Adverse effects of transfusion

Vivian Imbriotis | July 6, 2026

Immediate immune

  • Type 1 hypersensitivity ranging from urticaria to anaphylaxis (the allergen can be donor IgA in IgA deficiency, a plasma protein, another allergen (e.g. peanut epitopes), OR in a much more interesting scenario, donor IgE reacts with a recipient antigen).
  • Acute haemolytic transfusion reaction (e.g. ABO-incompatibility intravascular haemolysis). This causes haemolysis but also a cytokine storm from the massive amounts of antibody-antigen binding \(\to\) classical compliment activation \(\to\) tissue factor release from macrophages; causing fever, shock, DIC, renal failure from haemoglobin toxicity.
  • Febrile non-haemolytic transfusion reaction (due to cytokines in the product or anti-leukocyte antibodies in recipient). Diagnosis of exclusion.
  • Transfusion-associated acute lung injury (due to anti-leukocyte antibodies in donor plasma \(\to\) activate receipient leukocytes \(\to\) direct lung injury)

Immediate non-immune

  • Transfusion-associated fluid overload (i.e. acute pulmonary oedema)
  • Bacterial sepsis delivered straight to the bloodstream (most typically from platelets, which are kept at the ideal culturing temperature)
  • Hypothermic and dilutional coagulopathy
  • RBCs are stored citrated, therefore citrate toxicity - HAMGA, hypocalcaemia \(\to\) coagulopathy \(\pm\) negative inotropy \(\pm\) vasodilation
  • Hypo- or hyperkalaemia. Stored RBCs lose Na/K ATPase function and leak out their potassium \(\to\) hyperkalaemia when infused; but once infused and exposed to glucose, they resume normal Na/K ATPase function and take up potassium \(\to\) hypokalaemia
  • Oxyhaemoglobin dissociation curve left-shift by 2,3-DPG deficient cells \(\to\) impaired oxygen offloading

Delayed immune

  • Delayed haemolytic reaction - typically extravascular haemolysis due to antibodies against Kidd, Duffy, or Kell systems; rarely get DIC, shock, or renal injury
  • Post-transfusion purpura - immune reaction against an antigen on platelets with loss of self-tolerance \(\to\) dramatic thrombocytopaenia
  • Graft-vs-host disease - rare; almost universally in immunodeficient recipients. Transfused T-cells engraft, then react against the host \(\to\) marrow aplasia with 90% mortality. This is why blood products for immunodeificnty patients must be irradiated (i.e. all T-cells annihilated) rather than just leukodepleted by a mesh.
  • Alloimmunisation - i.e. sensitization to something in the product (D, Kell, Duffy, HLA, whatever).


Delayed non-immune

  • Iron overload
  • Blood-borne pathogen (virus, prion, malaria) transmission - less than 1:1,000,000 chance in Australia (about the same as death by lighting strike)