Abstract

Dear Sir, We concur with observations made by Dr. Ahmed in his letter “Anaerobic storage of red blood cells: the need for caution regarding donor red cells with sickle cell trait”1 about the potential unsuitability of anaerobic conditions for the storage of sickle cell trait (SCT) blood. Blood containing HbAS is well known to clog up leucoreduction filters and to enable unacceptable levels of leucocytes to escape during the filtering process2. At sufficiently low pO2, pH and high mean corpuscular haemoglobin concentration, HbAS in red blood cells (RBC) of SCT carriers polymerises. Although SCT is considered benign, symptoms and pathology suggesting occurrences of serious sickling events have been reported in numerous cases involving healthy SCT carriers placed under extremely demanding anoxic conditions3. Polymerisation of HbAS is well underway at a pO2 below 35 Torr for RBC with an HbS content of 40% or less, reducing RBC deformability and resulting in the well-described obstruction of leucoreduction filters2. In order to obtain significant anti-oxidative and metabolic benefits, we target anaerobic red blood cells to have less than 3% haemoglobin oxygen saturation (%SO2) before placing units in storage, and then maintain this low SO2 state throughout the storage period4. The pO2 required to achieve an SO2 below 3% is less than 5 Torr at 4 °C, and under such a low pO2, HbAS would polymerise. Even if it was permissible, inclusion of anti-sickling agents would be insufficient to prevent HbAS polymerisation, and storing RBC under a highly sickled state is known to be unacceptable because of prolonged mechanical stress to the cells and resulting haemolysis. If successful collection and storage of SCT blood is specifically desired, a test to exclude units with HbAS will be necessary to avoid subjecting these collected RBC to the anaerobic treatment. Further investigation will be required to determine the feasibility of storing SCT blood with a low HbS content. The AABB guidelines for transfusing erythrocytes containing sickle haemoglobin recommend avoiding transfusion of HbAS blood to foetuses and neonates, as well as to patients with sickle cell disease, but there is no definitive clinical evidence indicating a necessity to exclude RBC units containing HbAS for general transfusion5. Despite the fact that RBC containing HbAS are diluted in the recipient upon transfusion, under anoxic conditions that may exist in the recipient’s capillaries, these RBC may become rigid due to gelation of HbAS resulting in compromised oxygen delivery. Furthermore, RBC sickling in anoxic capillaries may result in capillary plugging and further harm the tissues. The safety of HbAS blood in the context of the general blood supply is an issue that lies outside the scope of Dr. Ahmed’s letter. For the reasons stated above however, we believe it is one that merits further careful scrutiny. In routine transfusion practice, we do not expect any harm to come from transfusing anaerobic blood to recipients, since infused RBC will be fully oxygenated at their first pass through the pulmonary capillaries. The effects of transfusing anaerobic blood to sickle cell disease patients will also need careful investigation.

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