NONE TOO S.M.A.LL: the global challenge of severe malarial anaemia and its transfusion support

Abstract

In endemic areas, the burden of malaria and anaemia converge together upon children, with severe malarial anaemia (SMA) accounting disproportionately for demands on limited blood supplies. The attributable morbidity and mortality from SMA remain high, and improved outcomes hinge in part on the timeliness, sufficiency and safety of transfusion support. The pathogenesis of SMA is complex, and depreciation kinetics (towards syndrome‐defining haemoglobin levels of <50 g/l) occur acutely or insidiously, and in relation to the parasite burden and host response. Beyond haemolysis of parasitized erythrocytes, mechanisms of bystander loss and reduced erythropoiesis figure prominently, with parallels to hyperhaemolysis syndrome. Involuntarily undertransfused children with SMA in low‐income countries (LIC) differ from those adults in high‐income countries (HIC) who deliberately renounce transfusion. Despite youth‐related advantages in the power to adapt to anaemia, critical reductions in oxygen‐carrying capacity illustrate the hierarchical impacts of organ anoxia, be it in terminal cardiorespiratory events or irreversible neurocognitive impairments in survivors. When resources permit, the dynamics of restored oxygen delivery by transfusion are particularly observable in SMA, as the triggers to transfuse are so much lower (and the odds of corresponding lactic acidosis are so much higher) than in HICs. Questions on the best haemotherapy approaches to SMA remain, be these in dosage, infusion rate, component preparation or matching options; these fundamental concerns now transcend those related to storage duration. As a persisting global scourge, SMA therefore keeps driving and facing the mandate to bank life‐preserving blood for those with the most to gain (and otherwise lose).