STORAGE LESIONS IN STORED BLOOD AND THEIR CLINICAL IMPLICATIONS

Blood component storage makes modern transfusion medicine possible by separating donation from clinical need, yet storage is not biologically neutral. Red cells, platelets and plasma undergo progressive biochemical, structural and functional alterations collectively termed storage lesions. These changes are measurable in the laboratory, but their importance after transfusion varies with the component, manufacturing process, storage conditions, dose, rate of administration and recipient vulnerability.Objectives:This review examines the mechanisms, clinical implications and prevention of storage lesions across major blood components. Methods: Relevant experimental studies, clinical trials, systematic reviews and professional guidelines addressing blood-component storage were critically reviewed. Evidence relating to red-cell metabolism and membrane integrity, platelet activation and survival, plasma coagulation-factor stability, transfusion outcomes and mitigation strategies was synthesized narratively. Results:Red-cell storage is characterized by depletion of adenosine triphosphate and 2,3-diphosphoglycerate, falling pH, potassium leakage, oxidative injury, loss of membrane integrity, vesiculation, reduced deformability and accumulation of cell-free haemoglobin, bioactive lipids and inflammatory mediators. Platelets stored at room temperature develop activation, receptor shedding, metabolic exhaustion, mitochondrial dysfunction and impaired post-transfusion survival, whereas refrigeration preserves aspects of immediate haemostatic function but accelerates clearance. Frozen and thawed plasma shows variable loss of labile coagulation factors and changes related to thawing and post-thaw storage.Conclusion: Although these lesions are biologically plausible causes of impaired oxygen delivery, inflammation, thrombosis, hyperkalaemia or reduced haemostatic efficacy, large randomized trials have not demonstrated a general mortality advantage for routinely transfusing the freshest available red cells. Clinical concern is therefore greatest in selected settings, including neonates, massive or rapid transfusion, extracorporeal circuits, severe trauma, chronic transfusion dependence and recipients of irradiated units. Effective mitigation includes appropriate component selection, validated processing, temperature control, leucoreduction, additive solutions, washing or potassium reduction when indicated, rational inventory rotation and patient blood management. Storage age alone is an incomplete measure of quality; future practice should integrate donor biology, component manufacturing, molecular quality markers and recipient risk.