Hierarchical improvement of regional tissue oxygenation after packed red blood cell transfusion

Abstract

Background It is well established that counter-regulation to hypoxia follows a hierarchical pattern, with brain-sparing in preference to peripheral tissues. In contrast, it is unknown if the same hierarchical sequence applies to recovery from hypoxia after correction of anemia with packed red blood cell transfusion (PRBCT). Objective To understand the chronology of cerebral and splanchnic tissue oxygenation resulting after correction of anemia by PRBCT in preterm infants using near-infrared spectroscopy (NIRS). Design Prospective cohort study. Setting Neonatal intensive care. Patients included Haemodynamically stable infants: <32 weeks gestation, <37weeks postmenstrual age, <1500 grams birth weight; and ≥120 mL/kg/day feeds tolerated. Intervention PRBCT at 15 mL/Kg over 4 hours. Main outcome measures Transfusion-associated changes were determined by comparing the 4-hour mean pretransfusion cerebral and splanchnic fractional tissue oxygen extraction (FTOEc0; FTOEs0) with hourly means during (FTOEc1-4; FTOEs1-4) and for 24 hours after PRBCT completion (FTOEc5-28; FTOEs5-28). Results Of 30 enrolled infants, 14[46.7%] male; median[IQR] birth weight, 923[655-1064]g; gestation, 26.4[25.5-28.1]weeks; enrolment weight, 1549[1113-1882]g; and postmenstrual age, 33.6[32.4-35]weeks, 1 infant was excluded because of corrupted NIRS data. FTOEc significantly decreased during and for 24 hours after PRBCT (p < 0.001), indicating prompt improvement in cerebral oxygenation. In contrast, FTOEs showed no significant changes during and after PRBCT (p>0.05), indicating failure of improvement in splanchnic oxygenation. Conclusion Improvement in regional oxygenation after PRBCT follows the same hierarchical pattern with a prompt improvement of cerebral but not splanchnic tissue oxygenation. We hypothesise that this hierarchical recovery may indicate continued splanchnic hypoxia in the immediate post-transfusion period and vulnerability to transfusion-associated necrotizing enterocolitis (TANEC). Our study provides a possible mechanistic underpinning for TANEC and warrants future randomised controlled studies to stratify its prevention.