Blood Transfusion Reaction
From Anvita Health Wiki
Introduction
- immediate immunologic transfusion reactions
- acute intravascular hemolysis
- etiology:
- clinical errors: misidentification of patient or patient's blood specimen accounts for the majority of fatal transfusion reactions
- caused by ABO incompatible plasma or red cells
- involves complement-fixing IgG & IgM antibodies
- fever
- tachycardia
- hypotension
- acute renal failure 5 pain at infusion site
- chest pain
- abdominal pain
- flank pain
- incidence < 1:50,000
- laboratory:
- red plasma & urine: hemoglobinuria
- plasma free hemoglobin;
- direct antiglobulin test ( Coomb's test) is positive
- management:
- stop transfusion
- clotted & EDTA-treated blood specimens along with patient's blood & tubing should be sent to lab
- send freshly voided urine to lab for free hemoglobin
- support blood pressure
- maintain urine output at 100 mL/hr with IV fluids, diuretics, & mannitol if necessary
- NaHCO3 to alkalinize urine may aid in excretion of hemoglobin
- urticarial reactions
- etiology: recipient sensitized to donor antigens
- epidemiology: incidence: 1-3% of all transfusion
- pathology: plasma contituents can react with patient's IgE on mast cells
- clinial manifestions: rapid onset of hives, rash, wheezing during or after transfusion
- treatment: antihistamines, corticosteroids
- anti- IgA antibodies in IgA-deficient individuals
- clinical manifestations: sudden hypotension & respiratory distress during transfusion
- incidence: < 1:1000
- prevention: use of washed RBC in IgA-deficient patients or use of blood components from IgA-deficient donors
- etiology:
- recipient response to donor leukocytes (antibodies)
- donor leukocyte cytokines
- incidence: 1-3%; more common in multiply transfused patients
- clinical manifestations: occur at the end of, or after transfusion complete; rapid onset fever & chills; headache; anxiety; myalgia; pulmonary distress (rare)
- laboratory: direct antiglobulin test to rule out hemolytic transfusion reaction
- treatment: antipyretics, glucocorticoids
- prevention:
- platelet alloantibodies
- HLA or platelet-specific antibodies, i.e. anti-PLA-1
- clinical manifestations: fever; edema; failure to maintain increased platelet count after transfusion; petechiae, purpura & severe thrombocytopenia within days with anti-PLA-1
- incidence: high-frequency of platelet alloantibodies in multiply transfused patients
- prevention: use of leukocyte filters for transfusion of cellular blood products
- transfusion-related acute lung injury
- etiology: donor antibodies reacting with recipient leukocytes causing leukocyte aggregation in the pulmonary capillary bed [4]
- epidemiology: rare
- clinical manifestations:
- fever/ chills, tachycardia, dry cough, hypoxemia
- non- cardiogenic pulmonary edema
- acute respiratory distress syndrome
- occurs 2-4 hours after initiation of transfusion
- laboratory: complete blood count ( CBC): eosinophilia
- radiology: chest X-ray: perihilar, patchy infiltrates
- treatment:
- stop transfusion
- respiratory support
- vasopressors for hypotension
- delayed immunologic transfusion reactions
- delayed immune hemolysis
- etiology: sensitization to RBC antigens (not ABO):
- esp. Rh, Kidd, Duffy, MNS antigens
- anamnsetic production of non- complement fixing IgG antibodies
- extravascular removal of antibody-coated RBCs
- anemia; fever; arthralgia; renal failure (mild)
- delayed hemolytic reaction typically occurs 4-13 days after transfusionb)
- incidence: 1 in 5000 (occurs in previously transfused patients or multiparous women)
- laboratory:
- complete blood count ( CBC): drop in hemoglobin
- serum LDH: increased
- serum bilirubin: hyperbilirubinemia;
- positive direct antiglobulin (Coomb's) test
- reticulocyte count: increased
- serum haptoglobin: decreased
- a new alloantibody appears in
- prevention
- wallet card identifying alloantibodies
- transfusion with compatible blood
- patient education
- graft vs host disease
- etiology:
- proliferation of donor-derived HLA-incompatible transfused lymphocytes
- occurs in immune compromised recipients & patients who receive blood components from relatives
- dermatitis; gastrointestinal & liver dysfunction
- immune suppression
- high mortality
- incidence: < 1 in 1000
- prevention:
- use of irradiated blood products (at least 2500 rads) if transfusing with relative's blood or in immunocompromised recipients
- use of irradiated blood components is an absolute requirement in bone marrow transplant recipients
- transfusion-related immune suppression
- etiology: unknown
- clinical manifestations:
- frequently subclinical;
- increased risk of bacterial infections
- increased cancer progression
- incidence: common; frequently unrecognized
- prevention: autologous blood transfusion
- immune-mediated thrombocytopenia ( ITP)
- thrombocytopenia occurring >= 1 week after transfusion
- most common in women
- prior pregnancy sensitizes women to platelet antigen-1 ( PlA1)
- laboratory: antibody to P1A1 ( HPA-1a)
- treatment is immune globulin
- immediate non- immunologic effects
-
- clinical manifestations: heart failure (right & left) pulmonary & peripheral edema
- incidence: common
- prevention: slow or incremental transfusion; careful monitoring; diuretics
- citrate toxicity
- etiology: sudden drop in serum ionized Ca+2
- clinical manifestations: hypotension & cardiac arrhythmias
- incidence: rare except in massive transfusions (> 12 units/hour in an adult)
- prevention: treatment with calcium gluconate or chloride washed RBCs in small recipients
- etiology: accidental infusion of air
- clinical manifestations: loss of consciousness; hemodynamic collapse; tachycardia; chest pain; dyspnea
- incidence: extremely rare, greatest risk with intra- operative blood salvage systems
- management: place patient on left side with head down & feet up
- potassium overload
- etiology: elevated K+ in older or irradiated RBCs
- clinical manifestations: hyperkalemia in massively transfused or smaller patients
- incidence: rare unless patient with pre-existing renal failure or acidosis
- prevention: use of washed RBCs
- delayed non- immunologic effects
- transfusion hemosiderosis
- etiology: 1 mg of iron/ mL of packed RBCs
- clinical manifestations: deposition of iron in heart, liver, lungs & bone marrow
- incidence: common in chronically transfused patients
- prevention:
- minimize unnecessary transfusion
- erythropoietin may be useful
- iron chelation therapy
- infectious complications
-
- etiology: failure to recognize asymptomatic donors infected with HIV-1, HIV-2, HTLV-1, HTLV-2, hepatitis viruses, CMV, & others
- clinical manifestations: related to transmitted virus
- incidence: (risk per unit of component transfused) HIV: < 1 in 200,000 hepatitis B: < 1 in 200,000 hepatitis C: < 1 in 3000 HTLV: < 1 in 60,000 CMV: 50-100% of donors are infected
- prevention:
- transmission of bacteria & bacterial endotoxins
- etiology:
- unrecognized bacteremia in donor
- contamination during processing
- bacterial contamination of donor platelets is the most common cause
- E. coli & Pseudomonas are associated with refrigerated components
- Yersinia, Serratia & Salmonella are associated with platelets
- shock & disseminated intravascular coagulation (DIC)
- high mortality
- incidence: < 1 in 500,000 as cause of death
- prevention:
- proper skin preparation with blood donation
- good blood banking practices
- deferring donors with febrile illnesses
- use of leukocyte-depleted blood components
- etiology: donors infected with parasites, i.e. Plasmodium ( malaria), Trypanosomes ( Chagas' disease)
- clinical manifestations: related to transmitted parasite
- incidence: rare in the USA
- prevention:
- donor screening
- development of serologic tests
More General Terms
References
- Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 615-616
- The Washington Manual of Medical Therapeutics, 29th edition, Carey, CF et al (eds), Lippincott-Raven, Philadelphia, 1998, pg 272-73
- Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 790
- Medical Knowledge Self Assessment Program (MKSAP) 11, 14, American College of Physicians, Philadelphia 1998, 2006
