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Patent ductus arteriosus


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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

Published in: Health & Medicine, Technology

Patent ductus arteriosus

  1. 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. 2. Time line 1939:Surgical ligation by Gross and Hubbard 1980:Maturation stages of ductus by Gittenberger-De Groot AC 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. 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. 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. 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. 6. Post natal After birth the duct closes functionally in 12 to 18 hours and anatomically in 2 to 3 weeks.
  7. 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. 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. 9. Krichencko • • • • 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. 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. 11. Reverse PDA • Pulmonary atresia • Tricuspid atresia • Inferior angle near 90 degree OK but if <60 deree ,needs ductal stenting
  12. 12. Ductal aneurysm  90% spontaneous closure except large size causing pressure effect Up to 8% reported of all PDA
  13. 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. 14. Histology • Mature:SMC are arranged longitudinally and circularly helping close by spasm
  15. 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. 16. Incidence  1/2000 births  5% to 10% of CHD  With silent PDA ,Incidence is 1:500  F>M(2:1)
  17. 17. Etiologic factors • Sporadic • Multifocal(genetic+environmental+ low O2(Asphyxia),rubella(First 4 weeks)/chemicals
  18. 18. Genetics  Chromosomal aberrations:Trisomy 21  Single-gene mutations:Holt-Oram syndrome/ Char syndrome(TFAP2B mutations )  X-linked mutations
  19. 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. 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. 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. 22. ECG • LAE • LVH • RVH
  23. 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. 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. 25. Catheterization • PDA closure • Hypertensive PDA
  26. 26. Management • • • • • Ignore Follow Transcathetor closure Surgical closure IE prophylaxis
  27. 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. 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. 29. Class III closure Silent PDA PDA with net right-to-left shunting
  30. 30. Closure method • Cox inhibitors has no role in grown up • Percutaneus Methods: Coil and device • Surgical
  31. 31. Transcathetor • Coils :<3 mm • Device:3-12mm
  32. 32. Post closure follow up Six months with IE prophylaxis
  33. 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. 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. 35. Complication • Mortality in 1 / 439 cases • major events 2.3% • Device embolisation 2%
  36. 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. 37. Thanks accompanying me until this page