Abstract
BackgroundThe factors that determine the effect of enteral feeding on intestinal perfusion after preterm birth remain largely unknown. We aimed to determine the effect of enteral feeding on intestinal oxygen saturation (rintSO2) in preterm infants and evaluated whether this effect depended on postnatal age (PNA), postmenstrual age (PMA), and/or feeding volumes. We also evaluated whether changes in postprandial rintSO2 affected cerebral oxygen saturation (rcSO2).MethodsIn a longitudinal observational pilot study using near-infrared spectroscopy we measured rintSO2 and rcSO2 continuously for two hours on postnatal Days 2 to 5, 8, 15, 22, 29, and 36. We compared preprandial with postprandial values over time using multi-level analyses. To assess the effect of PNA, PMA, and feeding volumes, we performed Wilcoxon signed-rank tests or logistic regression analyses. To evaluate the effect on rcSO2, we also used logistic regression analyses.ResultsWe included 29 infants: median (range) gestational age 28.1 weeks (25.1–30.7) and birth weight 1025 g (580–1495). On Day 5, rintSO2 values decreased postprandially: mean (SE) 44% (10) versus 35% (7), P = .01. On Day 29, rintSO2 values increased: 44% (11) versus 54% (7), P = .01. Infants with a PMA ≥ 32 weeks showed a rintSO2 increase after feeding (37% versus 51%, P = .04) whereas infants with a PMA < 32 weeks did not. Feeding volumes were associated with an increased postprandial rintSO2 (per 10 mL/kg: OR 1.63, 95% CI, 1.02–2.59). We did not find an effect on rcSO2 when rintSO2 increased postprandially.ConclusionsOur study suggests that postprandial rintSO2 increases in preterm infants only from the fifth week after birth, particularly at PMA ≥ 32 weeks when greater volumes of enteral feeding are tolerated. We speculate that at young gestational and postmenstrual ages preterm infants are still unable to increase intestinal oxygen saturation after feeding, which might be essential to meet metabolic demands.Trial registrationFor this prospective longitudinal pilot study we derived patients from a larger observational cohort study: CALIFORNIA-Trial, Dutch Trial Registry NTR4153.
Highlights
The factors that determine the effect of enteral feeding on intestinal perfusion after preterm birth remain largely unknown
We explored whether the cerebral oxygen saturation and extraction changed when postprandial Regional intestinal oxygen saturation (rintSO2) increased after enteral feeding
Three infants died during the study period after a median of 21 days after birth: one infant died of necrotizing enterocolitis (NEC), one of multi-organ failure as a result of sepsis, and one infant died of progressive respiratory failure
Summary
The factors that determine the effect of enteral feeding on intestinal perfusion after preterm birth remain largely unknown. Gastrointestinal (GI) motility of preterm infants is limited causing delay in gastric emptying and intestinal transit This in turn could result in intolerance to feeding [1]. The passage of enteral feeds leads to an increased metabolic demand on the small intestine This results in increased intestinal perfusion from the superior mesenteric artery (SMA) known as postprandial hyperaemia [3, 4]. If this increased metabolic demand after enteral feeding cannot be met, feeding intolerance (FI) may occur, resulting in delayed full enteral feeding (FEF) and possibly even necrotizing enterocolitis (NEC) [5,6,7,8]. As preterm infants are at risk of impaired cerebrovascular autoregulation, postprandial redistribution of blood in favour of the intestines may result in cerebral underperfusion [9,10,11]
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