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Complications of Blood Transfusion: An Overview

Complications of Blood Transfusion: An Overview. Clinical Pathology Conference Dean Fong, DO January 6, 2006. Case Presentation. 63 y/o male status post AVR 2 ° to AS on 11/18. Developed fevers, weakness, sternal erythema, SOB  readmitted on 12/3. + BC

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Complications of Blood Transfusion: An Overview

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  1. Complications of Blood Transfusion:An Overview Clinical Pathology Conference Dean Fong, DO January 6, 2006

  2. Case Presentation • 63 y/o male status post AVR 2° to AS on 11/18. • Developed fevers, weakness, sternal erythema, SOB  readmitted on 12/3. • + BC • Echo  vegetations c/w endocarditis • 12/10 AM • Received 2U FFP 2°  PT and PTT

  3. Case Presentation • Approximately 20 minutes after transfusion, pt. developed… • Shaking/rigors • Tachycardia • Hypoxia • No change in tempterature during transfusion • Pt. was given benadryl, lasix, intubation and ventilatory support • Pt. improved and was extubated later that afternoon

  4. Case Presentation • PMH: AVR S/P AS, endocarditis, left arm septic thrombophlebitis • CXR: • 12/9  “fluid overload, unchanged, LLL consolidation, pneumonia R base” • 12/10 (AM after transfusion)  “bibasilar atelectasis/consolidation” • 12/10 (later AM)  “↑ pulmonaty edema, unchanged LLL consolidation) • 12/11  “no change”

  5. Case Presentation • Labs: • HCT 11/20 32.8% 12/10 27.6% (16:00) 12/10 34.7% (20:00) 12/12 34.7% • Haptoglobin 100 mg/dl (30-200 mg/dl) • Blood bank: • Pt. is O+, DAT – • Backtype on both units FFP – • Gram stain -, cultures (after 7 days) – • Donor information: • 33 y/o female, O+, G2, CMV+ • 64 y/o male, O+, CMV+

  6. Case Presentation DIFFERENTIAL DIAGNOSIS?

  7. Differential Diagnosis • Circulatory overload • Pulmonary embolism • Anaphylactic reaction • TRALI • Bacterial/Sepsis

  8. Complications of Transfusion • Transfusion reactions occur in 2% of units or within 24 hours of use. • Most common adverse side effects are usually mild and non-life-threatening • Two categories: • Infectious complications • i.e HIV and HCV  1 transmission/2 million transfusion • Non-infectious complications

  9. Non-infectious Complications of Transfusions Technical Manual • Acute (< 24°) • Immunologic • Non-immunologic • Delayed (> 24°) • Immunologic • Non-immunologic

  10. Acute (< 24°) Immunologic • Hemolytic • Fever/chills, non-hemolytic • Urticarial/Allergic • Anaphylactic

  11. Acute (< 24°) Non-Immunologic • Hypotension associated with ACE inhibition • Transfusion-related acute lung injury (TRALI) • Circulatory overload • Nonimmune hemolysis • Air embolus • Hypocalcemia • Hypothermia

  12. Delayed (> 24°) Immunologic • Allo-immunization • RBC antigens • HLA • Hemolytic • Graft-versus-host disease (GVHD) • Post-transfusion purpura • Immuno-modulation

  13. Delayed (> 24°) Non-Immunologic • Iron overload

  14. Acute (< 24°) Immunologic Hemolytic Fever/chills, non-hemolytic Urticarial/Allergic Anaphylactic

  15. Hemolytic • Most severe hemolytic rxns. occur when transfused RBCs interact w/ preformed aby • Transfused aby rxns. w/ recipient’s RBCs rarely cause sxs. • May cause accelerated RBC destruction • Can occur after infusion of as little as 10-15 mL ABO-incompatible blood • Etiology • 1:38,000 to 1:70,000 • Clerical and other human error most common causes of ABO-incompatible transfusion • CAP survey – 3601 institution • 834 HTR over 5 year period w/ 50 (6%) fatality • Mortality estimated to be 1:1,000,000 transfusion

  16. Hemolytic • Highly variable in acuity and severity • Severe • Fevers and/or chills • Hypotension • Dyspnea • Tachycardia • Pain • DIC • ARF • Shock

  17. Hemolytic • Pathophysiology • Intravascular hemolysis, opsonization, generation of anaphylotoxins • Complement activation  classical pathway • IgM and IgG • C1q binds to Ig • C3 activation  cleavage of C3 leads to C3a being released into plasma and C3b deposition onto RBC membrane • C3a  proinflammatory effects • C3b  erythrophagocytosis • C5 cleaved  C5a into plasma • C5a  proinflammatory (100-fold more potent than C3a) • Assembly of remaining components of the MAC then occurs on RBC surface • Lysis of RBC • Cytokines activation • TNF, IL-1, IL-6, IL-8 • Coagulation activation • Bradykinin

  18. Hemolytic • Laboratory findings • Hemoglobinemia • Hemoglobinuria •  LDH • Hyperbilirubinemia •  Haptoglobin •  BUN, creatinine in ARF • DAT +

  19. Hemolytic • Differential diagnosis • AIHA • Nonimmune hemolysis • Microangiopathic hemolytic anemia • Drug-induced • Infections • Any causes of hemolysis

  20. Hemolytic • Treatment/Prevention • Stop transfusion • Supportive care to maintain renal function • Goal of urine O/P 100 mL/hr. in adults for at least 18-24 hours • Low dose dopamine • Treatment of DIC • ? Heparin – direct anticomplement effect • Prevention of clerical/human errors

  21. Acute (< 24°) Immunologic Hemolytic Fever/chills, non-hemolytic Urticarial/Allergic Anaphylactic

  22. Fevers/chills, non-hemolytic (FNHTR) • Defined as a rise in temperature of 1°C or greater. • Incidence • 43-75% of all transfusion rxn. • PRBCs 0.5-6% • Plts 1-38% • Signs/Symptoms • Chills/rigor • HA • Vomitting

  23. Fevers/chills, non-hemolytic (FNHTR) • Etiology • Reaction… • Between recipient WBC antibodies (HLA, WBC antigens) against transfused WBC in product • Cytokines that accumulates in blood bag during storage • Differential Diagnosis: • Other causes of fever ruled out • Hemolytic • Bacterial/Septic • Treatment/Prevention • Discontinue transfusion? • Acetaminophen/meperidine • Leukoreduced blood component

  24. Acute (< 24°) Immunologic Hemolytic Fever/chills, non-hemolytic Urticarial/Allergic Anaphylactic

  25. Uritcarial/Allergic • Continuum • Mild – urticarial • “Anaphylactoid” • Severe – anaphylactic • Incidence • 1-3% of all transfusion rxn. • Signs/Symptoms • Uriticarial/hives – upper trunk and neck • Fever • Pulmonary signs (10%) – hoarseness, stridor, “lump in throat”, bronchoconstriction • No cutaneous involvement • GI – N/V, abd. pain, diarrhea • Circulatory – tachycardia, hypotension

  26. Uritcarial/Allergic • Etiology • Circulating aby against soluable material in the blood • Proteins in donor plasma • Binds to preformed IgE aby on mast cells • Release of histamine • Vasoactive substances • C3a, C5a, leukotrienes • Differential Diagnosis: • Hemolytic • Bacterial • TRALI • Treatment/Prevention • Discontinue transfusion • Antihistamine/steroids • Washing of blood products, pretreatment,leukoreduction?

  27. Acute (< 24°) Immunologic Hemolytic Fever/chills, non-hemolytic Urticarial/Allergic Anaphylactic

  28. Anaphylactic • Rare • Incidence • 1:18,000 to 170,000 • Plt 1:1598-9630 • FFP 1:28,831 • RBCs 1:23,148-57,869 • Signs/Symptoms • In addition to uritcarial/allergic… • Cardiovascular instability • Cardiac arrhythmia • Shock • Cardiac arrest • More pronounced respiratory involvement

  29. Anaphylactic • Etiology • IgA aby (IgE, IgG, IgM) in IgA deficiency • Serum IgA < 5 mg/dL • Estimated 1 in 342 blood donors • C4 aby • Aby against nonbiologic origin • Haptoglobin deficiency (IgG or IgE anti-haptoglobin) • ? • Differential Diagnosis: • Hemolytic • Bacterial • TRALI • Circulatory overload

  30. Anaphylactic • Treatment/Prevention • Discontinue transfusion • Supportive care • Epinephrine • Antihistamine/steroids • In IgA deficient pts.  IgA-deficient product, wash blood product

  31. Acute (< 24°) Non-Immunologic Hypotension associated with ACE inhibition Transfusion-related acute lung injury (TRALI) Circulatory overload Nonimmune hemolysis Air embolus Hypocalcemia Hypothermia

  32. Hypotension associated with ACE inhibition • Pt. on ACEI  receiving albumin during plasma exchange • Etiology • Inhibition of bradykinin catabolism by ACEI • Bradykinin activation by activator (low level prekallikrein) in albumin • Bradykinin activation by prekallikrein in plasma protein • Differential diagnosis • Rule out hemolysis • Treatment/Prevention • Withdraw ACEI/supportative care • Avoid albumin • Avoid bedside leukofiltration

  33. Acute (< 24°) Non-Immunologic Hypotension associated with ACE inhibition Transfusion-related acute lung injury (TRALI) Circulatory overload Nonimmune hemolysis Air embolus Hypocalcemia Hypothermia

  34. Transfusion-related acute lung injury (TRALI) • What Is TRALI? • Transfusion related noncardiogenic pulmonary edema • Differential Diagnosis • Circulatory overload (TACO) • Allergic/Anaphylactic • Bacterial • Acute hemolytic reaction • Clinical presentation (“classic”, severe form) • Acute respiratory distress • Pulmonary edema • Hypoxemia • Hypotension • Transfusion usually within 6 hours (majority of cases during transfusion or within 2 hours of transfusion)

  35. TRALI • Clinical criteria • Insidious, acute onset of pulmonary insufficiency • Profound hypoxemia  PaO2/FiO2 < 300 mmHg • CXR  b/l fluffy infiltrates c/w pulmonary edema • Cardiac  PA wedge pressure  18 mmHg • No clinical evidence of LA HTN

  36. TRALI • Definition • TRALI w/out clinical risk factors for ALI: • New ALI temporally related to transfusion • Worsening of pre-existing pulmonary insufficiency temporally related to transfusion • TRALI in pts. w/ clinical risk factor for ALI: • New ALI temporally related to transfusion • New ALI thought to be mechasnistically related to the transfusion • Worsening of pre-existing pulmonary insufficiency temporally related to transfusion

  37. TRALI • Syndrome of TRALI (Weber KE et. al., Transfusion Med Rev, 2003) • Very common • Dyspnea, hypoxemia, pulmonary edema, hypotension, fever (1-2°C increase) • Common • Tachycardia, cyanosis • Uncommon • Hypertension • ? • Leukopenia, hypocomplements, monocytopenia

  38. TRALI • Implicated Blood Products • RBCs, FFP, apheresis platelets, platelet concentrates • Rare cases of IVIG, cryo- • No cases of albumin reported

  39. TRALI • Clinical Course • 100% TRALI patients require O2 and 72% require ventilation support • 81% resolves within 4 days and 17% resolve within 7 days • Most pts. recover with 72 hours • Mortality rate 6% (subsequent series up to 14-25%) • No long term sequela • Treatment • Respiratory support • No role for treatment w/ steroids or diuretics

  40. TRALI • Why Is TRALI Important? • Between 2001 – 2003, FDA report on causes of transfusion related deaths • TRALI 16.3% • ABO/Hemolytic transfusion reaction 14.3% • Bacterial contamination 14.1% • UK SHOT Data 7 years experience (from 1996) • Total 155 cases • 32 Deaths

  41. TRALI • Why Is TRALI Important? (cont.) • UK SHOT Data 7 years experience (from 1996) 2001/2002 Red cells 2.7 million Platelets 250K Fresh frozen plasma 385K Cryoprecipitate 88K TOTAL 3.4 million

  42. TRALI • Pathogenesis • Two current working model hypothesis • Both models are directed against increase in pulmonary microvascular permeability Bioactive Lipids “Two-Hit” Model Leukocyte Antibody  Pulmonary Microvascular Permeability Pulmonary Edema

  43. TRALI • UK and SHOT (7 Year Experience) • Data between 1996 to 2003 • Define TRALI as “Acute dyspnea, hypoxia, bilateral pulmonary infiltrates within 24 hours after transfusion with no other apparent causes” • 1996 < 10 cases • 2003  40 cases • Total 155 cases • 138 cases examined, others were excluded 94 Fully Recovered 4 Partial Recovery 32 Deaths 11 Other Demise

  44. TRALI 1 or more donors positive 71% • UK and SHOT (cont.) • Serological testing • Leukocyte antibody investigation • 71 cases of leukocyte antibodies Patient positive 8% Donor and patient negative 19% 16 HNA 50 HLA Class I or II 5 HLA and HNA Incomplete samples or not done 2% 18 Crossmatched 14 Antibody only in donor 18 Multiple antibodies

  45. TRALI • UK and SHOT (cont.) • Products implicated • 45/139 FFP/Cryo- • 34/139 RBCs • 27/139 Platelets • Estimation • FFP/Platelet 1 in 50-60K • RBC/Cryo- 1 in 500-600K • Frequency 1 in 1,000-2,500 patients transfused • Would expect to see 300-750 cases/year

  46. TRALI • UK and SHOT • What UK is doing • October 2003 Male donor ONLY for FFP • 2004 Import FFP for children • April 2004 Previously transfused donors excluded • Future Considerations • ? Male plasma only to suspend platelet pools • ? Female apheresis platelet donor for leukocyte antibody • ? Effects of decreased plasma (additive solution) in platelet concentrates/apheresis platelets • ? Mild TRALI. Does it exist?

  47. Acute (< 24°) Non-Immunologic Hypotension associated with ACE inhibition Transfusion-related acute lung injury (TRALI) Circulatory overload Nonimmune hemolysis Air embolus Hypocalcemia Hypothermia

  48. Circulatory overload • Acute pulmonary edema due to volume overload • Incidence • One of the most common complications of transfusion • Young children and elderly at risk • Cardiac and pulmonary compromise • Chronic anemia with expanded plasma volume • Infusion of 25% albumin • Shifts large volume of extravascular fluid into the vascular space • Signs/Symptoms • Dyspnea, cyanosis, orthopnea, severe HA, HTN, CHF during or soon after transfusion

  49. Circulatory overload • Differential diagnosis: • TRALI • Allergic rxn. • Other causes of CHF • Treatment/Prevention • Stop transfusion • Supportive care • Phlebotomy • Diuretic • Slow transfusion • Usually 4 hours, can be extended to 6 hours • Other strategies

  50. Acute (< 24°) Non-Immunologic Hypotension associated with ACE inhibition Transfusion-related acute lung injury (TRALI) Circulatory overload Nonimmune hemolysis Air embolus Hypocalcemia Hypothermia

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