- Definition
- Pathophysiology
- Systems Affected
- Genetics
- Incidence/Prevalence
- Geographic Distribution
- Signalment
- Signs
- Causes
- Risk Factors
BASICS
- Blood and/or blood components can be administered as biological therapeutic agents
- A TR is an adverse clinical consequence or reaction to the administration of blood or blood component
- Administration of nonideal BP may induce a TR due to the additional unnecessary components (usually plasma) of the BP
- TRs can be immune-mediated or nonimmune mediated; may or may not involve hemolysis of recipient or donor RBCs; can occur immediately or be delayed hours to days after administration; and may involve the transmission of an infectious agent
- Different methods of processing whole blood into components achieve different levels of purity and can affect the incidence of TR
- Improper methods and techniques of collection, processing, storage, or administration of the BP can induce a TR
- Sourced from other horses, BPs contain antigens that can be recognized by the recipient as foreign (alloantigens) and induce an immune-mediated reaction in the recipient
- Autologous alloantibodies to RBC surface antigens do not naturally occur in horses, thus hemolytic reactions are uncommon during first blood transfusions; alloantibodies to RBC antigens develop within 3–10 days of exposure (original transfusion) and therefore caution is indicated with subsequent transfusions
- Immune-mediated TRs can be induced by administered RBCs, WBCs, plasma proteins, or platelets interacting with the recipient's immune system
- Common immune-mediated reactions include hemolysis (acute or delayed), febrile nonhemolytic TR, allergic reactions ranging from mild urticaria to severe anaphylaxis, thrombocytopenia, transfusion-related acute lung injury, and post-transfusion purpura
- Anaphylaxis represents the most severe form of allergic transfusion reaction and can occur following administration of very small volumes of BP (a few mL)
- Common nonimmune-mediated reactions include circulatory volume overload; hypocalcemia, e.g. citrate toxicity; coagulopathy, e.g. excess anticoagulant administration; transmission of blood-borne infectious agents; hemosiderosis and hemoglobinemia; and hyperkalemia, e.g. administration of hemolyzed RBCs
- Blood-borne infectious agents transmissible by plasma include Theiler disease-associated virus (serum hepatitis) and equine infectious anemia virus and in whole blood include Babesia spp. and Anaplasma phagocytophilum
- Hepatic failure is a complication in foals receiving blood transfusion(s) especially those receiving >4 L of blood; deferoxamine enhances urinary iron elimination and decreases hepatic iron accumulation, reducing the risk of hepatic failure in these foals
Differences in inherited blood types, WBC and platelet antigens, and protein polymorphism contribute to incidence.
- Plasma—horses <7 days of age 9.7%; horses >7 days of age and adults <2% (commercial, plasmapheresis) and 10% (inhouse, gravity sedimentation)
- Whole blood—adult horses 16%
- Previous transfusion of blood or BP
- Transfusion of old, damaged, or hemolyzed blood or BP
- Improper aseptic technique for collection or administration of blood or BP
- Improper storage or handling of blood, BP, or transfusion supplies and equipment
- Acute hemolysis and delayed immune-mediated hemolysis; fever, restlessness, tachycardia, tachypnea
- Febrile nonhemolytic TR—increase in body temperature >1°C during transfusion with or without malaise, signs of abdominal pain, tachycardia, and tachypnea
- Allergic reaction—piloerection, pruritus, urticaria, tachycardia, tachypnea, dyspnea, nasal and/or pulmonary edema, signs of abdominal pain, muscle fasciculations
- Anaphylaxis—signs of abdominal pain, diarrhea, tachycardia, tachypnea, dyspnea, nasal and/or pulmonary edema, hypotension, shock, cardiac dysrhythmias, loss of consciousness, cardiac arrest, death, fever often absent
- Contaminated transfusion—fever, tachycardia, tachypnea
- Circulatory volume expansion—hypertension, jugular vein distention, pulmonary edema, cardiac dysfunction, dyspnea, tachypnea
- Hypocalcemia—cardiac dysrhythmias, ileus, signs of abdominal pain, synchronous diaphragmatic flutter (“thumps”), tachycardia (bradycardia if severe hypocalcemia), tachypnea, muscle fasciculations, trismus
- Hemolytic TRs involve either antibodies directed against recipient RBCs present in administered plasma or preexisting or acquired antibodies in the recipient's own plasma directed against transfused RBCs (inducing immediate or delayed TR respectively)
- Antibodies binding RBC surface alloantigens cause complement activation, RBC lysis, and cytokine release
- Febrile, nonhemolytic TRs are likely associated with leukocyte-derived cytokines and/or circulating antileukocyte antibodies in the recipient; most common TR
- Allergic/anaphylactic reaction is an IgE-mediated (type 1) hypersensitivity reaction due to interaction of a donor antigen with recipient IgE antibodies results in mast cell degranulation, histamine release, and complement activation
- Related to the physical volume of the administered BP into the vascular space if the recipient's circulating volume is not reduced, degradation of RBCs or WBCs in the BP, contamination of the BP at the time of collection (infectious agents), or the effect of the anticoagulant
- Pyrogens and proinflammatory substances can accumulate during storage or can be released by degradation of leukocytes during storage
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS