Transfusion Medicine-Printer Friendly Version
Last revised 8 September 2007
Copyright (c) 2007, PathologyOutlines.com, Inc.
See also Coagulation chapter
Bold and underlined topics are hypertext links
References in green are journals with free full text-no registration
Transfusion Medicine - table of contents
Transfusion reaction: general, acute hemolytic, allergic-mild, allergic-severe, delayed hemolytic, febrile nonhemolytic, graft versus host disease, immune system modulation, nonimmune hemolysis, red blood cell alloimmunization, transfusion related acute lung injury
Transfusion side effects: circulatory overload, coagulation effects, hemoglobinopathy (apparent), hypotension, iron overload, metabolic effects, platelet antibodies, post transfusion purpura, transfusion-associated microchimerism
Transfusion transmitted disease: general, pathogen inactivation, Babesiosis, bacteria, CMV, variant Creutzfeldt–Jakob, Hepatitis B, Hepatitis C, HIV, HTLV, malaria, Parvovirus, SEN virus, syphilis, Toxoplasma, transfusion transmitted virus, Trypanosoma cruzi, West Nile virus
Standards for blood banks: general
Primary references for Transfusion Medicine
American Journal of Clinical Pathology (AJCP), January 1975 to July 2007
Archives of Pathology and Laboratory Medicine (Archives), January 1976 to August 2007
Biomed Center, 1 March 1997 to 17 August 2007
Henry’s Clinical Diagnosis and Management by Laboratory Methods (2006, 21st ed)
Journal search terms: transfusion and each disease entity listed
Please refer to these primary references for more detailed discussions and additional images
Transfusion reaction
Usually identified during or shortly after transfusion
If identified during transfusion:
- stop transfusion; keep IV line open with saline
- report to blood bank/transfusion service using standard forms
- check labels of transfused components for clerical errors
- check post-transfusion serum/plasma for hemolysis compared to pre-transfusion sample
- perform DAT (direct antiglobulin test) on post-transfusion specimen, compare it to pre-transfusion sample
- document transfusion reaction in patient’s chart
If identified after transfusion:
- determine cause, document in patient’s chart
Algorithm for patient management and blood bank investigation
Acute hemolytic transfusion reaction
By definition, presents within 24 hours of transfusion
Usually due to accidental transfusion of ABO incompatible red blood cells (see Standards section below for prevention strategies)
Less commonly due to anti-Pk, anti-Vel or rarely anti-Lea (Lewis), anti-Jka, anti-Jkb (Kidd) or anti-K1 (Kell) antibodies
May be immune mediated due to effect of drugs (cefotetan-Am J Hematol 2000;64:67, oxaliplatin chemotherapy-Transfusion 2004;44:838)
Incidence of 1 per 14-38K red cell transfusions (20 annual deaths in US)
Severity is related to volume of incompatible blood transfused
Hemolytic antibodies cause complement mediated lysis of red blood cells in peripheral circulation; extravascular hemolysis is less common
Complement activation causes release of cytokines, leading to fever (increased temperature of at least 1°C), chills, hypotension, wheezing, chest pain, nausea and vomiting, flank pain
Variable patient symptoms - 47% have none; severe reaction causes DIC, bleeding, renal failure, shock, circulatory collapse and death (2%)
Laboratory: hemoglobulinemia and hemoglobinuria; elevated LDH, bilirubin, low haptoglobin (Eur J Clin Invest 2006;36:202); may have positive direct antiglobulin test (DAT)
May also occur due to ABO incompatible plasma in platelet products (Archives 2007;131:909)
- very rare; less than 20 case reports, all involving group O platelets
- usually occurs in group A patients or those with anti-A titers greater than 1:1000
- can prevent by removing plasma from platelets, or limiting number of incompatible group O platelets in a 24 hour period
Case reports: due to antibodies - ABO incompatible platelet products #1 (AJCP 1999;111:202), #2 in a baby (J Clin Apher 2005;20:225), anti-Bg HLA antibodies (Transfusion 2003;43:753), anti-Coa (Immunohematol 2001;17:45), anti-Dombrock(a) (Transfusion 2006;46:244), anti-Fy3 in a non sickle cell disease patient (Immunohematol 2005;21:48), anti-IH in a patient with sickle cell disease (Transfusion 2000;40:828), anti-Jka not detected by polybrene screen (Ann Clin Lab Sci 2006;36:101), anti-Jra (Transfusion 2004;44:197), anti-P1 (Transfusion 1998;38:373)
due to non-antibodies - chimeric red cells in a donor who was a twin (Transfusion 2003;43:1449), sickle cell disease (Transfusion 2001;41:323)
Treatment: stop transfusion but maintain IV access; hydration and diuretics (maintain renal perfusion but avoid fluid overload), possibly dopamine (maintain blood pressure and cardiac function); possibly exchange transfusion; report to blood bank promptly since another patient may be at risk if there is a name mix up
References: Merck Manual
Allergic transfusion reaction - mild
Common (1 per 2000 transfusions); occur with all types of blood components but less common with red blood cells
May occur with autologous blood products (Archives 2003;127:316)
Symptoms: pruritis, urticaria, erythema, cutaneous flushing, angioedema, nausea, vomiting, diarrhea, abdominal pain; 10% have only pulmonary symptoms
Prevention: pretreatment with diphenhydramine is common but controversial (Transfus Med Rev 2007;21:1, Br J Haematol 2005;130:781), removal of plasma because reaction may be due to antibodies to donor plasma proteins; washing red blood cells and platelets, but not if only cutaneous allergic reaction
Treatment: stop transfusion immediately and maintain IV access; intubate or administer oxygen if necessary; diphenhydramine (50-100 mg) is usually effective; may need epinephrine for severe reactions
Can restart the transfusion if reaction is mild; if reaction is severe, do not restart
Allergic transfusion reaction - severe / major (anaphylactic)
Symptoms similar to anaphylaxis but not mediated by IgE
Occurs in 1 per 30,000 transfusions
Death is rare (8 deaths in a 9 year period, Transfusion 1990;30:583); reaction may promote death in ill patients
Causes: IgA deficiency (< 0.05 mg/dL) plus anti-IgA antibodies (obtain quantitative IgA levels) causes <20% of cases (Immunohematol 2004;20:226); haptoglobin deficiency due to IgG or IgE antihaptoglobin (more common in Japan); also plasma proteins, chemicals used to sterilize tubing, penicillin or other drugs; cause is often unknown (Curr Opin Hematol 2003;10:419)
Symptoms: those of mild allergic reaction (above) plus hypotension, tachycardia, chest pain, loss of consciousness, arrhythmia, shock, cardiac arrest, dyspnea or stridor, wheezing; no fever
Prevention: premedication with antihistamines or corticosteroids; if IgA deficiency, use IgA deficient plasma or wash red cells and platelets; resuspending platelets in a nonprotein storage solution instead of fresh frozen plasma may be helpful (Transfusion 2002;42:556)
Case reports: 4 year old girl receiving blood from mother (Acta Anaesthesiol Scand 2002;46:1276)
Treatment: stop transfusion but maintain IV access; intubation, oxygen, IV fluids, epinephrine as needed, antihistamines as needed, particularly if urticaria, aminophylline for bronchospasm; steroids for chronic symptoms
Delayed hemolytic transfusion reaction
By definition, occurs 24 hours or more after transfusion, usually within 2 weeks
Due to anamnestic immune response in patients previously alloimmunized by certain RBC antigens; hemolysis is usually extravascular
Cannot be detected by pretransfusion antibody screening tests or crossmatches because antibodies are present in low concentrations, have low affinity for antigen or indicator antigen is missing from test red cells
Antibodies are usually IgG reactive at 37°C, fix complement; Duffy (Fya) and Kidd (Jka) are most likely
Associated with prolonged intervals between initial and subsequent transfusions, as antibodies decrease to undetectable levels
Rarely is due to a primary immune response with no prior exposure (Immunohematol 2004;20:184)
Symptoms: usually mild hemolysis, fever, falling hematocrit, jaundice; may have “bystander hemolysis” affecting non-transfused red cells, due to complement activation and deposition of C3d on non-transfused red cells
Sickle cell patients usually have non-severe symptoms (Transfusion 2002;42:37), but may have acute pain syndrome with life threatening anemia due to bystander hemolysis (hyperhemolysis, Pediatrics 2003;111:e661)
Laboratory: anemia, mild hemolysis, reticulocytes, hyperbilirubinemia (unconjugated), increased serum LDH and WBCs, low haptoglobin, positive DAT, new RBC antibody present, spherocytes due to removal of portions of red cell membranes by splenic phagocytic cells
Prevention: accurate recordkeeping of prior red cell alloantibodies and avoiding reexposure; obtain accurate patient history of other transfusions and contact those institutions for their records; minimize transfusions; sickle cell patients should have their extended red cell antigen phenotype determined (ABO, Rh, Kell, Kidd, Duffy, Lewis, MNS) before transfusion therapy and receive units phenotypically matched for C, E, and Kell (Transfusion 2001;41:1086)
Case reports: severe reaction due to anti-At(a) (Transfusion 1999;39:834), due to anti-D (Transfusion 1998;38:459), due to anti-Go(a) (Am J Hematol 1996;53:248), due to anti-Jk(a) (Acta Chir Iugosl 2005;52:111), due to anti-Jk3 after massive postpartum hemorrhage requiring transfusion (Archives 1999;123:949), multiple episodes due to different antibodies (Transfus Sci 2000;23:107)
sickle cell patients - due to anti-c (Sao Paulo Med J 1999;117 n.1), due to anti-Js(a) (AJCP 1997;108:658), due to anti-s (J Pediatr Hematol Oncol 1999;21:70), with pregnancy (Obstet Gynecol 2007;110:471), with Serratia marcescens infection and death (J Natl Med Assoc 2006;98:1697)
Treatment: usually careful followup only; may need exchange transfusion if large number of antigen positive red cells; IV immunoglobulin may prevent transfusion reactions if compatible blood cannot be obtained
Febrile nonhemolytic transfusion reaction
Temperature rise at least 1º C, usually associated with chills or rigors, but without hemolysis
Usually during or within 1 hour of transfusion completion
Incidence of 0.1% of RBC transfusions, 0.1-1.0% of platelet transfusions
Due to pyrogenic cytokines and intracellular contents released from donor leukocytes
A particular problem with platelet transfusions because platelets are stored at room temperature, which allows contaminating leukocytes to remain functional
No complications, but costs time and money to rule out more serious transfusion reactions
Some recommend continuing the transfusion after reaction has been diagnosed to minimize number of donor exposures
Others recommend against continuing the transfusion because may have continued reaction or may have subsequent severe reaction if initial reaction was actually due to bacterial contamination or hemolysis
Patients are often pretreated for transfusions by acetaminophen and diphenhydramine, which benefits recipient but does not necessarily save money (Archives 2004;128:991, Transfus Med Rev 2007;21:1)
These reactions are underreported in cancer patients (MedGenMed 2004;6:17)
Prevention: leukocyte reduction (Transfusion 2004;44:10, Transfusion 2004;44:25, but see Transfusion 2001;41:997); pre-storage reduction may be more effective than post-storage reduction; plasma removal is also helpful
Treatment: acetaminophen (optional, fever is usually self limited), diphenhydramine (commonly used, but may have no effect)
DD: bacterial contamination, hemolytic transfusion reaction, disease related fever, rise to normal temperature in initially hypothermic patient
Graft versus host disease - transfusion related
Rare
Viable donor CD8+ T cells proliferate and attack recipient’s bone marrow cells and possibly other organs (Osaka City Med J 1999;45:37); recipient’s immune system does not attack these donor T cells
Usually 2-50 days after transfusion
Rate markedly reduced after universal leukoreduction in United Kingdom (Transfusion 2007;47:1455)
Very rare in blood stored 4+ days due to WBC inactivation (Br J Haematol 2000;111:146)
Symptoms: skin rash, diarrhea, fever, abnormal liver function tests, pancytopenia, hypoplastic marrow
Risk factors: marked cellular immunodeficiency; recipient may have normal immunity if homozygous for a HLA haplotype and donor is heterozygous with one shared haplotype, which causes donor cells to see recipient cells as foreign, but recipient cells don’t see donor cells as foreign (high risk if directed donations from first or second degree relatives); rural areas where gamma radiation is not possible (Transfusion 2007;47:1405, Indian Pediatr 2004;41:1260)
Indications for irradiating blood components to inactivate donor lymphocytes:
absolute - chemotherapy with purine analogs, congenital cellular immunodeficiency (severe combined immunodeficiency, DiGeorge syndrome), hematopoietic progenitor cell transplantation, granulocyte transfusion, Hodgkin’s lymphoma, intrauterine transfusion, neonates who have received intrauterine transfusion, transfusion from relatives
probable - infants < 1200g, non-Hodgkin’s lymphoma/leukemia (Vox Sang 2002;83:279), HLA-matched platelet concentrates, high dose chemotherapy, radiation therapy or aggressive immunotherapy
controversial - solid organ transplants, large volume or exchange transfusions in infant who did not receive intrauterine transfusion, aplastic anemia, absolute lymphopenia
NOT indicated - HIV infection, hemophilia, humoral immunodeficiency (common variable immunodeficiency), small volume transfusions in term infant who did not receive intrauterine transfusion, elderly, immunosuppression other than purine analogs, pregnancy, red cell disorders (hemoglobin, membrane or metabolic)
Diagnosis: skin biopsy
Case reports: fatal case caused by blood from unrelated HLA homozygous donor #1 (AJCP 2000;113:732), #2 (Transfusion 2006;46:885); fatal cases caused by blood from related donors - father (Indian J Pediatr 2005;72:533), first-degree relatives (J Natl Med Assoc 2005;97:418)
Treatment: 90% mortality, usually due to infection
Immune system modulation due to transfusion
Also called transfusion related immune modulation (TRIM)
Transfusion is “liquid allogeneic transplant”, causing changes to immunologic profile of recipient (Archives 2007;131:708)
Transfusions may increase nosocomial infections in critically ill patients (Crit Care Med 2002;30:2249) and overall mortality (JAMA 2002;288:1499); for ICU patients, one study found reduced mortality with lower hematocrit trigger, possibly due to fewer transfusions (N Engl J Med 1999;340:409)
However, transfusions also decrease recurrence of Crohn’s disease (Colon Rectum 1989;32:749) and enhance graft survival after HLA-DR shared blood transfusions (Hum Immunol 2002;63:902)
No reduction in infectious complications from leukoreduction (Shock 2006;26:342)
References: Chest 2005;127:295, Transfus Clin Biol 2001;8:315.
Nonimmune hemolysis and transfusion
Must exclude immune causes
Hemolysis of red cells may occur from storage and handling, hyper- and hypoosmotic fluids, thermal injury
Lysed red cells may cause hemodynamic, renal and pulmonary problems, possibly death
Laboratory: hemoglobinemia, hemoglobinuria, possibly hyperkalemia (if renal failure)
Treatment: stop transfusion but maintain IV access, save blood bag, tubing and IV fluids; rule out hemolytic transfusion reaction, monitor serum potassium and urine output
DD: hemolytic transfusion reaction with no identifiable antibody, percutaneous mechanical thrombectomy (Transfusion 2005;45:1291), transfusion related infection (malaria, babesiosis)
Red blood cell alloimmunization and transfusion
Red cell antibodies occur in 3% of general population, 5-37% with thalassemia (Transfus Med 2006;16:200), 18-47% with sickle cell anemia (Transfusion 2002;42:37), 20% if prior transfusion but no hematologic or oncologic disease
Still occurs in pregnancy despite widespread antenatal and postpartum Rhesus immune globulin (RhIG), due to inadvertent failure to administer and antenatal sensitization prior to administration of RhIG (Semin Hematol 2005;42:169)
Incidence not affected by prestorage leukoreduction (Br J Haematol 2005;129:151)
Different antibodies appear at different times after transfusions (Transfusion 2006;46:250)
Recommended to match red cells for E antigens in thalassemia patients (Southeast Asian J Trop Med Public Health 2006;37:1015)
Usually no acute hemolytic transfusion reactions even if red cell antibodies present, if accurate antibody identification and component phenotyping occurs during compatibility testing
Delayed incompatibility occurs in 1 per 1500 units due to anamnestic response in previously sensitized patient; however, often no actual hemolysis and is termed delayed serologic transfusion reaction
May cause transfusion challenges in solid organ transplant patients (Transplantation 2007;84:527)
Appears to be regulated by CD4+ CD25+ T cells (Am J Hematol 2007;82:691)
Alloimmunization may be reduced by molecular testing (Curr Opin Hematol 2006;13:471, Transfusion 2006;46:841)
Transfusion related acute lung injury (TRALI)
Clinical diagnosis of acute respiratory distress, usually during or within hours of transfusion
#1 cause of death from transfusion therapy
Incidence of 1 per 5,000 units of packed RBC
Considered a subtype of ARDS, but associated with better outcome than non-TRALI ARDS
Computer screening identifies more cases of post-transfusion hypoxemia than are reported voluntarily (AJCP 2005;124:601)
Epidemiologic studies: allogeneic red blood cell transfusion is an independent risk factor for ARDS in the intensive care unit population; follows a dose-response relationship (Crit Care 2007 Jun 6;11(3):R63 [Epub ahead of print]), but see Eur J Anaesthesiol 2007;24:355; transfusions of plasma-rich blood products, FFP and platelets may have higher risk of ARDS than RBC transfusions (Chest 2007;131:1308); restrictive transfusion policies reduce late onset ARDS in trauma patients (J Trauma 2007;63:1)
Symptoms: vary from mild to life threatening; usually rapid onset of shortness of breath, severe hypoxemia (<90% pO2 on room air), tachycardia, fever, hypotension, cyanosis, noncardiogenic pulmonary edema; by definition, no findings of circulatory overload, no preexisting acute lung injury or ARDS
Chest Xray: necessary to confirm diagnosis; bilateral infiltrates resembling pulmonary edema, may persist after symptoms subside
Pathophysiology: endothelial damage likely due to donor antibodies against recipient HLA or other granulocyte antigens (Hematology Am Soc Hematol Educ Program 2006;497); testing for these antibodies is not required for diagnosis and is not predictive (Vox Sang 2007;93:70, Vox Sang 2007;92:247); granulocytes accumulate within pulmonary vasculature and extravasate into alveoli (AJCP 1999;112:216)
Risk factors: plasma from female donors (Transfusion 2007;47:599), particularly in critically ill patients (Crit Care Med 2007;35:1645), sepsis, chronic alcohol abuse; possibly presence of donor antigranulocyte or HLA class II antibodies (Am J Respir Crit Care Med 2007 [Epub ahead of print]), increasing number of units of whole blood transfused (AJCP 2007;128:128)
Case reports: transfusions between mother and daughter (AJCP 2004;121:590), 2 cases in children (Transfus Med 2006;16:343), 67 year old man with transfusion for iron deficiency anemia (CMAJ 2007;177:149), recurrence 2 years later (Transfus Med 2007;17:192)
Treatment: stop transfusion, maintain IV access and consult blood bank; antipyretics and fluids (for fever and hypotension), oxygen; ventilation if needed; usually resolves within 2-4 days but 20% die
DD: fluid overload from transfusion, bacterial contamination, allergic reaction, ARDS, pulmonary embolism, pulmonary hemorrhage
References: Transfusion 2004;44:1774 (consensus panel), summary of consensus panel, ASH update, Blood 2005;105:2266
Transfusion side effects
Circulatory (fluid / volume) overload due to transfusion
Also called transfusion associated circulatory overload (TACO)
Occurs when transfusion volume exceeds cardiovascular capacity
Common; 1 per 2,000 red cell transfusions, 1 per 400 red cell transfusions in ICU (Transfusion 2006;46:1478); 1% of elderly patients with total knee or hip replacement (Immunohematol 1996;12:87), 1 per 6,000 platelet pool recipients
May occur after only 1-2 units of red cells
Prevent by slowing rate of transfusion (longer infusion or breaking component into smaller aliquots and giving them over time)
Risk factors: compromised cardiovascular function, current volume overload, small intravascular volume (elderly, young children), severe chronic anemia
Symptoms: dyspnea, hypoxemia, elevated venous pressure, pulmonary edema and rales, orthopnea, possible congestive heart failure
Chest Xray: pulmonary edema, distended pulmonary artery, cardiomegaly
Laboratory: elevated B-natriuretic peptide (BNP) is 81% sensitive and 89% specific (Transfusion 2005;45:1056)
Case reports: 84 year old man with respiratory distress after receiving fresh frozen plasma
Treatment: diuresis
DD: TRALI (usually no cardiovascular history, difficult to distinguish in critically ill patients-Crit Care Med 2006;34:S109), allergic reaction, other causes of congestive heart failure
References: Archives 2007;131:708
Coagulation effects of transfusion
Due to dilution of patient’s blood with red blood cells lacking platelets and coagulation factors, and possibly also to direct effects of trauma or surgery itself
Massive transfusion
Transfusion greater than 1 blood volume (70 mL/kg in adults, 85-100 mL/kg in neonates) or 10 units of blood in an adult in 24 hours
Onset and severity may differ in elective surgery versus trauma (Vox Sang 2005;89:123)
Causes decrease in fibrinogen
May cause hypothermia if red cells are not warmed prior to transfusion, leading to prolongation of PT and PTT and impaired platelet function
See also Metabolic effects of transfusion, below
May cause metabolic acidosis and hypokalemia due to citrate in red blood cell units
May cause hyperkalemia due to red cell damage from storage or irradiation
Complex coagulopathy occurs in trauma patients with hypothermia, shock, tissue anoxia, DIC
Treatment: sufficient RBC for adequate oxygen delivery, keep platelet count > 50K, plasma to replace plasma factors (early may be better, J Trauma 2007;62:112), cryoprecipitate for fibrinogen, possibly early recombinant factor VIIa (J Trauma 2007;62:1095); 1:1:1 ratio of red cells:plasma:platelets may be helpful (J Trauma 2006;60:S91); monitor PT, PTT, platelet count, fibrinogen
Some advocate use of fresh whole blood (J Trauma 2006;60:S59)
Protocols: trauma.org, Royal Children’s Hospital of Australia (diagram), Australian Red Cross
References: Can J Anaesth 2004;51:293
Hemoglobinopathy (apparent) due to transfusion
Due to receiving blood from donor with hemoglobinopathy; hemoglobin C is most common
Abnormal hemoglobin ranges from 1-14% of recipient hemoglobin; recipient often has received multiple transfusions (Archives 2006;130:1830)
Important to identify to avoid unnecessary testing and treatment, and to notify donor
See also transfusion related microchimerism, below
Other causes of “chimerism” include transplants (Transfus Med Rev 2007;21:134)
Conversely, detection of hemoglobinopathies may rarely be suppressed by transfusions (Archives 2005;129:e107)
Case reports: hemoglobin C (Archives 1999;123:642)
Hypotension due to transfusion
Defined as hypotension during transfusion with no evidence of transfusion reaction (i.e. no fever, chills, shortness of breath, flushing or urticaria)
Drop of 10 mmHg or more in systolic or diastolic arterial blood pressure from pre-transfusion pressure
May be due to activation of contact coagulation pathway and release of bradykinin (Transfusion 2007;47:410)
Associated with ACE inhibitors (ACE breaks down bradykinin in circulation) and some filters which activate contact pathway (J Heart Lung Transplant 2001;20:759)
Rare in pediatric ICU (4 events per 2509 transfusions, Transfusion 2006;46:1899)
Treatment: stop transfusion and maintain IV access; put patient in Trendelenburg position (head down, feet up) and give fluids; resolves when transfusion is stopped
Iron overload due to transfusion
Also called secondary iron overload
Inevitable side effect of transfusions because body cannot eliminate additional transfused iron
One unit of red cells contains 250 mg of iron
Iron accumulates in reticuloendothelial cells and parenchymal cells, causing damage to liver (Mod Path 2007;20 Suppl:S31), heart (Haematologica 2006;91:ECR19), endocrine organs (Saudi Med J 2004;25:1347), GI mucosa (Histopathology 2006;48:808)
See also Liver-nontumor chapter (Hemochromatosis)
Iron overload is associated with HFE mutation H63D in thalassemia patients, regardless of transfusion history (Indian J Pathol Microbiol 2007;50:82); may be related to elevation of Growth differentiation factor 15 (GDF15) and suppression of iron regulatory protein hepcidin (Nat Med 2007 Aug 26; [Epub ahead of print])
Prevention: use of erythropoiesis stimulating agents instead of transfusion (Future Oncol 2007;3:397)
Early symptoms: abdominal discomfort, lethargy, fatigue; mild hepatomegaly
Treatment: chelation therapy (effective, but poor patient compliance with subcutaneous/IV treatment, better compliance with oral agents-Am J Health Syst Pharm 2007;64:606)
Metabolic effects of transfusions
Due to preservatives, anticoagulants or other additives, and biochemical changes in blood components during storage (Archives 2007;131:708)
Citrate
Chelates calcium and serves as anticoagulant for blood components (CPDA-1 is citrate-phosphate-adenine anticoagulant-preservative); may cause transient decrease in recipient’s plasma ionized calcium, causing QT interval prolongation, decreased left ventricular function, hypotension, hypomagnesemia, cardiac arrhythmias
Citrate is metabolized to bicarbonate in liver, so patients with liver failure or premature infants (immature liver function) are most susceptible
Prevention: continuous calcium-gluconate infusion during large-volume peripheral blood progenitor cell leukapheresis (Transfusion 2003;43:1615)
Treatment: may require slowing the rate of transfusion or providing calcium / magnesium replacement
Potassium
Accumulates in supernatant of whole blood and red cells during storage because ATP pump is impaired at this temperature
Leakage is accelerated by gamma irradiation
Total potassium in supernatant of most transfusions is clinically insignificant, but rapid infusion of large volumes (> 20 mL/kg) of stored or irradiated red cells may cause fatal hyperkalemia in infants, children and rarely adults
Increased susceptibility if oliguric renal failure, hepatic failure or poor cardiac function
Case reports: ventricular fibrillation (Anaesth Intensive Care 2007;35:110)
Prevention: washing red cells or reducing volume of additive solution (Transfusion 2007;47:248, Eur J Cardiothorac Surg 2007;31:659), use of autotransfusion devices (Transfus Med 2007;17:89), potassium adsorption filter (Can J Anaesth 2004;51:639)
Glucose
Transfusions to neonates may cause hypoglycemia unless continuous glucose infusion of 4-8 mg/kg/min
Transfusions may cause transient hyperglycemia due to glucose in preservative; this leads to insulin release and may cause hypoglycemia
Hypoglycemia more common with CPDA-1 red cells than AS-1 or AS-3, because CPD has lower glucose concentration
Transfusions usually not a factor in hyperglycemia in liver transplant patients (World J Gastroenterol 2005;11:2789)
Platelet antibodies and transfusions
Due to platelet transfusions for thrombocytopenia (post-chemoradiation therapy); also from chronic red cell transfusions (Transfusion 2005;45:761)
Usually occur within 21-28 days after primary exposure (pregnancy or transfusion) or 4 days after reexposure
Cause platelet refractoriness - inability of transfusions to increase platelet count
Other causes of platelet refractoriness are related to consumption of platelets - fever, infection, drugs, bleeding, hypersplenism, DIC
Usually 4-6 units of platelets or 1 unit of apheresis platelets raises platelet count by 50-100K/μL; if no rise in platelet count after 1 hour, cause is likely antibodies (refractoriness)
If platelet count increases after 1 hour but drops after 24 hours, cause is likely due to consumption (see above)
Refer to blood bank for workup if there are two inadequate 10 or 60 minute post transfusion platelet counts
Prevention: reduce leukocyte content of platelet components (Blood 1991;77:201, Blood 2004;103:333); prescreening for antibodies (Transfus Apher Sci 2005;33:157), giving larger doses of platelets (Blood 2005;105:4106)
Treatment: select HLA-matched or crossmatched platelets for transfusion to avoid crossreactive HLA or platelet antigens; ABO identical platelets and first degree relatives are helpful unless relatives may be source for stem cell transplantation; IV immunoglobulin may have short term benefit
DD: neonatal alloimmune thrombocytopenia (due to maternal antibodies, Transfusion 2007;47:901)
References: Archives 2003;127:409, Haematologica 2005;90:247
Rare complication of transfusions (1 per 50-100K transfusions)
Usually affects multiparous women
Abrupt, sudden onset of severe thrombocytopenia (less than 10K/ μL), usually days to weeks after transfusions of platelets, red cells or plasma
Destroys transfused platelets expressing a platelet antigen (often HP1a) as well as patient’s own platelets
Self limited, usually resolves within 3 weeks, but may cause intracranial bleeds
Case reports: patient with HPA-1a and GPIa/IIa antibodies (Transfus Med 2006;16:69), dramatic drop in platelet count 14 days after red cell transfusions for trauma induced anemia
Treatment: IV immunoglobulin (0.4 g/kg/day for 5-8 days), possibly plasmapheresis or corticosteroids; platelet transfusions usually NOT recommended
DD: heparin induced thrombocytopenia (Thromb Res 2000;100:115), DIC, SLE
References: National Blood Service (UK)
Transfusion-associated microchimerism
Stable persistence of an allogeneic cell population; may increase to 2-5% of circulating WBCs
Present in 50% of transfused, severely injured patients at hospital discharge (J Trauma 2004;57:702)
Injury induces immunosuppressive milieu, leading to persistence of donor WBCs
Not affected by leukoreduction (Transfusion 2006;46:1863)
No apparent increased risk of transfusion associated graft versus host disease (Blood 2001;98:272)
References: Semin Hematol 2007;44:24
Transfusion transmitted disease
Transfusion transmitted disease-general
Blood is nutritious media for microorganisms
Any blood pathogen can theoretically be transmitted via transfusions
Most transfusion transmitted infections occur during window period between infection and ability of tests to detect the agent
Prevention: donor education (don’t donate if sick), donor selection (volunteer, not paid donors), donor screening by specific direct questioning, geographic exclusions based on potential exposure, comparing donor to list of prior deferred donors, examining and preparing phlebotomy site to minimize skin related microorganisms, testing blood for selected known agents, discarding components if post donation evidence of exposure or illness
Can also limit unnecessary transfusions and increase autologous donations (may be infectious, but rarely are given to nondonors, Archives 2005;129:1212, Archives 2005;129:981)
In US as of 2006, testing occurs for hepatitis B, hepatitis C, HIV1, HIV2, HTLV-I and II, syphilis, usually West Nile Virus
Testing for HIV and hepatitis viruses does not occur in developing countries (Lancet 2007;370:415)
Testing increases safety of blood supply and provides diagnostic information to tested donor (when informed of results-not done in all countries)
Nucleic acid testing has improved sensitivity of testing
References: Crit Care 2004;8 Suppl 2:S18, Archives 2007;131:702
Pathogen inactivation and transfusions
Additional layer of protection from known and unknown infectious agents (Semin Hematol 2007;44:32); includes leukoreduction (filtration), chemicals and mechanical agents (heat, radiation, fractionation)
Techniques may damage blood products or have their own side effects
Examples: Methylene blue for fresh frozen plasma (Vox Sang 2007;92:319), photochemical treatment with amotosalen and ultraviolet A for parvovirus B19 (Transfusion 2007;47:1062), S-303 for red cells (Transfusion 2006;46:1778)
References: Archives 2007;131:719, Transfus Apher Sci 2006;35:189, Transfus Apher Sci 2006;35:83 (plasma), Best Pract Res Clin Haematol 2006;19:205
Most frequently reported tick-borne pathogen transmitted by blood transmission
Endemic in North American mammals
Often no/mild symptoms; more severe in immunocompromised or asplenic patients
Parasite survives within refrigerated red cells
40 cases of transfusion transmitted disease reported in US
Include within differential diagnosis of febrile illness in immunocompromised recipients of blood transfusion, particularly in Northeastern US (Transfusion 2000;40:285)
Case reports: asymptomatic donor #1 with multiple recipients (Transfusion 2002;42:1154), #2 (JAMA 1999;281:927), WA1-type Babesia transmission #1 (Transfusion 2002;42:1482), #2 (J Infect Dis 1997;175:1259), transfusions with heart transplant (Emerg Infect Dis [serial online] 2003 Jan), case in Canada (CMAJ 2001;164:1721), Japan (J Clin Microbiol 2000;38:4511)
References: Transfus Med Rev 2002;16:131, Am Fam Physician 2001;63:1969, eMedicine #1, #2
Bacterial contamination of transfusions
Greater risk than viral transmission in Western countries
#2 cause of transfusion related death after hemolytic reactions; cause 10% of transfusion associated deaths in US
Transfusions may be a small risk factor for surgical site infection (Infect Control Hosp Epidemiol 1999; 20:250)
Clinical presentation is usually dramatic with onset during or shortly after transfusion; fever, chills, hypotension, nausea, vomiting; may lead to shock, renal failure, DIC, death
Must usually treat with broad spectrum antibiotics before bacteria is identified
70% of cases of transfusion related sepsis are due to gram positive organisms associated with skin flora at phlebotomy site
80% of transfusion related deaths are due to gram negative organisms that circulate transiently in blood of healthy donors
References: Clin Microbiol Rev 2005;18:195
Platelet transfusions - contamination by bacteria
Bacterial testing of platelets is required in US (CAP Today) and Canada (Transfusion 2007;47:421)
Bacteria are usually from skin flora (Propionibacterium acnes, Staphylococcus epidermidis)
Cultures detect only half of contaminated units in median 0.7 days for aerobic cultures or 3.7 days for anaerobic cultures (Transfusion 2007;47:644)
Bacterial contamination is found by culture in 1 per 1-3K units; sepsis develops in 10-40% of those receiving contaminated platelet units
For apharesis, risk of bacterial contamination is 1 per 5K units; risk of death is 1 per 500K screened negative products; higher risk for two arm apharesis procedures (Transfusion 2007;47:1134)
Recommended to divert first 30-50 mL of blood containing the skin plug and associated bacteria and to use effective skin disinfection methods (Transfusion 2006;46:476)
Photochemical treatment with amotosalen and ultraviolet A may reduce risk (Transfusion 2007;47:1125)
CAP recently added a phase I item to the Laboratory Accreditation Checklist, TRM.44955: “Does the laboratory have a system to detect the presence of bacteria in Platelet components?” (Archives 2004;128:958); and is subject of AABB standard 5.1.5.1 (Archives 2004;128:279)
Reagent strips are inadequate for detection of bacteria (Archives 2004;128:852)
Case reports: fatal infections (MMWR Morb Mortal Wkly Rep 2005;54:168), Listeria monocytogenes in donor (Transfusion 2006;46:305), Morganella morganii (Transfus Med 2004;14:237), Streptococcus bovis (Am J Hematol 2004;77:282), Streptococcus pneumoniae (Rinsho Ketsueki 2003;44:381)
Red blood cell transfusions - contamination by bacteria
Bacterial contamination present in 1 per 40K units (FDA talk)
Risk of transfusion transmitted bacteremia is 1 per 500K units of RBCs
Risk of death is 1 per 8 million units
Case reports: Yersinia enterocolitica #1 (Archives 1996;120:499), #2 (J Clin Microbiol 2000;38:2788), #3 (Transfusion 2005;45:814)
CMV is almost always latent in immunocompetent individuals
Present in 50-85% of US adults, 93% of blood donors in Ghana (Ghana Med J 2006;40:99); risk of transmission is 1%
Can cause pneumonitis, hepatitis, retinitis or organ failure in immunocompromised recipients, who should get CMV negative or leukoreduced blood components (Bone Marrow Transplant 2005;36:499, Transfus Med Rev 2005;19:181)
variant Creutzfeldt-Jakob disease (vCJD) and transfusions
Caused by prion protein that assumes an abnormal configuration, which promotes change to abnormal configuration of other proteins
Resistant to enzymatic degradation
Three forms of classic CJD: sporadic (85%), hereditary and acquired (through corneal transplants, pituitary gland derived growth hormone, dura mater transplants, inadequately sterilized brain electrodes)
vCJD is human equivalent of “mad cow” disease, due to epidemic of bovine spongiform encephalopathy, possibly due to prion in cattle entering human food supply
vCJD is rarely transmitted by transfusions of blood components but not plasma products
As of 2007, in United Kingdom, 66 individuals have received transfusion products from donors who later developed vCJD; 3 have developed symptoms of vCJD, one had no symptoms of vCJD but evidence of abnormal prion proteins at autopsy for unrelated death
Excluding transfusion recipients from donating blood is unlikely to change epidemiology of disease (Emerg Infect Dis 2007;13:89)
Case reports (transfusion related): United Kingdom - confirmed (Lancet 2006;368:2061), possible transmission (Lancet 2004;363:417), preclinical disease in patient with unrelated death (Lancet 2004;364:527), epidemiologic study (Vox Sang 2006;91:221), Case #4 in UK
References: AABB, eMedicine, Centers for Disease Control
Hepatitis B virus (HBV) and transfusions
Previously the most serious transfusion risk
Due to serologic testing, risk of transfusion transmitted HBV is now 1 per 1.3 million units in Australia (Intern Med J 2005;35:592), 1 per 640K in France (Transfus Clin Biol 2005;12:239), 1 per 200-500K in US (Archives 2007;131:702), 1 per 150K in Canada (Transfusion 2007;47:316), 1 per 17,500 in Shenzhen, China (Transfusion 2007;47:529), 1 per 1500 in Mexico (Rev Invest Clin 2006;58:101)
To reduce rates even further, vigilance for errors and donor selection may be as important as further testing (Euro Surveill 2005;10:17)
Value of nucleic acid testing is controversial (helpful- Vox Sang 2006;91:1, Transfusion 2005;45:1247; not helpful in low endemic areas-Mol Diagn Ther 2006;10:77)
In US, blood banks use sensitive HBsAg and anti-HBc tests
In most of world, prevalence of anti-HBc is >10%, and use of HBc antibody test may exclude many otherwise healthy donors (J Clin Virol 2006;36:S33)
Pathogen inactivation has eliminated transmission in US licensed plasma derivatives since 1985; however cannot be used for cellular components (Archives 2007;131:719)
Only one confirmed transfusion related case in US in 2003; false positive seroconversions may occur due to administration of immunoglobulin (Dtsch Med Wochenschr 2006;131:1325)
Microarray multiplex assay may be useful to detect Hepatitis B, C and HIV (Biochem Biophys Res Commun 2007;356:1017)
Vaccinated children may be susceptible in endemic areas (J Hepatol 2006;44:39)
Hepatitis C virus (HCV) and transfusions
Historical risk for “non-A, non-B hepatitis” was 7% from volunteer donated blood and 28% from commercial blood
9% of Chinese patients with HCV due to unscreened blood have developed cirrhosis after mean 13 years (Zhonghua Gan Zang Bing Za Zhi 2006;14:199)
Recommended to offer screening to patients (particularly children) who received blood products in 1992 (US) or previously, when blood was not screen for HCV (Acta Paediatr 2007;96:1050, Transfusion 2007;47:615, Transfusion 2005;45:1020)
Serologic testing and nucleic acid–based testing have reduced risk, although developing countries may not screen (J Hepatol 2006;45:607)
Identified in 1 per 250K donors in US (Archives 2007;131:702); donors are usually asymptomatic; risk factors are injection drug use, hemodialysis, incarceration, receipt of blood products prior to HCV testing; also ozone-enriched transfusion of autologous blood in Italy (Infect Control Hosp Epidemiol 2005;26:762); antigen positive donors may not seroconvert (Transfusion 2000;40:1280)
Documented breakthrough cases from nonreactive nucleic acid testing components are rare (Lancet 2000;355:41)
Yield of HCV lookback in Canada is likely zero when prior donations were tested by second or third generation EIA (Transfusion 2006;46:690)
Pathogen inactivation has eliminated transmission in US licensed plasma derivatives since 1985; however technique cannot be used for cellular components (Archives 2007;131:719)
References: Nature Medicine 2000; 6:1082 (history), eMedicine
HIV (HIV1/HIV2) and transfusions
Pathogen inactivation has eliminated transmission in US licensed plasma derivatives since 1985; however technique cannot be used for cellular components (Archives 2007;131:719)
Possibility of transfusion associated HIV is frightening to many patients, but actual risk is only 1 per 2 million for HIV1 in US, no reported cases for HIV2
Risk in France is 1 per 3 million (Euro Surveill 2005;10:5), in Ivory Coast is 1 per 6K (Transfus Clin Biol 2006;13:242)
Infectivity is 90-100% for contaminated blood versus 0-2% for needlestick injuries (AIDS 2006;20:805)
Current standard is serologic antibody testing (1 per 33K positive) plus nucleic acid testing (reduces window of seronegativity between time of infection and development of antibodies, Transfus Med 2007;17:200)
Risk exists for blood donated through window of seronegativity, and 4 “breakthrough” cases have been identified (nonreactive by nucleic acid testing-Vox Sang 2004;86:171, Transfusion 2004;44:929)
Most transfusion medicine litigation focuses on transfusion acquired HIV (Archives 2007;131:615)
Transfusion associated HIV cases usually have acute viral syndrome; if untreated, progress to AIDS in 10 years
References: Archives 2007;131:702
HTLV (HTLV 1/2) and transfusions
Endemic in the Caribbean and parts of Africa, Japan and South America
Most positive donors are asymptomatic
HTLV-I is rare in US; HTLV-II is common in IV drug users in US; HTLV-III is another name for HIV virus
Prevalence in donors: Brazil HIV clinic-2% (Sex Transm Dis 2006;33:302), California (US)-1 per 900K (Transfusion 2006;46:703), India-0.2% (Indian J Pathol Microbiol 2006;49:532), Peruvian pregnant women-2% (J Acquir Immune Defic Syndr 2006;42:604), Saudi Arabia-< 0.01% (Saudi Med J 2004;25:1419), Senegal-0.2% (J Clin Microbiol 2006;44:1550)
Risk of transmission in US is 1 per 3 million
Leukoreduction may be effective in removing HTLV (Transfusion 2004;44:42 but see Blood 2002;100:677)
Common transfusion transmitted infection worldwide
In US, 1300 new cases of malaria/year, but only 1-2 cases are due to transfusion
Donor deferral based on travel history is used to minimize transmission (Vox Sang 2006;90:77)
Most donors in transmission cases had traveled to an endemic area; are often “semi-immune” with low parasite loads (Transfus Med Rev 2005;19:229)
May be marked difference in antigen versus antibody rate (Saudi Arabia - 0.2% vs. 8%, Ann Saudi Med 2002;22:329)
Prevalence in donors (in endemic regions): Brazil - 1-3% (Rev Inst Med Trop Sao Paulo 2007;49:1), Kenya - 9% (East Afr Med J 2005;82:565), Nigeria - 10% (Trop Doct 2007;37:32)
Countries with high donor infection rates may process donor blood in vivo with quinine or sulfadoxine-pyrimethamine to kill parasites (Saudi Med J 2006;27:986, Am J Trop Med Hyg 2005;73:1119)
Case reports: 69 year old man in Texas with blood donor from Ghana (MMWR Morb Mortal Wkly Rep 2003;52:1075), 49 year old man with blood donor from West Africa (Centers for Disease Control), 70 year old man with donor from Cameroon (Swiss Med Wkly 001;131:320), 47 year old woman with striking fever (Mikrobiyol Bul 2005;39:101), review of US cases (N Engl J Med 2001;344:1973), Canadian cases (CMAJ 2001;164:377)
References: US FDA Workshop
Parvovirus B19 and transfusions
Virus present in blood in 1:5000 donors, but most adults show evidence of prior exposure
Usually causes mild, self-limited febrile illness
Attacks erythroblasts, may cause acute anemic crisis in patients with accelerated erythropoiesis, immunocompromise or pregnancy, although usually recipients have no symptoms (Transfusion 2005;45:1811)
Immune response usually clears infection and provides lifelong protection, but virus may persist in blood or tissue (Transfus Med 2007;17:263)
In Germany, incidence was 13 and 262 per 100K donors for viral loads above and below 100K IU/mL; blood with levels below 100K is considered safe due to high level of neutralizing antibodies; blood with viral loads > 100K IU/mL should not be transfused (Transfusion 2007 Aug 21; [Epub ahead of print], Transfusion 2006;46:1593)
Virus is difficult to inactivate, although photochemical treatment with amotosalen combined with UVA light appears to be successful (Transfusion 2007;47:1062)
Newly described DNA virus, distantly related to transfusion transmitted virus (Infect Dis 2001;183:359)
Prevalence increases with transfusions (Pediatr Infect Dis J 2006;25:390)
Frequently occurs early in life; in eastern Taiwan, present in 25-31% of adolescents, may be associated with urbanization, probably not parenteral transmission in this group (J Gastroenterol Hepatol 2007;22:171)
D- and H-variants are present in 2% of US population (Hepatology 2001;33:1303)
Present in 40% of hemodialysis patients in Poland (Wiad Lek 2006;59:751)
Weak association, at most, with hepatitis (Minerva Gastroenterol Dietol 2002;48:73, Transfusion 2005;45:1084)
High levels are associated with poor survival in HIV+ patients (AIDS 2005;19:1091)
No cases of transfusion transmitted disease in US since 1966
Detected by serologic testing, although blood with positive test in US is unlikely to be infectious (Transfusion 2002;42:94)
1200 cases detected in US donors during 1995-2000 (J Infect Dis 2002;185:545)
Test may contribute little to transfusion safety (NIH Consensus Report, AABB statement), although some consider it a marker (although nonspecific) for high risk behavior associated with other sexually transmitted diseases
Donor positive rates: Brazil - 3% (Sex Transm Dis 2001;28:710), Cameroon - 9% (Transfus Med 2003;13:267), Tanzania - 13% (East Afr Med J 1999;76:167), Turkey - 0.2% (Mikrobiyol Bul 2004;38:445)
Can be transmitted by blood transfusion; refrigeration kills most (but not all) spirochetes within 1-2 days, but platelets are stored at room temperature and some red cells are transfused immediately without refrigeration
Toxoplasma gondii and transfusions
Tested using IgG or IgM ELISA
Rare in US
Presence in blood donors associated with cats at home
Donor positive rates: Mexico - 7% (IgG by EIA, BMC Infect Dis 2007;7:75), Malaysia - 28% (Med J Malaysia 2002;57:304), Turkey - 20% for IgG by ELISA (Ethiop Med J 2006;44:257), 43% using Sabin Feldman dye test (Mikrobiyol Bul 2006;40:375)
Also called Torque teno virus
Non-enveloped human virus with a circular negative-sense ssDNA genome (FEBS J 2007 Aug 22 [Epub ahead of print])
Has extremely high degree of genomic variability (Arch Virol 2007 Aug 23 [Epub ahead of print])
Association with disease is unclear - occasionally associated with mild non A-E hepatitis (Ann Univ Mariae Curie Sklodowska [Med] 2004;59:539); also associated with viral hepatitis and healthy populations (Archives 2006;130:1680)
May be cofactor in classic (Mediterranean) Kaposi’s sarcoma (Acta Derm Venereol 2007;87:14)
High viral loads correlate with bronchiectasis and peripheral airflow limitation in children (Pediatr Infect Dis J 2006;25:804)
92-97% similarity between strains in camels and humans in UAE (J Med Virol 2007;79:188)
Donor/control positive rates:), Egypt - 48% (J Egypt Public Health Assoc 2005;80:651), India - 27% (World J Gastroenterol 2006;12:2432), Poland - 78% (Przegl Epidemiol 2006;60:581), Saudi Arabia - 50% (Ann Saudi Med 2006;26:444), Taiwan - 37% (Ren Fail 2007;29:553), US - 10% (J Infect Dis 1999;179:1242)
References: Rev Med Virol 2007;17:45, World J Gastroenterol 2006;12:5122
Trypanosoma cruzi and transfusions
Causes Chagas disease, endemic in South and Central America
50-100K chronic carriers in US, due to immigration
Rarely transmitted by transfusion in US; seropositivity may overestimate infectivity
Canada to start screening in 2008 (CMAJ 2007;177:242); Red Cross and other blood collection centers are screening in US
Photoinactivation may be useful for red cell suspensions (Transfus Apher Sci 2007 Aug 13; [Epub ahead of print]), platelets (Transfusion 2007;47:434) or plasma (Vox Sang 2006;91:285)
Donor/control positive rates: Brazil - 2% (Rev Soc Bras Med Trop 2006;39:530), Columbia - 0.4% (Biomedica 2005;25:527), Mexico - 0.5% (Salud Publica Mex 2006;48:13), US high risk regions - 1 per 5000 (MMWR Morb Mortal Wkly Rep 2007;56:141)
Case reports: transfusion from Bolivian blood donor to US child (Transfusion 2007;47:540)
West Nile Virus (WNV) and transfusions
Entered North America in 1999; still epidemic in North America due to mosquito and bird vectors
Symptoms: headache, new rash, generalized weakness (Transfusion 2006;46:272); may cause meningoencephalitis (AJCP 2003;119:749)
Detected by nucleic acid based testing, although virus adheres to human red blood cells in whole blood (Clin Infect Dis 2007;45:181)
In 2003-2005, 1425 infected blood donors were identified in US (Transfusion 2006;46:2038)
In 2003, only 6 cases of transfusion-transmitted WNV were documented in US from 12.6 million blood units donated and 23 million blood transfusions; fewer since strategy changed from minipool to individual nucleic acid testing method in epidemic areas (Dev Biol (Basel) 2007;127:43, N Engl J Med 2005;353:460)
Viral inactivation systems may be useful (Vox Sang 2006;91:345, Antiviral Res 2005;68:84)
Cost effectiveness models: In areas with high levels of WNV transmission, seasonal screening of individual samples and restricting screening to blood donations designated for immunocompromised recipients is cost saving; in areas with low levels of infection, using a standard questionnaire is cost-effective (PLoS Med 2006;3:e21, PLoS Med 2006;3:e99; see also Ann Intern Med 2005;143:486 and Ann Intern Med 2005;143:537)
Donor prevalence rates: Mexico - 0.03% (Transfusion 2006;46:111), Netherlands - 0% (Vox Sang 2006;90:166)
Epidemiologic reports from Centers for Disease Control (2002-2007): MMWR 2002;51:790, MMWR 2002;51:823, MMWR 2002;51:884, MMWR 2002;51:973, MMWR 2003;52:769, MMWR 2003;52:916, MMWR 2004;53:281, MMWR 2004;53:842, Emerg Infect Dis 2005;11:1167, MMWR 2007;56:76
References: Transfus Med Rev 2006;20:97 (Canadian policy), Wikipedia, AABB-Biovigilance Network
Standards for blood banks
Standards for blood bank - general
Responsibility for quality should be instilled into all employees at all levels (AJCP 2005;124:594)
Specimen labeling errors should be tracked (Archives 2006;130:1196)
Identification often does not meet accreditation standards (Archives 2003;127:541)
Patients commonly have similar names, causing errors at registration or bedside (Ann Clin Biochem 2007;44:106)
“Near miss” events are much more common than adverse events (Vox Sang 2007;92:233)
Electronic systems with bar codes may improve transfusion practice (Transfusion 2006;46:352)
References: Quality Management (WHO)
Methods to independently verify accuracy of patient name whose blood is in tube
(a) label all blood samples at time of collection with patient’s first and last name, unique identification number and date of collection (CAP); use of bar codes or specially trained nursing staff may be helpful; use at least two patient identifiers (neither being the room number) when taking blood samples (Joint Commission)
(b) compare ABO typing with historical values (computer systems for intraoperative ordering and delivering have low error rates, AJCP 2005;124:124)
(c) for non-group O patients that were previously untyped and likely to require transfusion, independently draw a second tube (AJCP 2006;126:422)
Note: should have positive identification of transfusion recipients and blood components (CAP Checklist, TRM.41000)
End of Transfusion Medicine chapter / outline