1. Patent Ductus Ateriosis PDA Muhammad Syed MD Heart

2. Low vascular resistance of the placenta High vascular resistance of the fluid-filled fetal lung Right-to-left shunts

4. Two right-to-left shunts occur in the fetus Foramen ovale — Blood shunted from the right to left atrium Ductus arteriosus — Blood shunted from the pulmonary artery to the aorta Ductus Arteriosus Foramen Ovale

5. Two right-to-left shunts occur in the fetus Foramen ovale — Blood shunted from the right to left atrium Ductus arteriosus — Blood shunted from the pulmonary artery to the aorta

6. TRANSITION AT DELIVERY Alveolar fluid clearance Lung expansion Circulatory changes

7. clamping of the umbilical cord, rise in neonatal systemic blood pressure. lung expansion reduces both pulmonary vascular resistance and the pulmonary artery pressure. increased pulmonary arterial blood flow raises pulmonary venous return to the left atrium and left atrial pressure. As the left atrial pressure increases and the right atrial pressure falls, right-to-left shunting across the foramen ovale decreases.

8. Patent Foramen Ovale If the flap forms incompletely or does not completely seal close, then deoxygenated blood can pass from the right atrium to the left atrium. A patient with an open or patent foramen ovale will have a heart murmur. Unfortunately, this heart murmur maybe undetectable and the patient will exhibit no other obvious symptoms.

9. If the ductus arteriosus remains open after birth and fails to close it is referred to as a patent ductus arteriosus. Patent Ductus Arteriosus

10. PDA occurs commonly in premature infants, especially in those with respiratory distress syndrome Among very low birth weight (VLBW) infants (birth weight below 1500 g) PDA occurred in 30 percent

11. Because of the large volume of blood flow, the ductus becomes a large vessel with a diameter similar to that of the descending aorta

12. Patency of the ductus Mainly on Low arterial oxygen content Also is influenced by dilators, prostaglandins nitric oxide

13. HYDROCORTISONE Facilitates ductal constriction Hydrocortisone treatment decreases the sensitivity of the ductus to the dilating action of PGE2

14. CLOSURE Constrictors (Increased O2) PGE2, a vasodilator Anatomic closure usually is complete within one to three months.

15. Gestational age In term infants, functional closure after birth 24 hours 50 % 48 hours in 90 % 72 hours in virtually all In preterm infants, ductal closure can be delayed and the ductus can reopen following constriction.

16. Delayed closure Occurs especially when accompanying respiratory disease is present. Severe respiratory distress syndrome; in ill infants less than 30 W gestation, PDA persists on the fourth day in approximately 65 % Two other factors may be important: Contractile capacity in ductal tissue is less in immature Ductus in preterm infants continues to dilate in response to PGE2 and NO, in contrast to term infants whose ductus loses responsiveness shortly after birth

17. Reopening The histological changes following constriction of the ductus occur rapidly in term infants and prevent subsequent reopening. Reopening may occur because the effects of ductal constriction on events that lead to anatomic closure are influenced by immaturity. In one study, for example, constriction resulted in hypoxia, cell death, VEGF expression, endothelial proliferation, and intimal mound formation in the ductus of term but not preterm baboons

18. Shunting of blood flow through a PDA in prematures is essentially all left-to-right

19. Excessive flow through the pulmonary circulation Pulmonary edema Pulmonary hemorrhage Bronchopulmonary dysplasia

21. Systemic and cerebral blood flow effects Preterm animals and infants with a PDA increase their cardiac output. However, postductal blood flow is reduced, which may lead to organ dysfunction. NEC IVH

22. CLINICAL FEATURES Machinery Murmur ( infraclavicular region and upper left sternal border) Prominent left ventricular impulse Bounding pulses, and widened pulse pressure (greater than 25 mmHg) "silent," especially in the first three days (deterioration of respiratory status )

23. Diagnosis ECHO A transductal diameter that exceeds 1.5 mm is the most commonly used definition of a significant PDA

24. PDA closure indications Significant left-to-right shunt + symptomatic Evidence of left-sided volume overload (ie, left atrial or ventricular enlargement), reversible pulmonary arterial hypertension PDA closure is not recommended in patients with severe and irreversible PAH

25. Small PDA Recommend closure of a small audible PDA even in the absence of a significant L-to-R right shunt Silent PDA Never have hemodynamic consequences Risk Of endocarditis

26. Infants with a persistent PDA had a four-fold increased risk of death compared to infants who never had a significant PDA

27. Management Supportive therapy — During evaluation and treatment, supportive measures are applied. A neutral thermal environment and adequate oxygenation minimize demands on left ventricular output. Positive end-expiratory pressure (PEEP) may improve gas exchange in infants with respiratory compromise. Maintaining the hematocrit at 35 to 40 percent may increase pulmonary vascular resistance and reduce the left-to-right shunt Not recommend routine use of furosemide or any other loop diuretic, which stimulates renal synthesis of PGE2.furosemide

28. THERAPEUTIC INTERVENTIONS Interventions for PDA closure include: Pharmacologic therapy, which is used exclusively in premature infants Surgical ligation Percutaneous catheter occlusion

29. Pharmacologic therapy Inhibitors of prostaglandin synthesis, such as indomethacin and ibuprofen, are used asindomethacinibuprofen the initial interventions for PDA closure in preterm infants. IndomethacinIndomethacin has proven to be ineffective in term infants and older patients with a PDA.

32. Thank you