Impact of red blood cell transfusions on intestinal barrier function in preterm infants

Ajayi, O.O., Davis, N.L., Saleem, B., Kapoor, S., Okogbule-Wonodi, A.C., Viscardi, R.M., Sundararajan, S.* | JNPM 2019;

: To determine the relationships of red blood cell (RBC) transfusion and enteral feeding to changes in intestinal permeability (IP) measured by the relative intestinal uptake of lactulose (La) and rhamnose (Rh) in preterm infants <33 wk gestation.
DESIGN/METHODS: Infants 240–326wk gestation received La/Rh solution enterally on study days 1, 8 and 15.Urinary La/Rh ratio was measured by HPLC. Hematocrit preceding transfusion, total RBC transfusion volume, volume/kg, and feeding status during each study interval (birth-d1; d1-d8, and d8-d15) were determined.
RESULTS: Of the seventeen (40.5%) subjects who received≥1 transfusion during the study period, 12 (70.6%) infants were <28 wk gestation and 5 (29.4%) infants were≥28 wk gestation, p < 0.0001. Lower pre-transfusion hematocrit was observed in intervals preceding high IP (La/Rh > 0.05) than in intervals preceding low IP (La/Rh≤0.05) measurements (33 vs 35.8, p = 0.1051). RBC transfusions occurred more frequently in intervals preceding high IP than in intervals preceding low IP (26.8%; vs 8.3%, p = 0.0275) with 5-fold higher total RBC volume and volume/kg in intervals preceding any time point with high IP. RBC transfusion during an interval was associated with a three-fold increased risk of high IP (aOR 2.7; 95% C.I 0.564–12.814; p = 0.2143). Exclusive breast milk exposure and post-menstrual age reduced the risk for high IP following RBC transfusion.
CONCLUSIONS: Both RBC transfusion number and volume was associated with subsequent high IP measurements in preterm infants <33 weeks gestation and potentially may contribute to impairment of the preterm intestinal barrier.

*Corresponding Author: 

Sripriya Sundararajan, MBBS, MD, Department of Pediatrics, University of Maryland School of Medicine, Division of Neonatology, 110 S Paca Street, 8th floor, Baltimore, 21201, Maryland. USA. Tel.: +1 410 328 6003; Fax: +1 410 328 1076; E-mail: