Indomethacin therapy for patent ductus arteriosus: When is prophylaxis not prophylactic?

Clyman, Ronald I.; Campbell, Donnie

doi:10.1016/s0022-3476(87)80248-2

Cited by 20 publications

(8 citation statements)

References 38 publications

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“…Rationale for eliminating ductal ligation was to minimize surgical trauma to the lung and postoperative edema, inflammation, infection, and atelectasis. Pharmacological closure, using indomethacin (42) or ibuprofen (122), has not been used in this model. Our experience is that the ductus is physiologically closed during the first days of life.…”

Section: Animal Models As Tools To Identify Pathogenic Mechanisms Leamentioning

confidence: 99%

Utility of large-animal models of BPD: chronically ventilated preterm lambs

Albertine

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Albertine KH. Utility of large-animal models of BPD: chronically ventilated preterm lambs. Am J Physiol Lung Cell Mol Physiol 308: L983-L1001, 2015. First published March 13, 2015; doi:10.1152/ajplung.00178.2014.-This paper is focused on unique insights provided by the preterm lamb physiological model of bronchopulmonary dysplasia (BPD). Connections are also made to insights provided by the former preterm baboon model of BPD, as well as to rodent models of lung injury to the immature, postnatal lung. The preterm lamb and baboon models recapitulate the clinical setting of preterm birth and respiratory failure that require prolonged ventilation support for days or weeks with oxygen-rich gas. An advantage of the preterm lamb model is the large size of preterm lambs, which facilitates physiological studies for days or weeks during the evolution of neonatal chronic lung disease (CLD). To this advantage is linked an integrated array of morphological, biochemical, and molecular analyses that are identifying the role of individual genes in the pathogenesis of neonatal CLD. Results indicate that the mode of ventilation, invasive mechanical ventilation vs. less invasive high-frequency nasal ventilation, is related to outcomes. Our approach also includes pharmacological interventions that test causality of specific molecular players, such as vitamin A supplementation in the pathogenesis of neonatal CLD. The new insights that are being gained from our preterm lamb model may have important translational implications about the pathogenesis and treatment of BPD in preterm human infants.neonatal chronic lung disease; alveolarization; alveolar simplification; pulmonary hypertension; airway expiratory resistance; nitric oxide; vitamin A; endothelial nitric oxide synthase; nasal CPAP; insulin-like growth factor-1; epigenetics ACUTE RESPIRATORY FAILURE of preterm human infants reflects immaturity of the lung following preterm birth, disrupted developmental processes, and dysregulated repair responses. This reflection occurs in the neonatal intensive care setting of continuous invasive mechanical ventilation support with oxygen-rich gas that is necessary to keep many preterm human infants alive. Among survivors of preterm birth and initial days of ventilation support with oxygen-rich gas, human infants who require prolonged invasive ventilation support with oxygen-rich gas frequently develop bronchopulmonary dysplasia (BPD). BPD is a significant pediatric health problem because, almost four decades after its initial description (134), this disease of preterm infants remains the most common cause of long-term pour outcomes, including postnatal growth failure, recurrent hospitalization for respiratory tract infections, and intraventricular hemorrhage (53, 178). In the United States, since 2006, the overall rate of prematurity is 1 in 8 births, or ϳ12% (74, 118). However, the underlying pathogenic mechanisms are incompletely understood.Gaps in knowledge about the underlying pathogenic mechanisms that contribute to BPD are related, in p...

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Section: Animal Models As Tools To Identify Pathogenic Mechanisms Leamentioning

confidence: 99%

Utility of large-animal models of BPD: chronically ventilated preterm lambs

Albertine

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The differences among these management possibilities were not large, but some adverse events could have occurred more frequently when indomethacin was unfavorably included as part of initial therapy [5]. Notwithstanding, our data do not clarify the complex mechanisms by which PDA increasing pulmonary flow and edema formation in the lung, complicates RDS recovery, decreasing lung compliance and interfering with the functional properties of surfactant [2,3,11,12,14,15].…”

Section: Resultsmentioning

confidence: 69%

“…However, the most compelling support for a relationship between pulmonary edema and BPD comes from reports linking pulmonary edema and PDA directly to BPD [3,4,5].…”

Section: Introductionmentioning

confidence: 99%

“Silent” patent ductus arteriosus and bronchopulmonary dysplasia in low birth weight infants

Zanardo¹,

Trevisanuto²,

Dani³

et al. 1995

Jpme

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We conducted a clinical study on the antecedents of bronchopulmonary dysplasia (BPD) in 290 premature RDS infants with < or = 1.75 kg birth weight (BW). They were enrolled in a prospective trial of indomethacin treatment for "silent" patent ductus arteriosus (PDA), screened by 2-D echocardiographic and pulsed Doppler evaluation on the third day of life. The trial took place at the NICU of the Pediatric Department of Padua University between January 1987 and December 1991. Out of 290 infants screened, 96 had evidence of "silent" PDA (33%) and 77 responded to indomethacin treatment (80%). Comprehensively 79 (27%) developed BPD, and from these the incidence of BPD was statistically increased in infants with "silent" PDA, 47 out of 96 (49 +/- 9%), with respect to 32 out of 194 (16 +/- 3%) preterm infants without PDA. Statistical analysis showed that in preterm infants with "silent" PDA the development of BPD was correlated at 99% C.L. to their low BWs (mean BW = 1.13 kg): in fact the mean and the mode of BW distributions were statistically lower in the presence of BPD, 1.03 kg versus 1.24 kg, and 0.88 kg versus 1.65 kg respectively. Moreover, the preterm infants with "silent" PDA unresponsive to the first course of indomethacin and/or submitted later to surgical closure, presented a statistically lower BW with respect to the early responders, 1.06 kg versus 1.18 kg, and at the same time a statistically higher incidence of BPD (63 +/- 20% versus 43 +/- 9%). From these data we conclude that, although "silent", PDA increase per se the incidence of BPD, even if benefits from an early induced closure. Furthermore, a lower BW of infants affected by "silent" PDA represents a contributing factor to the development of BPD.

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“…They observed no difference in the pulmonary morbidity in these infants compared with control infants. Others have urged caution in the prophylactic management of ductus arteriosus in low-birth-weight infants [13].…”

Section: Discussionmentioning

confidence: 99%