Does re-feeding stomach aspirates in preterm infants promote growth without causing feeding problems?
Monitoring of stomach aspirates to diagnose feed intolerance and necrotising enterocolitis is a common practice for preterm infants on tube feeds. There is no consensus on whether to re-feed or discard the stomach aspirates. Although re-feeding the aspirates may replace partially digested milk and gastrointestinal secretions that are essential for gastrointestinal maturation, re-feeding abnormal aspirates may result in vomiting, necrotising enterocolitis, or sepsis. We have looked for evidence from clinical trials that assessed whether re-feeding stomach aspirates is beneficial or harmful in preterm infants.
The thorough literature search is up-to-date as of Febraury 2018. We found only one small randomised controlled trial (with 72 preterm infant participants) that addressed this question.
We are uncertain as to whether re-feeding stomach aspirates has an effect on important outcomes such as incidence of necrotising enterocolitis, mortality before discharge, time to regain birth weight, time to reach full enteral feeds, duration of parenteral nutrition and duration of hospital stay.
Quality of evidence
Available evidence is insufficient to support or refute re-feeding of stomach aspirates in preterm infants. More trials are needed to examine whether re-feeding the stomach aspirates is beneficial or harmful in preterm infants.
We found only limited data from one small unblinded trial on the efficacy and safety of re-feeding gastric residuals in preterm infants. The quality of evidence was low to very low. Hence, available evidence is insufficient to support or refute re-feeding of gastric residuals in preterm infants. A large, randomised controlled trial is needed to provide data of sufficient quality and precision to inform policy and practice.
Routine monitoring of gastric residuals in preterm infants on gavage feeds is a common practice in many neonatal intensive care units and is used to guide the initiation and advancement of feeds. No guidelines or consensus is available on whether to re-feed or discard the aspirated gastric residuals. Although re-feeding gastric residuals may replace partially digested milk, gastrointestinal enzymes, hormones, and trophic substances that aid in digestion and promote gastrointestinal motility and maturation, re-feeding abnormal residuals may result in emesis, necrotising enterocolitis, or sepsis.
To assess the efficacy and safety of re-feeding compared to discarding gastric residuals in preterm infants. The allocation should have been started in the first week of life and should have been continued at least until the baby reached full enteral feeds. The investigator could have chosen to discard the gastric residual in the re-feeding group, if the gastric residual quality was not satisfactory. However, the criteria for discarding gastric residual should have been predefined.
To conduct subgroup analysis based on gestational age (≤ 27 weeks, 28 weeks to 31 weeks, ≥ 32 weeks), birth weight (< 1000 g, 1000 g to 1499 g, ≥ 1500 g), type of milk (human milk or formula milk), quality of the gastric residual (fresh milk, curded milk, or bile-stained gastric residual), volume of gastric residual replaced (total volume, 50% of the volume, volume of the next feed, or prespecified volume, irrespective of the volume of the aspirate, e.g. 2 mL, 3 mL), and whether the volume of gastric residual that is re-fed is included in or excluded from the volume of the next feed (see "Subgroup analysis and investigation of heterogeneity").
We used the standard search strategy of Cochrane Neonatal to search the Cochrane Central Register of Controlled Trials (CENTRAL; 2018, Issue 1), MEDLINE via PubMed (1966 to 19 February 2018), Embase (1980 to 19 February 2018), and the Cumulative Index to Nursing and Allied Health Literature (CINAHL) (1982 to 19 February 2018). We also searched clinical trial databases, conference proceedings, and the reference lists of retrieved articles for randomised controlled trials and quasi-randomised trials.
Randomised and quasi-randomised controlled trials that compared re-feeding versus discarding gastric residuals in preterm infants.
Two review authors assessed trial eligibility and risk of bias and independently extracted data. We analysed treatment effects in individual trials and reported the risk ratio and risk difference for dichotomous data, and the mean difference for continuous data, with respective 95% confidence intervals. We used the GRADE approach to assess the quality of evidence.
We found one eligible trial that included 72 preterm infants. This trial was not blinded.
We are uncertain as to the effect of re-feeding gastric residual on efficacy outcomes such as time to regain birth weight (mean difference (MD) 0.40 days, 95% confidence interval (CI) -2.89 to 3.69 days; very low quality evidence), time to reach enteral feeds ≥ 120 mL/kg/d (MD -1.30 days, 95% CI -2.93 to 0.33 days; very low quality evidence), number of infants with extrauterine growth restriction at discharge (risk ratio (RR) 1.29, 95% CI 0.38 to 4.34; very low quality evidence), duration of total parenteral nutrition (MD -0.30 days, 95% CI -2.07 to 1.47 days; very low quality evidence), and length of hospital stay (MD -1.90 days, 95% CI -25.27 to 21.47 days; very low quality evidence).
Similarly, we are uncertain as to the effect of re-feeding gastric residual on safety outcomes such as incidence of stage 2 or 3 necrotising enterocolitis and/or spontaneous intestinal perforation (RR 0.71, 95% CI 0.25 to 2.04; very low quality evidence), number of episodes of feed interruption lasting ≥ 12 hours (RR 0.80, 95% CI 0.42 to 1.52; very low quality evidence), or mortality before discharge (RR 0.50, 95% CI 0.14 to 1.85; low-quality evidence). We are uncertain as to the effect of re-feeding gastric residual in the subgroups of human milk-fed and formula-fed infants. We found no data on other outcomes such as linear and head growth during hospital stay, postdischarge growth, number of infants with parenteral nutrition-associated liver disease, and neurodevelopmental outcomes.