Blood storage lesion in blood bag during cold storage

changes in blood during storage

1. Blood storage lesion

2. introduction Erythrocyte prone to modification due to : High oxygen concentration (prone to oxidative stress and hemoglobine auto oxidation) No nucleus – no repairing mechanism Ex-vivo storage of blood: Nonbiological container in non biological temperature Changes in cellular biochemistry Changes in normal aging process

3. Biochemical changes Shape changes are accompanied by biochemical changes within the cells and byproduct accumulation in the storage medium. Stored RBCs accumulate lactic acid and potassium, and pH progressively decreases . Routine storage of RBCs results in an early loss (within hours) of nitric oxide bioactivity, which may lead to impaired vasodilation in response to hypoxia

4. Morphologic changes With longer storage, RBCs change shape from a normal biconcave disk to echinocytes (reversible) and spheroechinocytes (nonreversible) These changes reduce their deformability and increase their likelihood of occluding the microcirculation The cause of decreased deformability is thought to be, in part, oxidative-induced membrane changes or depletion of adenosine triphosphate and 2, 3-diphosphoglycerate As RBC storage duration increases, concentration of microvesicles increases. Microvesicle come from tip of echinocyte spine Many of these microvesicles express phosphatidylserine, which facilitates thrombin generation in vitro. This is a possible mechanism by which stored RBCs contribute to thrombotic and other complications associated with transfusion

5. Oxidative injury Freshly stored RBCs in a standard blood bag undergo very little oxidation apart from normal spontaneous (autoxidation) reactions of Hb, resulting in little metHb accumulation (left). Reductive and antioxidant enzymes/proteins such as NADPH reductase and GSH maintain metHb to a minimum. Under prolonged storage conditions or when RBCs are exposed to UV light, Hb oxidative side reactions are increased, mainly Hb's own pseudoperoxidative pathways (right). These pathways result in the production of ferryl Hb ( HbFe 4+ ) which attacks other biological targets including band 3, resulting in band 3 clustering. Ferryl Hb crosslinks the major RBC membranes band 3 into clusters and the ultimate release of Hb-laden microparticles (MPs), with modifications. prolonged RBC storage was associated with increased plasma nontransferrin -bound iron, leading to acute tissue iron deposition and inflammation. This nontransferrin -bound iron enhanced bacterial growth in vitro.

6. Formability changes Implications of the storage lesion: reduced red blood cell deformability and impaired microvascular tissue flow. (A) Normal capillary. (B) Capillary blocked by abnormally shaped red blood cells.