Potentially fatal noninfectious complications of allogeneic blood transfusion
| Complication . | Definition . | Mechanism . |
|---|---|---|
| Transfusion-related acute lung injury (TRALI) | New acute lung injury (ALI) occurring within 6 hours after a transfusion, with a clear temporal relationship to the transfusion, in patients without risk factors for ALI other than transfusion21 * | Donor anti-WBC antibodies attacking the recipient's WBCs in the microcirculature of the lungs |
| “Two-hit” hypothesis implicating biologic response modifiers accumulating in supernatant plasma during storage† | ||
| Hemolytic transfusion reactions (HTRs) | Immune destruction of the transfused donor RBCs which are attacked by the recipient's: “naturally occurring” antibodies to the A or B antigens of the ABO blood group system, and/or alloantibodies to other RBC antigens produced following immunization through a previous transfusion or pregnancy | Acute HTR: Destruction of “incompatible” donor RBCs intravascularly or extravascularly (in the liver and/or spleen) by preexisting circulating antibody within 24 hours of a transfusion‡ |
| Delayed HTR: Destruction of “compatible” donor RBCs 7-10 days after a transfusion, following an anamnestic immune response to a donor RBC antigen to which the recipient has been alloimmunized by a previous transfusion or pregnancy | ||
| Transfusion-associated graft-versus-host disease (TA-GVHD) | Immune attack against the recipient's tissues and organs by donor lymphocytes which engraft, proliferate, and mount an immune assault against the recipient | Donor lymphocytes not cleared by:immunocompromised patients andpatients who receive components from donors (eg, relatives) with whom they partially share HLA haplotypes survive and engraft in the recipient |
| Transfusion-associated circulatory overload (TACO) | Acute pulmonary edema secondary to congestive heart failure precipitated by transfusion of a volume of blood greater than what the recipient's circulatory system can tolerate | Usually rapid infusion or massive transfusion of blood in patients with diminished cardiac reserve, chronic anemia, infants, and the elderly, although no patient is immune |
| Anaphylaxis | Anaphylactic response of a presensitized patient to various proteins contained in donor plasma | Often, donor IgA infused into an IgA-deficient recipient with preexisting circulating anti-IgA triggers anaphylaxis |
| Posttransfusion purpura (PTP) | Sudden, severe thrombocytopenia occurring 7-10 days after transfusion in a patient previously alloimmunized (by pregnancy or transfusion) to a platelet-specific antigen | Production of potent alloantibody to a platelet-specific antigen through an anamnestic immune response that follows reexposure to the antigen on the donor's platelets. Paradoxically, the antibody destroys the recipient's own (antigen-negative) platelets as well |
| Complication . | Definition . | Mechanism . |
|---|---|---|
| Transfusion-related acute lung injury (TRALI) | New acute lung injury (ALI) occurring within 6 hours after a transfusion, with a clear temporal relationship to the transfusion, in patients without risk factors for ALI other than transfusion21 * | Donor anti-WBC antibodies attacking the recipient's WBCs in the microcirculature of the lungs |
| “Two-hit” hypothesis implicating biologic response modifiers accumulating in supernatant plasma during storage† | ||
| Hemolytic transfusion reactions (HTRs) | Immune destruction of the transfused donor RBCs which are attacked by the recipient's: “naturally occurring” antibodies to the A or B antigens of the ABO blood group system, and/or alloantibodies to other RBC antigens produced following immunization through a previous transfusion or pregnancy | Acute HTR: Destruction of “incompatible” donor RBCs intravascularly or extravascularly (in the liver and/or spleen) by preexisting circulating antibody within 24 hours of a transfusion‡ |
| Delayed HTR: Destruction of “compatible” donor RBCs 7-10 days after a transfusion, following an anamnestic immune response to a donor RBC antigen to which the recipient has been alloimmunized by a previous transfusion or pregnancy | ||
| Transfusion-associated graft-versus-host disease (TA-GVHD) | Immune attack against the recipient's tissues and organs by donor lymphocytes which engraft, proliferate, and mount an immune assault against the recipient | Donor lymphocytes not cleared by:immunocompromised patients andpatients who receive components from donors (eg, relatives) with whom they partially share HLA haplotypes survive and engraft in the recipient |
| Transfusion-associated circulatory overload (TACO) | Acute pulmonary edema secondary to congestive heart failure precipitated by transfusion of a volume of blood greater than what the recipient's circulatory system can tolerate | Usually rapid infusion or massive transfusion of blood in patients with diminished cardiac reserve, chronic anemia, infants, and the elderly, although no patient is immune |
| Anaphylaxis | Anaphylactic response of a presensitized patient to various proteins contained in donor plasma | Often, donor IgA infused into an IgA-deficient recipient with preexisting circulating anti-IgA triggers anaphylaxis |
| Posttransfusion purpura (PTP) | Sudden, severe thrombocytopenia occurring 7-10 days after transfusion in a patient previously alloimmunized (by pregnancy or transfusion) to a platelet-specific antigen | Production of potent alloantibody to a platelet-specific antigen through an anamnestic immune response that follows reexposure to the antigen on the donor's platelets. Paradoxically, the antibody destroys the recipient's own (antigen-negative) platelets as well |