The effect of haemoglobin and blood transfusion on preterm infant gut perfusion and injury

Claire Howarth; Christian Mifsud; Jayanta Banerjee; Simon Eaton; Terence Leung; Paul Fleming; Joan Morris; Narendra Aladangady

doi:10.3389/fped.2024.1440537

The effect of haemoglobin and blood transfusion on preterm infant gut perfusion and injury

Front Pediatr. 2024 Nov 22:12:1440537. doi: 10.3389/fped.2024.1440537. eCollection 2024.

Authors

Claire Howarth¹, Christian Mifsud^{2

3}, Jayanta Banerjee⁴, Simon Eaton², Terence Leung⁵, Paul Fleming¹, Joan Morris⁶, Narendra Aladangady¹

Affiliations

¹ Neonatal Unit, Homerton Healthcare NHS Foundation Trust and Queen Mary University of London, London, England.
² Great Ormond Street Institute of Child Health, University College London (UCL), London, England.
³ School of Science and Technology, Centre for Health, Ageing and Understanding Disease (CHAUD), Nottingham Trent University, Nottingham, England.
⁴ Neonatal Unit, Imperial College Healthcare NHS Trust and Imperial College London, London, England.
⁵ Department of Medical Physics and Biomedical Engineering, University College London, London, England.
⁶ Population Health Research Institute, St George's University of London, London, England.

Abstract

Introduction: There is significant uncertainty regarding the role that anaemia or red blood cell transfusion (RBCT) plays in the development of gut injury in preterm infants. This study evaluated Near Infrared Spectroscopy (NIRS) together with a range of known biomarkers of gut inflammation to identify their relationship with anaemia and RBCT.

Method: A prospective observational study of preterm infants born at <30 weeks gestation was conducted from birth until either 36 weeks post conceptional age or discharge home. Gut perfusion and biomarkers of gut injury were assessed weekly by: 60 min NIRS measurements (splanchnic tissue oxygenation index [sTOI] and fractional tissue oxygenation extraction [sFTOE]); stool calprotectin; urine intestinal and liver fatty acid binding proteins (I-FABPs and L-FABPs); and trefoil factor 3 (TFF-3). Exclusion criteria included Fetal Growth Restriction (FGR), and abnormal antenatal Dopplers. Haemoglobin (Hb) levels were measured in parallel with NIRS measurements. NIRS, together with urine and stool biomarkers of gut injury, were evaluated up to 72 h pre/post RBCT and pre/post measurements compared.

Results: Forty-eight infants were studied. Median (range) gestational age was 26 ⁺ ³ (23 ⁺ ⁰ to 29 ⁺ ⁶) weeks and birthweight 883.5 g (460-1,600). Seven (14.6%) infants developed ≥ Bells stage 2 NEC. 28 (58.3%), 5 (10.4%) and 24 (50%) infants had ECHO confirmed PDA, haemorrhagic parenchymal infarct (HPI) and IVH respectively. There were 22 episodes of sepsis. Infants were in the study for a median of 7.3 (1-13) weeks. There was no significant association between Hb divided into three categories (<80 g/L, 80-111.9 g/L and ≥120 g/L) or continuous values and sTOI, sFTOE or any of the gut injury biomarkers measured (p > 0.05). 283 RBCTs were administered; 117 (41.3%) within the first two weeks of life. Pre and post blood transfusion changes in splanchnic NIRS oxygenation, urine and stool gut injury biomarkers were measured in 165, 195 and 175 episodes of RBCT respectively. There was no significant post RBCT changes in splanchnic NIRS or gut injury biomarker levels (p > 0.05). However, post RBCT calprotectin was significantly reduced during the first 14 days of life (mean difference -114%, CI -185 to -42 & p 0.002).

Conclusion: There was no association between anaemia or RBCT with NIRS measurements of tissue oxygen saturation and biomarkers of intestinal inflammation or gut injury in preterm infants enrolled in this study. Further studies with standardised methods of examining the relationship between anaemia, RBCT and gut injury are needed.

Keywords: NEC; blood transfusion; gut injury; gut perfusion; haemoglobin; preterm infants.

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was funded by a Barts Charity Grant Award (Grant reference number MGU0388). The authors have no financial relationships relevant to this article to disclose. Dr Howarth was funded through the Barts Charity Grant, but none of the other authors had a financial relationship with the charity or the fund. Dr Eaton acknowledges support from NIHR Biomedical Research Centre at Great Ormond Street Hospital and UCL Great Ormond Street Institute of Child Health.