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Patent Ductus Arteriosus
Ramachandra
The bottle neck of large PDA:Occasional missed large PDAs with or without
Eisenmenger syndrome by even renowned cardiologist.
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
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
Signature of PDA
• 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
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
Post natal
After birth the duct closes functionally in 12 to
18 hours and anatomically in 2 to 3 weeks.
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
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
•
Krichencko et.al:1989
• Angiography
• Dead left lateral
• Left angiograms
• Types
– 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
Hemodynamic classification
• 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
Reverse PDA
• Pulmonary atresia
• Tricuspid atresia
• Inferior angle near 90 degree OK but if <60
deree ,needs ductal stenting
Ductal aneurysm
 90% spontaneous closure except large size
causing pressure effect
Up to 8% reported of all PDA
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.
Histology
• Mature:SMC are arranged longitudinally and
circularly helping close by spasm
Physiology in foetus
• 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
Incidence
1/2000 births
5% to 10% of CHD
With silent PDA ,Incidence is 1:500
F>M(2:1)
Etiologic factors
• Sporadic
• Multifocal(genetic+environmental+ low
O2(Asphyxia),rubella(First 4 weeks)/chemicals
Genetics
Chromosomal aberrations:Trisomy 21
Single-gene mutations:Holt-Oram syndrome/
Char syndrome(TFAP2B mutations )
X-linked mutations
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)
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%
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
ECG
• LAE
• LVH
• RVH
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
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
Catheterization
• PDA closure
• Hypertensive PDA
Management
• Ignore
• Follow
• Transcathetor closure
• Surgical closure
• IE prophylaxis
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
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
Class III closure
Silent PDA
PDA with net right-to-left shunting
Closure method
• Cox inhibitors has no role in grown up
• Percutaneus Methods: Coil and device
• Surgical
Transcathetor
• Coils :<3 mm
• Device:3-12mm
Post closure follow up
Six months with IE prophylaxis
The basic of transcathetor technique
• 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
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.
Complication
• Mortality in 1 / 439 cases
• major events 2.3%
• Device embolisation 2%
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
Thanks accompanying me until this page

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Patent ductus arteriosus A long case presentation

  • 1. Patent Ductus Arteriosus Ramachandra The bottle neck of large PDA:Occasional missed large PDAs with or without Eisenmenger syndrome by even renowned cardiologist.
  • 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 • 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 • Angiography • Dead left lateral • Left angiograms • Types – 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 • 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 • 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
  • 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
  • 26. Management • 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 • 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