Abstract
Anemia should preferably be managed without red blood cell transfusion (RBCT); instead, therapy should be focused on causes of anemia along with efforts to minimize blood loss. Lactate could potentially be used as a physiologic RBCT trigger, although there are some limitations to its interpretation. The aim of our study was to analyze the impact of RBCT on blood lactate with consideration of factors known to increase its concentration and to assess the usefulness of blood lactate as a potential physiologic RBCT trigger. We performed a retrospective analysis of all RBCT episodes in non-bleeding critically ill patients. We retrieved demographic data, data on RBCT itself (duration, type of RBC, volume of RBC, age of RBC), laboratory parameters (lactate, hemoglobin, glucose, total bilirubin), and factors potentially increasing lactate. We analyzed 77 RBCTs with elevated pre-RBCT lactate. The median age of patients was 66 (IQR 57–73) years and the distribution of sexes was even. The named factors potentially influencing lactate had no impact on its concentration. The median pre-post RBCT lactate was 2.44 (IQR 2.08–3.27) and 2.13 (IQR 1.75–2.88) mmol/L, respectively (p < 0.01); the median decrease was 0.41 (IQR 0.07–0.92) mmol/L. We conclude that RBCT did not normalize mildly elevated lactate. Common causes of elevated lactate probably had no impact on its concentration. Therefore lactate may have a limited role as a physiologic RBCT trigger in non-bleeding severely anemic critically ill patients.
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7 articles.
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