Abstract
The management of enteral feeds in preterm infants with a hemodynamically significant patent ductus arteriosus (hs-PDA) is a major challenge for neonatologists due to the fear of gastrointestinal (GI) complications. This review aims to analyze the available evidence on the complex relation between the presence and management of PDA, enteral feeding practices, and GI outcomes in the preterm population. There is limited evidence, based on small and heterogeneous trials, that hs-PDA may affect the splanchnic hemodynamic response to enteral feeds. While the presence of PDA seems a risk factor for adverse GI outcomes, the benefits of feeding withholding during pharmacological PDA treatment are controversial. The lack of robust evidence in support of or against a timely feeding introduction or feeding withholding during pharmacological PDA closure in preterm neonates does not allow to draw any related recommendation. While waiting for further data, the feeding management of this population should be carefully evaluated and possibly individualized on the basis of the infants’ hemodynamic and clinical characteristics. Large, multicentric trials would help to better clarify the physiological mechanisms underlying the development of gut hypoperfusion, and to evaluate the impact of enteral feeds on splanchnic hemodynamics in relation to PDA features and treatment.
Highlights
A persistent patent ductus arteriosus (PDA) is a common condition among preterm neonates.A complex interplay of factors, such as increased sensitivity to the vasodilating effects of prostaglandinE2 (PGE2) and nitric oxide [1], a less muscular and thin-walled ductal structure, early adrenal insufficiency, and impaired platelet function, contribute significantly to prolonged ductal patency in the preterm population [2]
Compared to pre-prandial values, animals with a closed ductus showed a significant increase in diastolic and mean superior mesenteric artery (SMA)–blood flow velocity (BFV), and a significant relative vascular resistance (RVR) decrease 10 min after feeding; by 30 min, these parameters returned towards pre-prandial baselines
We recently investigated the 3-h averaged mean values of SrSO2 and splanchnic–cerebral oxygen ratio (SCOR), which has been proposed as a marker of gut hypoxia–ischemia [58], at the time of enteral feeding introduction in very preterm infants with hemodynamically significant patent ductus arteriosus (hs-PDA), defined by the evidence of a pulsatile trans-ductal shunt pattern and left atrium to aortic root (LA/Ao) ratio ≥ 1.5 (n = 11), restrictive PDA, defined by the evidence of a restrictive trans-ductal shunt pattern and left atrium-to-aortic root (LA)/Ao < 1.5 (n = 11), and no evidence of PDA (n = 28) [59]
Summary
A persistent patent ductus arteriosus (PDA) is a common condition among preterm neonates.A complex interplay of factors, such as increased sensitivity to the vasodilating effects of prostaglandinE2 (PGE2) and nitric oxide [1], a less muscular and thin-walled ductal structure, early adrenal insufficiency, and impaired platelet function, contribute significantly to prolonged ductal patency in the preterm population [2]. As pulmonary vascular resistances decline over the first days after birth, the blood flow proportion that is diverted by the PDA from systemic to pulmonary circulation progressively increases. As such, prolonged ductal patency is associated with higher mortality rates [4] and several adverse outcomes, including intraventricular hemorrhage, periventricular leukomalacia, impaired renal function, and necrotizing enterocolitis (NEC) [5]. To which extent these conditions are attributable to the hemodynamic consequences of PDA has not been fully elucidated; the development of gastrointestinal (GI)
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