Device :Antegrade veno-arterial
7Fr venous and 6Fr arterial sheath
Pigtail angio in dead left lateral to decide
Device size is 2mm more than PA end
Cross with multipurpose and Terumo
Confirm with repeat angio
6month F/U SBE prophylaxis

34. Success story of TCC
• ADO is 99%
• immediate closure at the time of
implantation of 76%
• day 1 of 89%
• 6 to 12 months of 99% by echocardiography.

35. Complication
• Mortality in 1 / 439 cases
• major events 2.3%
• Device embolisation 2%

36. Surgical
 very large PDA
 unusual ductal anatomy
 Ductal aneurysm
 Significant endarteritis
 Abscess
• Methods: lateral thoracotomy,median
sternotomy, or VAT ligation
• 100% success
• Morbidity:long hospital stay,laryngial palsy

37. Thanks accompanying me until this page