Acute Hypotensive Transfusion Reactions

Acute hypotensive transfusion reactions (AHTRs) are characterized by early and abrupt onset of hypotension as the predominant clinical manifestation. The drop in blood pressure typically resolves quickly once the transfusion is stopped. Disturbances in the production and metabolism of bradykinin cause the pathophysiology of these reactions. Bradykinin is produced after Factor XII becomes activated due to contact with negatively charged surfaces such as tubing systems, dialysis membranes, and blood filters used for leukoreduction. Bradykinin, a vasoactive peptide that binds to receptors on the endothelium and causes hypotension, is primarily metabolized by the angiotensin converting enzyme (ACE). An increase in the recognition of AHTRs has been due to the growing use of ACE inhibitors, the use of negatively charged leukoreduction filters and both genetic and induced alterations in bradykinin kinetics. This review describes the epidemiology of AHTRs, current understandings about the pathophysiology, and prevention measures.

[1]  N. Heddle,et al.  Hypotensive transfusion reactions can occur with blood products that are leukoreduced before storage , 2004, Transfusion.

[2]  A. Adam,et al.  Hypotensive reaction during staphylococcal protein A column therapy in a patient with anomalous degradation of bradykinin and Des‐Arg 9 ‐bradykinin after contact activation , 2002, Transfusion.

[3]  J. Rouleau,et al.  Bradykinin metabolism and hypotensive transfusion reactions , 2001, Transfusion.

[4]  A. Adam,et al.  Anomaly of the des‐Arg9‐bradykinin metabolism associated with severe hypotensive reactions during blood transfusions: a preliminary study , 1999, Transfusion.

[5]  P. Thibault,et al.  Des-Arg9-bradykinin metabolism in patients who presented hypersensitivity reactions during hemodialysis: role of serum ACE and aminopeptidase P , 1999, Peptides.

[6]  M. Dupuis,et al.  Hypotensive reactions to red cells filtered at the bedside, but not to those filtered before storage, in patients taking ACE inhibitors , 1998, Transfusion.

[7]  H. Abe,et al.  Hypotensive reactions with a white cell‐reduction filter: activation of kallikrein‐kinin cascade in a patient , 1998, Transfusion.

[8]  İ. Yenicesu,et al.  Hypotensive reactions during platelet transfusions , 1998, Transfusion.

[9]  H. Oberman,et al.  Hypotensive reactions associated with white cell‐reduced apheresis platelet concentrates in patients not receiving ACE Inhibitors , 1998, Transfusion.

[10]  K. Tadokoro,et al.  Activation of the contact system by filtration of platelet concentrates with a negatively charged white cell‐removal filter and measurement of venous blood bradykinin level in patients who received filtered platelets , 1997, Transfusion.

[11]  N. Key,et al.  Hypotensive reactions to white cell‐reduced plasma in a patient undergoing angiotensin‐converting enzyme inhibitor therapy , 1996, Transfusion.

[12]  K. C. Anderson,et al.  Hypotensive reactions: a previously uncharacterized complication of platelet transfusion? , 1996, Transfusion.

[13]  H. Abe,et al.  Bradykinin generation during filtration of platelet concentrates with a white cell‐reduction filter , 1995, Transfusion.

[14]  M. Brecher,et al.  Atypical reactions associated with use of angiotensin‐converting enzyme inhibitors and apheresis , 1994, Transfusion.

[15]  A. Stalenhoef,et al.  ACE inhibitors and LDL-apheresis with dextran sulphate adsorption , 1992, The Lancet.

[16]  J. V. van Mourik,et al.  Bradykinin-mediated hypotension after infusion of plasma-protein fraction. , 1982, Journal of Laboratory and Clinical Medicine.

[17]  R. Buckingham,et al.  Hypotension associated with prekallikrein activator (Hageman-factor fragments) in plasma protein fraction. , 1978, The New England journal of medicine.