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Patent ductus arteriosus: Perspectives on a ‘persistent’ problem
Early Human Development 85 (2009) 141
Contents lists available at ScienceDirect
Early Human Development j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / e a r l h u m d e v
Introduction
Patent ductus arteriosus: Perspectives on a ‘persistent’ problem The ductus arteriosus (DA) develops from the distal portion of the sixth embryonic aortic arch, and connects the left pulmonary artery near its origin to the descending aorta just distal to the left subclavian artery [1]. Galen (A.D. 129–200) was the first to describe this ‘special fetal channel’, which shunted blood from the right side of the heart into the aorta, bypassing the lungs, as “…a lung still contained in the uterus and in the process of formation does not require the same arrangements of a perfected lung endowed with motion” [2]. Persistent patent ductus arteriosus (PDA) was first recognized as a ‘congenital malformation’ by Carl von Rokitansky (1804 to 1878), a professor of pathologic anatomy at the University of Vienna (Vienna, Austria). The classic murmur of a PDA was described in 1900 by G.A. Gibson of Edinburgh, Scotland, and is still called Gibson's murmur [3]. In 1938, Robert E. Gross of Boston, Massachusetts was the first surgeon to report successful ligation of PDA in a 7 year-old child, a landmark event in the history of management of PDA [4,5]. Closure of PDA with indomethacin, a nonselective PG inhibitor, was first reported in 1976 [6]. The first large and comprehensive randomized controlled trial evaluating the role of indomethacin and establishing its role in the management of PDA was published in 1983 [7]. Persistent patency of the DA is a common occurrence in premature neonates, especially in the extremely-low-birth-weight population. We have chosen to discuss this topic by grouping them into three review sections. The aim of the first review is to present up-to-date information on the pathophysiology of persistent PDA. A clear understanding of the various factors that play a role in constriction and closure of the DA in premature neonates is of utmost importance in the management of PDA. There is strong disagreement on the definition for ‘significance’ of a PDA, and hence its management varies accordingly. Timing of pharmacologic or surgical intervention depends on the clinician's perception of this significance. Is a left-to-right shunt significant when certain criteria are met on a scheduled early postnatal echocardiogram, or when one or more early, nonspecific and subjective clinical signs of a PDA are present, or when it causes overt congestive heart failure? Can we identify a select subgroup of neonates in whom early diagnosis and intervention would help improve outcome. These issues are discussed in the review article on clinical and echocardiographic diagnosis of the Journal.
0378-3782/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.earlhumdev.2008.12.004
Three decades since the first reported closure of PDA with indomethacin, controversy surrounds its management. PDA has been associated with several important neonatal morbidities, including chronic lung disease and necrotizing enterocolitis. Although this is conceivable because persistent patency of the DA can lead to redistribution of blood flow, with increased pulmonary blood flow and systemic hypoperfusion, to date a cause-and-effect relationship has never been established. In the final article, the authors review the various treatment strategies implemented for PDA management, scrutinize the available evidence justifying these strategies and provide practical guidelines for the clinician. References [1] Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation Oct 24 2006;114 (17):1873–82. [2] McManus BM. In: Roberts WC, editor. Patent ductus arteriosus. Philadelphia: FA Davis; 1987. p. 455–76. [3] Kaemmerer H. Surgical treatment of patent ductus arteriosus: a new historical perspective. Am J Cardiol 2004;94:1153–4. [4] Gross RE. Surgical management of the patent ductus arteriosus: with summary of four surgically treated cases. Ann Surg Sep 1939;110(3):321–56. [5] Gross RE, Hubbard JP. Landmark article Feb 25, 1939: surgical ligation of a patent ductus arteriosus. Report of first successful case. By Robert E. Gross and John P. Hubbard. JAMA Mar 2 1984;251(9):1201–2. [6] Friedman WF, Hirschklau MJ, Printz MP, Pitlick PT, Kirkpatrick SE. Pharmacologic closure of patent ductus arteriosus in the premature infant. N Engl J Med Sep 2 1976;295(10):526–9. [7] Gersony WM, Peckham GJ, Ellison RC, Miettinen OS, Nadas AS. Effects of indomethacin in premature infants with patent ductus arteriosus: results of a national collaborative study. J Pediatr Jun 1983;102(6):895–906.
Mambarath A. Jaleel Department of Pediatrics, Division of Neonatal–Perinatal Medicine, University of Texas, Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9063, United States Tel.: +1 214 648 3903; fax: +1 214 648 2481. E-mail address: [email protected].
Contents lists available at ScienceDirect
Early Human Development j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / e a r l h u m d e v
Introduction
Patent ductus arteriosus: Perspectives on a ‘persistent’ problem The ductus arteriosus (DA) develops from the distal portion of the sixth embryonic aortic arch, and connects the left pulmonary artery near its origin to the descending aorta just distal to the left subclavian artery [1]. Galen (A.D. 129–200) was the first to describe this ‘special fetal channel’, which shunted blood from the right side of the heart into the aorta, bypassing the lungs, as “…a lung still contained in the uterus and in the process of formation does not require the same arrangements of a perfected lung endowed with motion” [2]. Persistent patent ductus arteriosus (PDA) was first recognized as a ‘congenital malformation’ by Carl von Rokitansky (1804 to 1878), a professor of pathologic anatomy at the University of Vienna (Vienna, Austria). The classic murmur of a PDA was described in 1900 by G.A. Gibson of Edinburgh, Scotland, and is still called Gibson's murmur [3]. In 1938, Robert E. Gross of Boston, Massachusetts was the first surgeon to report successful ligation of PDA in a 7 year-old child, a landmark event in the history of management of PDA [4,5]. Closure of PDA with indomethacin, a nonselective PG inhibitor, was first reported in 1976 [6]. The first large and comprehensive randomized controlled trial evaluating the role of indomethacin and establishing its role in the management of PDA was published in 1983 [7]. Persistent patency of the DA is a common occurrence in premature neonates, especially in the extremely-low-birth-weight population. We have chosen to discuss this topic by grouping them into three review sections. The aim of the first review is to present up-to-date information on the pathophysiology of persistent PDA. A clear understanding of the various factors that play a role in constriction and closure of the DA in premature neonates is of utmost importance in the management of PDA. There is strong disagreement on the definition for ‘significance’ of a PDA, and hence its management varies accordingly. Timing of pharmacologic or surgical intervention depends on the clinician's perception of this significance. Is a left-to-right shunt significant when certain criteria are met on a scheduled early postnatal echocardiogram, or when one or more early, nonspecific and subjective clinical signs of a PDA are present, or when it causes overt congestive heart failure? Can we identify a select subgroup of neonates in whom early diagnosis and intervention would help improve outcome. These issues are discussed in the review article on clinical and echocardiographic diagnosis of the Journal.
0378-3782/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.earlhumdev.2008.12.004
Three decades since the first reported closure of PDA with indomethacin, controversy surrounds its management. PDA has been associated with several important neonatal morbidities, including chronic lung disease and necrotizing enterocolitis. Although this is conceivable because persistent patency of the DA can lead to redistribution of blood flow, with increased pulmonary blood flow and systemic hypoperfusion, to date a cause-and-effect relationship has never been established. In the final article, the authors review the various treatment strategies implemented for PDA management, scrutinize the available evidence justifying these strategies and provide practical guidelines for the clinician. References [1] Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation Oct 24 2006;114 (17):1873–82. [2] McManus BM. In: Roberts WC, editor. Patent ductus arteriosus. Philadelphia: FA Davis; 1987. p. 455–76. [3] Kaemmerer H. Surgical treatment of patent ductus arteriosus: a new historical perspective. Am J Cardiol 2004;94:1153–4. [4] Gross RE. Surgical management of the patent ductus arteriosus: with summary of four surgically treated cases. Ann Surg Sep 1939;110(3):321–56. [5] Gross RE, Hubbard JP. Landmark article Feb 25, 1939: surgical ligation of a patent ductus arteriosus. Report of first successful case. By Robert E. Gross and John P. Hubbard. JAMA Mar 2 1984;251(9):1201–2. [6] Friedman WF, Hirschklau MJ, Printz MP, Pitlick PT, Kirkpatrick SE. Pharmacologic closure of patent ductus arteriosus in the premature infant. N Engl J Med Sep 2 1976;295(10):526–9. [7] Gersony WM, Peckham GJ, Ellison RC, Miettinen OS, Nadas AS. Effects of indomethacin in premature infants with patent ductus arteriosus: results of a national collaborative study. J Pediatr Jun 1983;102(6):895–906.
Mambarath A. Jaleel Department of Pediatrics, Division of Neonatal–Perinatal Medicine, University of Texas, Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9063, United States Tel.: +1 214 648 3903; fax: +1 214 648 2481. E-mail address: [email protected].