LAUSR

Dear Editor, We read with great interest the article by Boutboul et al. [1] and would like to comment on a physiological perspective. Oxygen delivery (DO2) is calculated by the following equation: DO2 = Cardiac output (CO) × arterial oxygen content (CaO2) with CaO2 = 1.34 × Hemoglobin × SaO2 + 0.0031 × PaO2. Thus, PaO2 plays a minor, if not negligible, role in DO2 as long as SaO2 is within standard ranges. As a consequence, nasal oxygen administration, as proposed by the authors, is very unlikely to significantly increase DO2 in non-hypoxemic patients (Fig. 1) and might even be deleterious as there is growing evidence that hyperox(em)ia is associated with poorer outcomes in various situations [2]. In this specific setting, hyperox(em)ia, by increasing reactive oxygen species production might enhance hemoglobin-driven lipid peroxydation and subsequent oxidative kidney damage [3]. Furthermore, oxygen administration is not mentioned in the recent guidelines of the British Society for Haematology about the management of primary autoimmune hemolytic anemia [4], and, despite extensive literature review, we did not find any guidelines recommending such therapy beyond the objective of correcting hypoxemia. In the general situation of acute hemolysis, we would recommend using oxygen only in hypoxemic patients with the only objective to target normoxemia. In contrast, CO is a crucial determinant of DO2, its increase representing the compensatory mechanism of lowered CaO2 during hemolysis (Fig. 1). Thus, highest risk patients are those unable to increase their CO to maintain the DO2 above a critical dysoxia threshold, due to underlying pathology (cardiac insufficiency) and/ or medication (beta-blockers). Patients at risk of hypoxic complications should be identified based on this rationale and might benefit from earlier transfusion. As evaluation of DO2 determinants is difficult in the ward, we suggest that such patients should be managed within the intensive care unit where central venous oxygen saturation (ScvO2), as a reflection of DO2 adequacy to oxygen consumption (VO2), can be monitored. Given its major contribution to DO2, a non-invasive punctual evaluation of CO (transthoracic echocardiography estimation), seems mandatory as part of initial evaluation and should be repeated according to the evolution. In situations of low cardiac output, continuous monitoring could be discussed in a case-by-case basis.