Patent ductus arteriosus medical therapy in preterm infants: Difference between revisions
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In term infants the ductus closure occur by 24 hours of bith in 50% of babies , by 48 hours in 90% of babies and by 72 hours in most of them. However, the ductal closure is delayed in preterm infants. | In term infants the ductus closure occur by 24 hours of bith in 50% of babies , by 48 hours in 90% of babies and by 72 hours in most of them. However, the ductal closure is delayed in preterm infants. | ||
Ductal constriction occurs after birth due to following reasons- | '''Ductal constriction occurs after birth due to following reasons'''- | ||
* The increased oxygen tension after birth with onset of breathing | * The increased oxygen tension after birth with onset of breathing | ||
* Decreased prostaglandin E2 due to removal of placenta | * Decreased prostaglandin E2 due to removal of placenta | ||
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'''Medical therapy''' | '''Medical therapy''' | ||
*Circulating [[prostaglandin]] E2 has been found to play a key role in maintaining the patency of ductus arterisus(DA)in the fetal life. Thus, use of inhibitors of prostaglandin synthesis (eg, indomethacin and ibuprofen) have been found to be effective in the treatment of PDA. These drugs were also found to be useful in ductus closure if given antenatally.Patients with cases involving the [[transposition of the great vessels|transposition of the great vessels (TGV)]] may need the ductus arteriosus kept open with prostaglandin E1 (PGE1). | *Circulating [[prostaglandin]] E2 has been found to play a key role in maintaining the patency of ductus arterisus(DA)in the fetal life. Thus, use of inhibitors of prostaglandin synthesis (eg, indomethacin and ibuprofen) have been found to be effective in the treatment of PDA. These drugs were also found to be useful in ductus closure if given antenatally.Patients with cases involving the [[transposition of the great vessels|transposition of the great vessels (TGV)]] may need the ductus arteriosus kept open with prostaglandin E1 (PGE1). | ||
*Steroids like hydrocortisone have been found to decrease the sensitivity of ductus to PGE2.Thus, facilitating ductal constriction. | *Steroids like hydrocortisone have been found to decrease the sensitivity of ductus to PGE2.Thus, facilitating ductal constriction. | ||
*Nitic oxide synthesized from endothelial cells have been shown to cause ductus constriction in animal studies. | *Nitic oxide synthesized from endothelial cells have been shown to cause ductus constriction in animal studies. | ||
Revision as of 14:56, 16 August 2011
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Priyamvada Singh, M.B.B.S. [2], Cafer Zorkun, M.D., Ph.D. [3]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]
Overview
Medical therapy
In term infants the ductus closure occur by 24 hours of bith in 50% of babies , by 48 hours in 90% of babies and by 72 hours in most of them. However, the ductal closure is delayed in preterm infants.
Ductal constriction occurs after birth due to following reasons-
- The increased oxygen tension after birth with onset of breathing
- Decreased prostaglandin E2 due to removal of placenta
- Increased removal of prostaglandin E2 from lung
Medical therapy
- Circulating prostaglandin E2 has been found to play a key role in maintaining the patency of ductus arterisus(DA)in the fetal life. Thus, use of inhibitors of prostaglandin synthesis (eg, indomethacin and ibuprofen) have been found to be effective in the treatment of PDA. These drugs were also found to be useful in ductus closure if given antenatally.Patients with cases involving the transposition of the great vessels (TGV) may need the ductus arteriosus kept open with prostaglandin E1 (PGE1).
- Steroids like hydrocortisone have been found to decrease the sensitivity of ductus to PGE2.Thus, facilitating ductal constriction.
- Nitic oxide synthesized from endothelial cells have been shown to cause ductus constriction in animal studies.
ACC/AHA recommendations for medical therapy in patients with patent ductus arteriosus[1](DONOT EDIT)
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Class I 1. Routine follow-up is recommended for patients with a small PDA without evidence of left-sided heart volume overload. Follow-up is recommended every 3 to 5 years for patients with a small PDA without evidence of left-heart volume overload. (Level of Evidence: C) Class III 1. Endocarditis prophylaxis is not recommended for those with a repaired PDA without residual shunt. (Level of Evidence: C)
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For ACC/AHA Level of evidence and classes click:ACC AHA Guidelines Classification Scheme
References
- ↑ Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA; et al. (2008). "ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". J Am Coll Cardiol. 52 (23): e1–121. doi:10.1016/j.jacc.2008.10.001. PMID 19038677.