1 / 75

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

dante
Download Presentation

Complications of Blood Transfusion: An Overview

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related