blood transfusion reactions revisited dr. edwin rodriguez

8/3/2019 Blood Transfusion Reactions Revisited Dr. Edwin Rodriguez

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Blood and blood components aresimilar to DRUGS.

Blood has both THERAPEUTICBlood has both THERAPEUTIC

INDICATIONS and ADVERSEINDICATIONS and ADVERSE

EFFECTS.EFFECTS.


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Blood has THERAPEUTIC USES.

Blood can be used to TREATBlood can be used to TREAT

anemia and clotting factoranemia and clotting factor

deficiencies.deficiencies.


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Blood has unwanted adverseBlood has unwanted adverseeffects in the form of bloodeffects in the form of blood

transfusion reactions.transfusion reactions.Blood must then be usedBlood must then be used

cautiously and consciously.cautiously and consciously.


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Blood transfusion must thereforebe INDIVIDUALIZED.

Blood must be transfused on a caseBlood must be transfused on a case--

toto--case basis using the patient riskcase basis using the patient risk--

benefit ratio as a guide.benefit ratio as a guide.


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Transfusion

irreversible event that carries potential

benefits and risks to the recipient

intravenous administration of whole blood

or components


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Transfusion Reaction

any unfavorable transfusion-related event

occurring in a patient during or after transfusion

of blood components

may be immune-mediated or non-immune

mediated (mechanism/ pathophysiology)

maybe acute or delayed (onset/ timing)


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Blood Transfusion Reactions (BTRs)

occurwithin 24 hours after transfusion in 2% ofcases

may be life-threatening and even fatal

require immediate recognition and management

must be treated if indicated and prevented intransfusion practice


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RISKS OF BLOODTRANSFUSION


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Risks of Immune-Mediated BTRs

NHFTR 1-2%

allergic 1-2%

IHTR 1:6000

DHTR 1:6000

fatal immediate BTR 1:100,000


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BTR-Induced Morbidity and Mortality

acute hemolytic reaction 1:25,000

delayed hemolytic reaction 1:2500

non-cardiogenic PE 1:1000

TA-GVHD and related donor 1:7000

TA-GVHD and unrelated donor 1:39,000


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Transfusion Associated Deaths (TAD)

acute hemolysis (ABO incompatible blood component)

acute pulmonary edema

bacterial contaminationdelayed hemolytic reactions

anaphylaxis

external hemolysis

acute hemolysisTA-GVHD


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Differential Diagnoses of BTR

PNH

AIHA

G6PDmalignant hyperthermia

hemoglobinopathies

RBC membrane defects


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HEMOLYTIC TRANSFUSIONHEMOLYTIC TRANSFUSIONREACTIONSREACTIONS


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Hemolytic Transfusion Reactions

(HTRs)

donor RBC infused is incompatible with an

antibody pre-existing in the recipient resulting in

intravascular destruction of RBC

may lead to hypotension, shock, consumptive

coagulopathy and acute renal failure


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IMMEDIATE OR ACUTEIMMEDIATE OR ACUTE

HEMOLYTIC TRANSFUSIONHEMOLYTIC TRANSFUSION

REACTIONSREACTIONS


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Acute Hemolytic Transfusion Reactions

(AHTRs)

rapid destruction of blood cells immediately after

or within 24 hours of a transfusion

commonly associated with whole blood

transfusion

mortality is high and depends on the amount of

blood infused


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(AHTRs)

Pathophysiology of AHTRs:

transfusion ofwhole blood or RBC that are

immunologically incompatible with antibodies

pre-existing with the recipient

commonly involve antibodies to A, Kell, Jk(a),

Fy(a)

ABO incompatibility accounts for74% of allfatal reactions


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(AHTRs)

Incompatible RBC infused binding of antibodyto the surface of transfused cells by complementactivation - intravascular hemolysis - release

of hemoglobin, RBC stroma and enzymes

Hemolysis primarily intravascular butextravascular component possible - antibody

and complement coating of RBC - ingestion ofmononuclear phagocytes of the RES


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(AHTRs)

Interplay of biochemical mediators:

anaphylatoxins: C3a, C5a

histamine and serotonin kallikrein

cytokines: TNF-alpha, IL-1, IL-8, MCP

PF3

pro-coagulant and pro-inflammatory

molecules


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(AHTRs)

Signs and symptoms of AHTRs:

Factors affecting clinical manifestations

antigen involved

quantity of RBC infused

titer of antibody

thermal range of antibody activity


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(AHTRs)

Signs and symptoms of AHTRs: fever

chills/ rigors

anxiety and feeling of dread nausea and vomiting

diarrhea

pallor

icterus chest pain

hypotension

flushing


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(AHTRs)


diffuse bleeding

hemoglobinuria, hemoglobinemia

jaundice

oliguria or anuria

pain in the abdomen, flanks, back, head, infusion site

shock (severe cases)

pallor

dyspnea


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(AHTRs)


Atypical presentation

anesthesized: changes in blood pressure, diffuse

bleeding, hemoglobinuria, chills and rigors are

NOT seen with paralysis


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(AHTRs)

Major complications of immune-mediated

hemolysis:hypotension

vasoconstriction and renal ischemia

activation of platelets and coagulation cascade

resulting in DIC


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(AHTRs)

Differential Diagnosis of AHTRs:

microbial contamination

physical, chemical and drug-related damage to stored

RBC AIHA: development of minor blood group antigens

congenital hemolytic anemias

microangiopathic hemolytic anemia

PNH

infections


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(AHTRs)

Prevention and Management of AHTRs: Avoid blood transfusion.

Define clear-cut indications for blood transfusion.

Consider blood substitutes. Use autologous blood if feasible.

Use a sensitive antibody screening tests.

Avoid, trace, correct clerical errors.

Implement strict quality assurance programs


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DELAYEDH

EMOLYTICDELAYEDH

EMOLYTICTRANSFUSION REACTIONSTRANSFUSION REACTIONS


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Delayed Hemolytic Transfusion Reactions

(DHTRs)

occurs 3-10 days

classically associated with previousimmunization with transfusion or pregnancy but

in whom the antibody was not detected in pre-transfusion testing

with generally milderclinical manifestations

present with fever, unexplained anemia,

jaundice, hemoglobinuriacommon with antibodies to Kidd and Rhantigens


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(DHTRs)previously called delayed bloodtransfusion incompatibility reaction

common features of DHTRs: previous alloimmunization due to previous

pregnancies or transfusions

low titer of reactivity allows antibody to be undetectedor missed in pre-transfusion antibody screening orcompatibility testing

occurs 3-10 days after blood transfusion antibody undetected in previous pre-transfusion

screening is readily identified in the post-transfusionsample


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(DHTRs)

Prevention of DHTRs Apply extensive phenotyping.

Perform prophylactic antigen matching of donor RBCwith recipients complete phenotype.

Use artificial blood substitutes.

Use more sensitive antibody screening tests.


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IMMEDIATE NONIMMEDIATE NON--H

EMOLYTICH

EMOLYTICTRANSFUSION REACTIONSTRANSFUSION REACTIONS


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Febrile Non-Hemolytic Transfusion

Reactions (FNHTRs)

temperature rise of at least 1C occurring with or

without chills in association with transfusion or

shortly thereafter (up to 4 hours) that is not

attributable to other causes including hemolysis

or underlying disease

recurrence rate: 15%incidence: 0-5-1.4%


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Febrile Non-Hemolytic Transfusion Reactions

(FNHTRs)

Pathophysiology of FNTHRs: Donor white cells- donor cytokines -recipient antibodies and/

or cytokines - FNTHRs

Donor white cells -- recipient antibodies/ and or cytokines --FNTHRs

Donor white cells - FNHTRs

Donor cytokines- recipient antibodies and/or cytokines -

FNHTRs

Other donor biologic response modifiers- recipient antibodiesand/or cytokines -- FNHTRs


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(FNHTRs)

Diagnosis of FNHTRs: Clinical manifestations: newly developed fever, chills

or both in a recipient during or shortly aftertransfusion

Presence of fever in a recipient during transfusionwarrants DISCONTINUATION of the transfusion.

To avoid confusion, it is recommended that bloodtransfusion be done during anAFEBRILE period.

Transfusion reaction evaluation should be initiated for

temperature elevation greater than 1C during bloodtransfusion.


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(FNHTRs)

Differential Diagnosis of FNHTRs: HTRs

Reactions to bacterially contaminated blood products Fever only temporally related to transfusion in

addition to FNHTRs


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(FNHTRs)

Treatment of FNHTRs:

Immediate discontinuation of blood transfusion

IV line should be maintained

Formal transfusion reaction report should be initiated

Pharmacologic antidotes: anti-pyretics, anti-

histaminics, steroids

Clinical manifestations resolve with or without

treatment and do not typically lead to additional orlong-term adverse sequelae.


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(FNHTRs)

Prevention/ Recurrence of FNHTRs:

pre-transfusion administration of antidotes documented BTR, warrants pre-transfusion medications

30 minutes before blood transfusion

use leukocyte-depleted blood removal of buffy coat

sedimentation

red cell washing

use of micro-aggregate filtration

(leukoreduction)


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Allergic and Anaphylactic Reactions

Types of allergic and anaphylactic reactions:

Uncomplicated allergic reactions consisting of

localized or diffuse urticaria (IgE-mediated)

Anaphylactic allergic reactions (IgE-mediated)High potential for adverse events and outcomes

including death

Require immediate recognition and intervention

Avoidance of all plasma-containing products Anaphylactoid allergic reactions (non-IgE mediated)


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Allergic and Anaphylactic Reactions

Diagnosis:

Nephelometry for IgA detection

Treatment:

Discontinuation of transfusion Antidotes: anti-histaminics, epinephrine

Prevention: Avoidance of plasma-containing blood products

Use immunodiffusion screening methods

Use confirmatory passive hemagglutination assays Modification of transfused blood products (washing,

autologous, freezing with deglycerolization)


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Transfusion-Associated Lung Injury

(TRALI)

occurs during or within 4 hours of transfusion

also called non-cardiogenic pulmonary edema,

pulmonary HPS reaction, allergic pulmonaryedema; consists of symptoms of adultrespiratory distress (ARDS)

manifested radiographically by the presence ofbilateral pulmonary infiltrates

clinical manifestations: chills, fever, tachypnea,cough, tachychardia


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(TRALI)

Pathophysiology of TRALI:

due to donor antibodies directed against WBC

antigens

donor profile: multiparous females, donors withmultiple exposure to various HLA types

involves antibodies directed toward NA2, NB2 and

anti-5b (granulocytic antigens)

antigen-antibody interaction leads to agglutinins

trapped within the pulmonary circulation with resultant

release of toxic substances and pulmonary edema


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(TRALI)

Treatment and Prevention of TRALI:

Supportive care is advised.

Endotracheal intubation may be needed. Resolution occurs in 81% of cases and

happens usually within 3-5 days from onset.

TRALI does not usually recur in the same

patient when the reaction is due to recipientantibodies.

TRALI is a donor-specific phenomenon.


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Transfusion Associated Circulatory Overload

(TACO)

incidence: 1 in 100 transfusions

often unrecognized or mistaken with TRALI

clinical manifestations: dyspnea, hypertension,

tachychardia, cough, chest tightness, cyanosis

iatrogenic transfusion reaction


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(TACO)

Pathophysiology:

Intravascular volume may be overtaxed by

either an inappropriate rate of transfusion or

an inappropriate volume of transfusion inaddition to other infused substances - high

CVP - LV failure - pulmonary congestion

and edema


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(TACO)

CXR: cardiomegaly, prominent pulmonary

arteries and septal lines, diffuse clouding of

both lung fields

Timing: immediate during blood transfusion

delayed after 24 hours from blood transfusion

Patients with CHF or pulmonary disease are

predisposed to these types of reactions.


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(TACO)

Treatment of TACO:

Cessation or reduction of the rate or

blood products.

Use of diuretics

Supportive therapy


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(TACO)

Prevention and Recurrence of Circulatory

Overload:

Vigilant assessment and recording of fluid

input and output

Slowed infusion rates

Diuretics

Identification of high risk groups


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Bacterial Contamination

Presentation and Prevalence:

PRBC

extremely severe transfusion reactions

high mortality: 70%

clinical manifestations: fever >38.5C,chills, hypotension begin during thetransfusion, nausea, vomiting, dyspnea,

diarrhea


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PRBC

microbial contaminants: gram negative

microbes (Yersinia enterocolitica-endotoxin)


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PRBC

prediposing factor:prediposing factor: PRBC stored >21 daysPRBC stored >21 dayswhich carried a high bacterial andwhich carried a high bacterial and

endotoxin loadendotoxin load

pathophysiology: infusion ofpathophysiology: infusion ofendotoxinendotoxin

followed by massive release of recipientfollowed by massive release of recipientcytokines (TNFcytokines (TNF--alpha)alpha)


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PLATELET CONCENTRATES

clinical manifestation: fever, chills,clinical manifestation: fever, chills,

hypotension beginning during or shortlyhypotension beginning during or shortlyafter transfusionafter transfusion

mortality rate:mortality rate: 25%25%

predisposing factor: platelet concentratespredisposing factor: platelet concentrates>3 days old>3 days old


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FFP AND CRYOPRECIPITATE

clinical manifestations: wound

infections, endocarditis, septicemiawith unusual organisms several

days after transfusion


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Microorganisms Implicated

PRBCYersinia enterocolitica

Enterobacter speciePseudomonas putida, fluorescens

Platelet ConcentratesCONS

FFP and CryoprecipitatePseudomonas cepacia, aeruginosa

Borrelia burgdorferi


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Mechanisms of Contamination:

Donor bacteremia

Patients with gastroenteritis (Yersinia,

Campylobacter)Patients with URI (Strep pyogenes)

Patients with septicemia (Staph aureus)

Patients with Lyme disease (Borrelia)


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Mechanisms of Contamination:

Donor bacteremia

Chronic low grade infection

Toe ulceration (Serratia)

Osteomyelitis (Salmonella)

After dental or medical procedure (Staph aureus)

Syphilis (Treponema)


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Blood CollectionBlood Collection Inadequate skin disinfection (Staph epidermidis,

aureus, diphteroids)

Scarred phlebotomy site (enterococci, Staph) Contaminated vacuum tubes (Serratia)

Contaminated apheresis solutions (Enterobacter)


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Blood processing

Contamination during thawing (Pseudomonas)

Container damage or defect

Leaky seals (Serratia)

Cracked vials (Enterobacter)

Blood bag manufacture

Contaminated bag exterior (Serratia)

Contamination during manufacture and/ or

fractionation (Pseudomonas)


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Prevention of TransfusionPrevention of Transfusion--AssociatedAssociated

Bacterial Sepsis:Bacterial Sepsis:

Extensive donor screening Improved donor skin disinfection

Removal of first aliquot of donor blood

Limitation of component storage time

Pre-transfusion detection


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Altered blood processing Leukocyte reduction

Reduced holding temperature and time prior to

component preparation

Component storage temperature

Waterbath disinfection

Chemical or photochemical decontamination psoralens


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Physically or Chemically Induced

Transfusion Reactions (PCITRs)

heterogenous group of conditions including:

physical RBC damage

depletion and dilution of coagulation factorsand platelets

hypothermia

citrate toxicity hypokalemia / hyperkalemia


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Physical Damage to RBCs

intravascular lysis due to hypertonic or hypotonic

solutions

heat damage from blood warmers, during shipping, in

hot rooms

freeze damage in absence of cryoprotective agent

during shipping


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Mechanical Damage

blood pumps, roller pumps infusion under pressure through small bore needles


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Patients with Intrinsic Abnormal Cells

congenital hemolytic anemias sickle cell crisis

PNH or AIHA


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Clinical manifestations: nonClinical manifestations: non--specificspecific

facial/ generalized numbness, chills, muscle

twitching, perioral tingling, altered respiration. anxiety

Laboratory tests:Laboratory tests:

electrolyte levels, serum ionized calcium, blood pH,blood glucose, urinalysis, hemoglobin, hematocrit,

PLT count, PT, aPTT


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Treatment of PCITRs:

correction of underlying cause preventive measures


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Citrate toxicityCitrate toxicity

ACD/ CPD has 1.4ACD/ CPD has 1.4--1.6 g of citrate1.6 g of citrate -- no toxicityno toxicity citrate > 100 mg/ dlcitrate > 100 mg/ dl -- citrate toxicitycitrate toxicity

CausesCauses

ADULTSADULTS

rate of BT > 1 liter/ 10 min or BT volume exceeds 6 Lrate of BT > 1 liter/ 10 min or BT volume exceeds 6 L

administered in < 2 hoursadministered in < 2 hours

CHILDRENCHILDREN

exchange transfusionexchange transfusion -- hypocalcemiahypocalcemia


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Clinical manifestations:Clinical manifestations:

involuntary muscle tremors, cardiac arrhythmia,involuntary muscle tremors, cardiac arrhythmia,

ventricular fibrillationventricular fibrillation

ECG findings:ECG findings:

ST prolongationST prolongation

T wave delayT wave delay


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Potassium toxicity:Potassium toxicity:

Mechanism: high potassium load with prolongedMechanism: high potassium load with prolonged

blood storageblood storage -- hyperkalemiahyperkalemia Clinical manifestations: cardiac excitabilityClinical manifestations: cardiac excitability -- cardiaccardiac

standstillstandstill

ECG findings: peak T wavesECG findings: peak T waves

Laboratory findings: hyperkalemiaLaboratory findings: hyperkalemia Management: calcium gluconateManagement: calcium gluconate


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DELAYED NONDELAYED NON--HEMOLYTICHEMOLYTIC

TRANSFUSION REACTIONSTRANSFUSION REACTIONS


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Post-Transfusion Purpura (PTP)

Consists of profound thrombocytopenia

occurring 1-2 weeks after transfusion

Pathophysiology:

Effect ofantibody directed against donor

platelet antigens that the recipient lacks

Commonly associated with human

platelet-specific alloantigen 1a (HPA-1a)


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Pathophysiology:

Causes destruction of both autologous

platelets as well as donor platelets

(innocent bystander effect)Nonspecific antibody adherence

Soluble proteins taken up by recipient platelets

against which an antibody has been formed

Immune complex deposition on platelet surfaces

with resultant recipient platelet destruction


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Treatment and Prevention of PTP:Treatment and Prevention of PTP: IVIGIVIG

plasmapheresis

steroids avoidance of antigen-positive platelet transfusion with

previous PTP


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If PTP does not lead to death due tohemorrhage, it is a SELF-LIMITED disease withrecovery within 4-5 days of therapy.

Recovery may be hastened by the use ofantigen-negative platelets if the specificity of theantibody has been determined and antigen-negative platelets are available.


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Transfusion Associated Graft versus

Host Disease (TA-GVHD)

disorder marked by attack and destruction ofrecipient cells by engrafted immune cells

remains a serious and common complication intransplantation

T f i A i d G f


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Criteria for diagnosis:

presence ofimmunocompetent cells in the

graft capable of reacting against the recipient major histocompatibility differences between

donor and recipient

inappropiate recognition of self-antigens

(autoimmunity)

inability of the recipient to reject donor cells

T f i A i t d G ft


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Pathophysiology of GVHD:

Immunocompetent donor lymphocytes that

are not cleared because of a compromised

host immune system go on to proliferate inthe recipient --- attack and destruction of

host tissues in target organs (liver, intestines,

skin, lungs)

T f i A i t d G ft


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One-Way HLA Match --- donor cells are

homozygous for an HLA type + recipient cells

which are heterozygous for the same HLAtype --- recipient immune cells do not

recognize the donor cells as foreign and fail to

mount an immune response that would

normally clear donor cells - donor cellsrespond to the mismatched haplotype - GVH

reaction

T f i A i t d G ft


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Role of dysregulated cell activation and

cytokine release

Upregulating effects: T-helper 1 cytokines -- IL-2, gamma interferon, pro-inflammatory

cytokines IL-1 and TNF-alpha

Downregulating effects: T-helper 2

cytokines-- IL-4, IL-10

T f i A i t d G ft


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Clinical Manifestations of GVHD:

onset: 7-10 days from transfusion

fever

reddish, raised rash spreading from trunk orface to extremities - bullous lesions --erythroderma

hepatitis

watery diarrhea (profuse) non-specific signs: anorexia, nausea and

vomiting

T f i A i t d G ft


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Pancytopenia is the usual cause of deathdue to hemorrhage and overwhelminginfection.

Death occurs within 1-3 weeks aftertransfusion.

Diagnosis of GVHD:

Identification of donor-derived lymphocytes inthe circulation or tissues of the affected host.(PCR amplification strategy)

T f i A i t d G ft


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Treatment of GVHD: Immunosuppressive therapy

Patient Groups at RISK for developing transfusion-associated GVHD:

Selected immunodeficiency (congenital, HD, CLL onfludarabine)

Newborns with erythroblastosis foetalis

Recipients of intrauterine transfusions

Recipients of hematopoietic stem cell transplants

Recipients of blood products donated by relativesRecipients of HLA selected (matched) platelets or plateletsknown to be homozygous

T f i A i t d G ft


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Prevention of GVHD:

Gamma irradiation of blood components containing

viable lymphocytes is 100% effective in preventing

GVHD.

Prevention of lymphocyte proliferation through DNA cross-

linkage.

Uses 25 cGy to the midplane of the blood container with a

minimum of 15 cGy to any point of the irradiated field

Adverse effects: moderate decrease in survival of RBC and

leakage of potassium from intracellular stores


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Iron Overload

common in patients with chronic diseases

requiring multiple and prolonged transfusions

(thalassemia)

on the average, 1 unit PRBC = 200 mg ironalso transfusion hemosiderosis

chronic iron overload leads to hepatic, cardiac

and pancreatic disease.

prevention:

iron chelation therapy (desferoxamine)


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Alloimmunization

results from priorexposure to donor blood

components

AE: difficulty in finding compatible RBC units

because of the presence of clinically significantRBC antibodies, transfusion reactions or platelet

refractoriness


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Alloimmunization

Pathophysiology:

after first exposure to donor antigen -

recipient memory lymphocytes are invoked --

moderate production of IgG and IgM on second exposure to donor antigen --

rapid and large production of IgG within the

first 2 days


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Alloimmunization

Clinical manifestations:

mild to severe

Laboratory tests:

antibody screening


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Alloimmunization

Treatment of Alloimmunization:

Accurate matching of donor and recipient

RBC phenotypes


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Immunosuppression

generalized non-specific effect diminishing the

activity of the recipients immune system soon

after blood transfusion

pathophysiology:

unknown

rapid uptake of blood component cellularmatter into the RES


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Immunosuppression

clinical manifestations:

non-specific

blood component transfusion may increaserisk of suppressive effect on the recipient

treatment of immunosuppression:

non-specific

prevention

risk-benefit ratio evaluated


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IMMEDIATE BTR PROCEDURES ATIMMEDIATE BTR PROCEDURES AT

BEDSIDEBEDSIDE


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Bedside BTR Procedures

1. STOP blood transfusion at once!1. STOP blood transfusion at once!

2. Keep IV2. Keep IV line open with isotonic solution.

3. Seek medical attention.

4. Monitor clinical condition of patient.5. Perform bedside clerical checks.

6. Return unit, set and attached solution to BB.

7. Collect appropriate blood specimens for

evaluation.8. Document BTR.


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SAFETY DURING BLOODSAFETY DURING BLOOD

TRANSFUSIONTRANSFUSION


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Safety During Blood Transfusion

Flow rates Infuse the first 25 mL of blood (smaller volume for pediatric

patients) slowly at no more than 25 drops/ minute toallow for recognition of an acute adverse reaction.

Remainder can be infused at 60-80 drops/ minute. Complete transfusion within 2 hours unless the patient cantolerate only gradual expansion of the intravascularvolume.

Transfusion should not exceed 4 hours.

Platelets, plasma and cryoprecipitate are generally transfused at

10 mL/ min


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Safety in Blood Transfusion

During the blood transfusion:

Document patients vital signs.

Check for urticaria.

During the infusion, VS should bedocumented after the 1st 15 and 30

minutes and hourly until 1 hour after

completion of transfusion.

Any transfusion that stops or slows thetransfusion should be investigated.


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Measures to enhance blood flow:

elevate IV pole

change filter and tubing

reposition patients arm

change to a larger gauge needle


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Medications:

Do not add medications directly to a unit of

blood during transfusion

Medications by IV push:stop transfusion

clear the line at the medical injection site with 5-10

mL NSS

administer the medication

re-flush the line with NSS and re-start transfusion


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SAFETY IS THE BESTSAFETY IS THE BEST

POLICY.POLICY.

blood transfusion reactions revisited dr. edwin rodriguez

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