Serious Hazards of Transfusion

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    Serious hazards of transfusion

    Dr Kenneth S Charles

    MB.BS (UWI), FRCP (UK), FRCPath(UK)

    Senior Lecturer in Haematology

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    Introduction

    Case study

    Definition of adverse effect

    Classification Pathophysiology

    Management

    Prevention

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    Red cell concentrate

    Cryoprecipitate Fresh frozen

    plasma

    Platelet concentrate

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    Case study

    26 year old man

    Relapsed Hodgkins Lymphoma

    Chemotherapy Sepsis/Disseminated Intravascular

    Coagulation

    2 U RBC, 6 U platelets, 6 U FFP 6 hours later, dyspnoea, hypoxia

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    Adverse reaction

    Any untoward event occurring within a few

    hours, weeks or months of and as a direct

    result of administration of a blood

    component

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    Classification

    Immediate/Delayed

    Infectious/Non-infectious

    Immune/Non-immune Clinical presentation

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    Adverse reactions classified by

    clinical presentation

    Febrile

    Haemolysis

    Acute haemolytic transfusion reactionDelayed haemolytic transfusion reaction

    Sepsis

    Bacterial contamination of componentAntileucocyte antibodies

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    Adverse reactions classified by

    clinical presentation

    Dyspnoeic

    Transfusion related acute lung injury

    Congestive cardiac failureAnaphylaxis caused by IgA deficiency

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    Adverse reactions classified by

    clinical presentation

    Urticarial

    Allergy to plasma proteins

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    Adverse reactions classified by

    clinical presentation

    OtherIron overload

    Transfusion Transmissible infectionsHIV

    HBV

    HCV

    Syphilis

    HTLV1

    Graft versus host disease

    Posttransfusion purpura

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    FEBRILE

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    Acute Haemolytic Febrile Transfusion

    Reaction (AHFTR)

    As little as 20 mls incompatible RBCs

    1 in 7 000 transfusions

    Mortality 10% Anti-A, anti-B, anti-Kell, anti-Kidd, anti-

    Duffy, anti-Lewis

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    AHFTR contd

    Abs in recipients serum activate

    complement to initiate intravascular lysis

    Catecholamines and kinins released

    DIC in 30-50%

    Fever, chills, nausea, pain at IV site,

    chest and back pains (intravascularocclusion by agglutinated red

    cells),hypotension, dark urine

    Nephrotoxic effects of anti-red cell stroma

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    AHFTR

    Stop transfusion

    IV hydration - Normal Saline to systolic BP

    > 100 mmHg, UO > 100 ml/hr

    Diuresis - +/- IV Frusemide or mannitol

    Appropriate samples to blood bench

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    Conditions mimicking AFHTR

    Improperly warmed blood

    Blood piggy-backed

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    (D)Some technical aspects of the

    administration of blood and blood

    components: blood warming

    Rarely indicated

    Only with specifically designed blood warmers

    with visible thermometer and audible warningNOT hot water bath, microwave, radiator.

    Massive transfusions in adults, exchangetransfusions in neonates, clinically

    significant cold agglutinins

    BCSH, 1998

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    Bacterial contamination

    Especially platelet concentrate

    Sourcesdonor bacteraemia, donor arm,

    contamination during processing

    Fever, chills, shock, ARF, DIC

    G- and G+ bacteria

    Mortality 26%

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    Fate of unused red cells

    25

    1

    Domestic refrigerator

    Returned to Blood

    Bench

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    (B) Collection of blood or blood components from

    the hospital blood bank or blood transfusion issue

    refrigerator and its delivery to the ward or operatingtheatre

    The transfusion of blood and blood components should

    begin as soon as possible after delivery to the ward oroperating theatre. If not possible, return to bloodtransfusion refrigerator. If > 30 mins return to hospitalblood bank for disposal (risk of bacterial infection)

    If the ward or operating room does not have a

    refrigerator that is approved for storing blood, theblood should not be released from the blood bankuntil immediately before transfusion

    BCSH, 1999

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    Wastage: Blood returned from

    wards

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    DYSPNOEIC

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    Non-haemolytic febrile

    transfusion reactions (NHFTR)

    Most common type of transfusion reaction

    Granulocyte and HLA-specificantileucocyte Abs develop in recipient by

    pregnancy, previous transfusion Lysis of donor WBCs and release of

    cytokines

    1 in 200-500 transfusions

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    Leucocyte antigens

    HLA Class I and II

    Neutrophil specific antigensNA-1, NA-2,NB

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    HLA Antigens

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    Febrile Non-haemolytic Transfusion

    Reaction (FNHTR)

    Fever, otherwise well

    Stop transfusion

    Exclude haemolysis, bacterialcontamination

    Acetominophen 650 mg

    Resume transfusion If recurs, leucocyte filter

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    Non-cardiogenic pulmonary oedema

    (TRALI)

    1 in 5 000 transfusions

    Donor antileucocyte Abs (previous

    transfusions, pregnancy) passively

    transfused to recipient

    Any blood component

    Ag/Ab complexes trapped in pulmonary

    vasculature

    Dyspnoea, hypoxia, chills, fever

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    TRALI

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    TRALI

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    Congestive Cardiac Failure

    (CCF)

    Safe rate for 1U RBCs 2-3 hrs

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    Anaphylaxis

    Hereditary IgA deficiency 1 in 700 in USA

    Complement-fixing IgG anti-IgA through

    pregnancy or transfusion

    Dyspnoea, chest pain, nausea, abdo

    cramps, hypotension

    IV epinephrine, methylprednisolone

    Washed red cells, IgA deficient donors

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    URTICARIAL

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    Urticaria

    Allergic reaction to plasma proteins

    Usually FFP but any component

    Skin rash, pruritis Antihistamine and continue transfusion

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    OTHER

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    Infective risks of blood transfusion

    Risk factor Estimated frequency

    Hepatitis A 1 in 1 000 000

    Hepatitis B 1/30 000-1/250 000

    Hepatitis C 1/30 0001/150 000

    HIV 1/200 0001/2 000 000

    HTLV1 1/250 000-1/2000 000

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    Centralized screening for TTIs

    HTLV1, Chagas

    Syphilis,HCV

    HIV, HBsAg

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    0

    50

    100

    150

    200

    250

    300

    350

    Voluntary Replacement Paid

    Risk of HIV seropositivity per 100,000 donors

    WHO,2002

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    Serological markers NBTS

    Year Sample

    (no)

    HIV HBsAg HTLV1 HCV TP Chagas

    200014 882 0.19 0.83 0.94 0.37 0.55 ND

    2004 13742 0.21 0.58 1.46 0.77 2.16 0.05

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    1866

    11275

    78

    1808

    11817

    66

    1551

    18055

    165

    1322

    19589

    106

    2707

    19209

    95

    2908

    19867

    95

    0

    5000

    10000

    15000

    20000

    25000

    NUMBER

    2004 2005 2006 2007 2008 2009

    YEAR

    ANNUAL DONATIONS BY TYPE

    AUTOLOGOUS

    REPLACEMENT

    VOLUNTARY

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    TTIs 2009

    HIV HBV HCV SYPH HTLV CHAGAS ALL

    REPLACEMENT 43(0.21) 68(0.33) 41(0.20) 275(1.3) 195(0.97) 11(0.05) 633(3.2)

    VOLUNTARY 3(0.14) 1(0.05) 5(0.23) 5(0.23) 14(0.64) 0(0) 28(1.3)

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    0

    0.2

    0.4

    0.6

    0.8

    1

    1.2

    2005 2006 2007 2008 2009

    JA

    TR

    CU

    0

    0.1

    0.2

    0.3

    0.40.5

    0.6

    0.7

    0.8

    0.9

    1

    2005 2006 2007 2008 2009

    BAR

    JAMTRT

    CUR

    Voluntary donor % HIV in donors

    %

    HBsAg in donors %HCV in donors

    %

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    Window period/days

    Virus ELISA NAT (PCR)

    HCV 88 23

    HBV 56 31

    HIV 22 12

    VIP Blood Screening LATAM meeting, Pleasanton, CA, Oct 2007

    Blood donation rate per 10 000 inhabitants and

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    Blood donation rate per 10,000 inhabitants and

    proportion of units reactive/positive for

    infectious markers in 2005

    Country Donation rate % TTI markers

    Jamaica 83.6 5.0

    Trinidad and Tobago 104.4 4.69

    Curacao 368.6 0.03

    From : PAHO, CD 48/11 Annex

    A

    W t S iti it f

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    Wastage: Seropositive units for

    discard

    T f i A i t d G ft

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    Transfusion Associated Graft

    Versus Host Disease

    Engraftment of donor lymphocytes in the

    blood of patients with impaired cellular

    immunity

    Congenital SCID, organ transplantrecipients, Intrauterine Transfusions,

    Hodgkins Disease, purine analogues

    7-10 days. Skin, gut, liver, pancytopaenia

    90% mortality. No effective Rx

    15 Gy irradiation of blood components

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    Post Transfusion Purpura (PTP)

    Middle aged, multiparous

    PlA1 negative

    Severe thrombocytopenia 7-10 days after

    transfusion

    AlloAb to PlA1 destroys transfused and

    recipient platelets

    Rx - IVIg

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    Iron overload

    IU red cells contains 250 mg iron

    No iron excretion mechanism

    Skin, joints, liver, heart, endocrine glands

    Iron chelationintravenous, s/c

    - oral

    thalassaemia major patients

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    Case study

    26 year old man

    Relapsed Hodgkins Lymphoma

    Salvage chemotherapy

    Sepsis/Disseminated Intravascular

    Coagulation

    2 U RBC, 6 U platelets, 6 U FFP 6 hours later, dyspnoea, hypoxia

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    Case study

    TRALI

    IPPV

    Later succumbed to malignancy

    Female donor anti NA-1 Abs

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    Summary

    Case study

    Definition of adverse effect

    Classification

    Pathophysiology

    Management

    Prevention

    When do patients require

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    When do patients require

    transfusion?

    Red cellsHb < 7.0 or acute blood loss

    - Hb < 9.0 pre-op

    Platelets- Active bleeding + platelets < 50

    - Prophylactic/ platelets < 10 Fresh frozen plasmaprolonged PT and/or

    APTT + active

    bleedingor planned procedure

    Cryoprecipitateno response to FFP

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