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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

Complications of Blood Transfusion:An Overview

Clinical Pathology Conference

Dean Fong, DO

January 6, 2006

case presentation
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
case presentation3
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
case presentation4
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”
case presentation5
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+
case presentation6
Case Presentation

DIFFERENTIAL DIAGNOSIS?

differential diagnosis
Differential Diagnosis
  • Circulatory overload
  • Pulmonary embolism
  • Anaphylactic reaction
  • TRALI
  • Bacterial/Sepsis
complications of transfusion
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
non infectious complications of transfusions
Non-infectious Complications of Transfusions

Technical Manual

  • Acute (< 24°)
    • Immunologic
    • Non-immunologic
  • Delayed (> 24°)
    • Immunologic
    • Non-immunologic
acute 24 immunologic
Acute (< 24°) Immunologic
  • Hemolytic
  • Fever/chills, non-hemolytic
  • Urticarial/Allergic
  • Anaphylactic
acute 24 non immunologic
Acute (< 24°) Non-Immunologic
  • Hypotension associated with ACE inhibition
  • Transfusion-related acute lung injury (TRALI)
  • Circulatory overload
  • Nonimmune hemolysis
  • Air embolus
  • Hypocalcemia
  • Hypothermia
delayed 24 immunologic
Delayed (> 24°) Immunologic
  • Allo-immunization
    • RBC antigens
    • HLA
  • Hemolytic
  • Graft-versus-host disease (GVHD)
  • Post-transfusion purpura
  • Immuno-modulation
acute 24 immunologic14

Acute (< 24°) Immunologic

Hemolytic

Fever/chills, non-hemolytic

Urticarial/Allergic

Anaphylactic

hemolytic
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
hemolytic16
Hemolytic
  • Highly variable in acuity and severity
    • Severe
      • Fevers and/or chills
      • Hypotension
      • Dyspnea
      • Tachycardia
      • Pain
      • DIC
      • ARF
      • Shock
hemolytic17
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
hemolytic18
Hemolytic
  • Laboratory findings
    • Hemoglobinemia
    • Hemoglobinuria
    •  LDH
    • Hyperbilirubinemia
    •  Haptoglobin
    •  BUN, creatinine in ARF
    • DAT +
hemolytic19
Hemolytic
  • Differential diagnosis
    • AIHA
    • Nonimmune hemolysis
    • Microangiopathic hemolytic anemia
    • Drug-induced
    • Infections
    • Any causes of hemolysis
hemolytic20
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
acute 24 immunologic21

Acute (< 24°) Immunologic

Hemolytic

Fever/chills, non-hemolytic

Urticarial/Allergic

Anaphylactic

fevers chills non hemolytic fnhtr
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
fevers chills non hemolytic fnhtr23
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
acute 24 immunologic24

Acute (< 24°) Immunologic

Hemolytic

Fever/chills, non-hemolytic

Urticarial/Allergic

Anaphylactic

uritcarial allergic
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
uritcarial allergic26
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?
acute 24 immunologic27

Acute (< 24°) Immunologic

Hemolytic

Fever/chills, non-hemolytic

Urticarial/Allergic

Anaphylactic

anaphylactic
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
anaphylactic29
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
anaphylactic30
Anaphylactic
  • Treatment/Prevention
    • Discontinue transfusion
    • Supportive care
    • Epinephrine
    • Antihistamine/steroids
    • In IgA deficient pts.  IgA-deficient product, wash blood product
acute 24 non immunologic31

Acute (< 24°) Non-Immunologic

Hypotension associated with ACE inhibition

Transfusion-related acute lung injury (TRALI)

Circulatory overload

Nonimmune hemolysis

Air embolus

Hypocalcemia

Hypothermia

hypotension associated with ace inhibition
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
acute 24 non immunologic33

Acute (< 24°) Non-Immunologic

Hypotension associated with ACE inhibition

Transfusion-related acute lung injury (TRALI)

Circulatory overload

Nonimmune hemolysis

Air embolus

Hypocalcemia

Hypothermia

transfusion related acute lung injury trali
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)
trali
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
trali36
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
trali37
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
trali38
TRALI
  • Implicated Blood Products
    • RBCs, FFP, apheresis platelets, platelet concentrates
    • Rare cases of IVIG, cryo-
    • No cases of albumin reported
trali39
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
trali40
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
trali41
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

trali42
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

trali43
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

trali44
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

trali45
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
trali46
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?
acute 24 non immunologic47

Acute (< 24°) Non-Immunologic

Hypotension associated with ACE inhibition

Transfusion-related acute lung injury (TRALI)

Circulatory overload

Nonimmune hemolysis

Air embolus

Hypocalcemia

Hypothermia

circulatory overload
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
circulatory overload49
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
acute 24 non immunologic50

Acute (< 24°) Non-Immunologic

Hypotension associated with ACE inhibition

Transfusion-related acute lung injury (TRALI)

Circulatory overload

Nonimmune hemolysis

Air embolus

Hypocalcemia

Hypothermia

nonimmune hemolysis
Nonimmune hemolysis
  • Lysis of RBCs as a result of storage, handling, or transfusion condition
  • Incidence
    • Rare
  • Signs/Symptoms
    • Transient hemodynamic
    • Pulmonary impairment
    • Renal impairment
    • Hemoglobinemia and hemoglobinuria
    • Hyperkalemia (renal failure)
    • Fever
nonimmune hemolysis52
Nonimmune hemolysis
  • Differential diagnosis
    • Hemolytic
    • Autoimmune
    • Bacterial/sepsis
    • PNH, drug-induced, oxidative stress, etc.
    • Diagnosis of exclusion
  • Treatment/Prevention
    • Stop transfusion
    • Investigation of blood bag and tubing
    • Investigate for hemolytic transfusion rxn.
    • Check serum K
    • Supportive care
    • Maintain urine O/P (except for contraindication…i.e. renal failure)
acute 24 non immunologic53

Acute (< 24°) Non-Immunologic

Hypotension associated with ACE inhibition

Transfusion-related acute lung injury (TRALI)

Circulatory overload

Nonimmune hemolysis

Air embolus

Hypocalcemia

Hypothermia

air embolus
Air embolus
  • Air infusion via line
  • Rare
  • Cough, dyspnea, chest pain, shock
  • If suspected…
    • Pt. placed on left side with head down
      • Displace air bubble from pulmonary valve
hypocalcemia
Hypocalcemia
  • Large volumes of FFP, whole blood, plts. transfused rapidly  plasma citrate levels may rise  binds iCa+2
    • Citrate rapidly metabolized  manifestations transient
    • Prolonged apheresis
  • Periorbal/peripheral tingling paresthesias, shivering, lightheadedness, tetanic sxs., hyperventilation, depressed cardiac function
  • Ca+2 replacement
hypothermia
Hypothermia
  • Rapid infusion of large volumes of cold blood
    • Ventricular arrhythmias
    • More likely via central catheters
    • Increased toxicity of hypocalcemia and hyperkalemia
    • Impaired hemostasis
    • Increase caloric requirement
  • Blood warmer
delayed 24 immunologic57

Delayed (> 24°) Immunologic

Allo-immunization

Hemolytic

Graft-versus-host disease (GVHD)

Post-transfusion purpura

Immuno-modulation

allo immunization
Allo-immunization
  • Occurs weeks to months after transfusion
  • Incidence
    • 1-1.6% to RBC antigens
    • 10% to HLA
  • Signs/Symptoms
    • PRBCs  hemolysis
    • Plts.  refractoriness
  • Treatment/Prevention
    • Plts.
      • Leukoreduction
      • Cross-matched and/or HLA-matched plts.
delayed 24 immunologic59

Delayed (> 24°) Immunologic

Allo-immunization

Hemolytic

Graft-versus-host disease (GVHD)

Post-transfusion purpura

Immuno-modulation

hemolytic60
Hemolytic
  • Once allo-immunization has occurred, abys may diminish to undetectable levels
    • Especially Kidd system (anti-Jka and anti-Jkb)
    • Hemolysis typically extravascular
  • Anamnestic response
    • W/in hours or days (up to 6 weeks), IgG aby reacts with transfused red cells
    • Prospective study
      • 58 of 2082 (2.8%) RBC recipients were found to have alloabys (previous undetected) w/in 7 days of transfusion
  • Incidence
    • Based on above study, only 1 recipient w/ new aby w/in 7 days of transfusion was shown to have hemolysis
    • Estimated rate
      • 1 in 2082 recipients
      • 1 in 11,328 units
    • Other reports at 0.02 to 0.009%
hemolytic61
Hemolytic
  • Signs/Symptoms
    • Fever
    • Declining Hb
    • Mild jaundice
    • Hemoglobinuria
    • ARF – uncommon
  • Check for alloaby in both serum and RBC
  • Treatment/Prevention
    • Rarely necessary
    • May need to monitor urine O/P, renal function, coagulation functions
    • IVIG
    • Appropriate units for transfusion
delayed 24 immunologic62

Delayed (> 24°) Immunologic

Allo-immunization

Hemolytic

Graft-versus-host disease (GVHD)

Post-transfusion purpura

Immuno-modulation

graft versus host disease gvhd
Graft-versus-host disease (GVHD)
  • Fatal complication cause by engraftment and clonal expansion of donor lymphocytes in susceptible host
    • Attack recipient tissues
    • Immunocompromised pts.
      • Hematologic malignancies or certain solid tumors receiving chemotherapy radiation
      • Stem cell transplant
      • Recipients of HLA matched products or familial blood donation
      • Lupus or CLL requiring fludarabine
      • Not reported in AIDS pts.
  • 2-30 days after transfusion
  • Incidence
    • Rare (0.002-0.005%)
slide64
GVHD
  • Signs/Symptoms
    • Appears w/in 10-12 days of transfusion
    • Skin – whole body erythroderma, desquamation
    • GI  N/A, diarrhea
    • Liver
    • BM  failure leading to pancytopenia
  • Treatment/Prevention
    • No effective treatment
    • Gamma irradiation
      • Render T-cells incapable of replication
      • FDA requirement
        • Minimum of 2500 cGy target to the midline of the container
        • Minimum of 1500 cGy target to all other part of component
delayed 24 immunologic65

Delayed (> 24°) Immunologic

Allo-immunization

Hemolytic

Graft-versus-host disease (GVHD)

Post-transfusion purpura

Immuno-modulation

post transfusion purpura ptp
Post-transfusion Purpura (PTP)
  • Characterized by abrupt onset of severe throbocytopenia (< 10K)
    • Average of 9 days (range 1-24 days)
    • PRBCs or whole blood
    • Reported in plts., plasma, frozen deglycerolized PRBCs
  • Incidence
    • Rare
    • Over 200 cases published
    • Male:Female 1:5
    • Median age 51 years (range 16-83)
  • Clinical course
    • Usually self-limited, recovery w/in 21 days
    • 10-15% mortality
      • Intracranial hemorrhage
slide67
PTP
  • Signs/Symptoms
    • Profound thrombocytopenia
    • Purpura
    • Bleeding
    • Fever (reported)
  • Etiology
    • Plt. specific IgG aby that are auto-aby
      • All HPA implicated but HPA-1a most common
    • 3 mechanisms
      • Immune complex – pt. aby and donor antigen
      • Concersion of antigen- autologous plts. to aby targets to antigen in transfused components
      • Cross-reactivity of pts. autoaby w/ autologous plts.
slide68
PTP
  • Differential diagnosis
    • ITP
    • TTP
    • Alloimmunization
    • Sepsis
    • DIC
    • BM failure
    • Drug-induced
  • Treatment/Prevention
    • Steroids – controversial
    • Plasma exchange – achieves plts. counts to 20K in 1-2 days (up to 12 days)
    • IGIV – recovery of plts. Counts of 100K w/in 3-5 days
      • Block aby-mediated clearance
    • Splenectomy – refractory pts., high risk of life-threatening hemorrhage
    • Plts. transfusion not effective
    • Antigen-negative blood product
delayed 24 immunologic69

Delayed (> 24°) Immunologic

Allo-immunization

Hemolytic

Graft-versus-host disease (GVHD)

Post-transfusion purpura

Immuno-modulation

immuno modulation
Immuno-modulation
  • ? Increases risk of recurrent cancer and bacterial infection
  • WBCs  cytokines during storage  interfere w/ immune function
  • Uncertain clinical significance
  • Leukoreduction of blood products
iron overload
Iron overload
  • Each unit of PRBC  200-225 mg of Fe
  • Chronic transfusion
  • > 50-100 units of PRBC
  • Storage in RE sites  saturation  other sites
    • Heart, liver, endocrine glands (pancreas)
  • Removal of Fe
    • Desferoxamine – Fe-chelating agent
  • Chronic transfusion in hemoglobinopathy
    • Prolong intertransfusion interval or PRBC exchange
case presentation74
Case Presentation
  • Donor FFP from 33 y/o female (G2)
    • Anti-HLA aby resulted positive for several anti-HLA aby
  • Recipient
    • Positive anti-HLA aby, HLA Class II antigen, HLA DQ1
    • But…
      • Pt. had received 11 units PRBCs and 2 units Plts. Over plast 1 month
  • Conclusion…
    • ? TRALI
      • Pt. was transfused with 2 U FFP over a 6 hour period w/out incident
    • ? Other
  • Recommendation…
    • ? What to do with donor
    • ? What to do with patient
references
References
  • Brecher ME et. al., Technical Manual, 14th Ed., AABB Press, 2002.
  • Davenport RD, “Pathophysiology of Hemolytic Transfusion Reactions” Seminars in Hematology 2005; 42: 165-168.
  • Gilstad CW, “Anaphylactic transfusion reactions”, Current Opinion in Hematology 2003; 10: 419-423.
  • Kuriyan M, Carson JL, “Blood transfusion risks in the intensive care unit”, Crit Care Clin 2004; 20: 237-253.
  • MacLennan S, Barbara JAJ, “Risks and side effects of therapy with plasma and plasma fractions”, Best Practice and Research Clinical Haematology 2006; 19(1): 169-189.
  • Mintz PD, Transfusion Therapy Clinical Principles and Practice, AABB Press, 2005.
  • Shander A, Popovsky MA, “Understanding the Consequences of Transfusion-Related Acute Lung Injury”, Chest 2005; 128: 598-604.
  • Silliman CC, McLaughlin NJD, “Transfusion-related acute lung injury”, Blood Reviews 2005; article in press.