Fact Sheets Final Web 0908

8/2/2019 Fact Sheets Final Web 0908

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New York State Council on Human Blood and Transfusion Services*and

New York State Board for Nursing

TRANSFUSION REACTION

FACT SHEETS

A Companion Reference To Guidelines For

Monitoring Transfusion Recipients

First Edition

2008

*New York State Council on Human Blood and Transfusion ServicesNew York State Department of Health

Wadsworth CenterEmpire State Plaza - P.O. Box 509

Albany, New York 12201-0509

New York State Board for NursingNew York State Education Department

Education Building89 Washington Avenue, Second Floor, West Wing

Albany, New York 12234


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First Edition 2008

Requests for copies of this publication may be directed to:

Blood and Tissue Resources ProgramNew York State Department of HealthWadsworth CenterEmpire State PlazaP.O. Box 509

Albany, New York 12201-0509

Telephone: (518) 485-5341Fax: (518) 485-5342E-mail: [email protected]: www.wadsworth.org/labcert/blood_tissue
mailto:[email protected]://www.wadsworth.org/labcert/blood_tissuehttp://www.wadsworth.org/labcert/blood_tissuehttp://www.wadsworth.org/labcert/blood_tissuemailto:[email protected]


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NEW YORK STATECOUNCIL ON HUMAN BLOOD AND TRANSFUSION SERVICES

AND

NEW YORK STATEBOARD FOR NURSING

Appendix B

Transfusion Reaction Fact Sheets

Table of Contents

Acute Reactions

Acute Hemolytic Reactions .............. 6B

Sepsis/Bacterial Contamination ....... 7B

Transfusion-Related Acute Lung Injury (TRALI) ...... 8B

Allergic (Severe) Anaphylactic or Anaphylactoid Reactions ........... 9B

Transfusion-Associated Circulatory Overload (TACO) .......... 10B

Febrile Nonhemolytic Reactions ........ 11B

Allergic (Mild) Reactions ....... 12B

Delayed Reactions

Graft-vs-Host Disease (GVHD) ... 13B

Delayed Hemolytic Reactions ..... 14B

Posttransfusion Purpura (PTP) ........... 15B

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Appendix B

Transfusion Reaction Fact Sheets

Acute Reactions

Acute Hemolytic Reactions (< 24 Hours)

Clinical Presentation Pathophysiology Treatment/Prevention

Fever 1C/2F

Rigors

Nausea

Lower back pain

Chest pain or tightness

Acute hypotension orhypertension

Tachycardia

Tachypnea, wheezing, or

hypoxemia Shock

Wine- or cola-coloredurine or jaundice

Pain at infusion site oralong infusion vein

Urticaria, pruritis, flushingor angioedema

Anxiety

Unexplained bleedingfrom mucous membranesor infusion sites

Hemoglobinuria Renal failure

Hemoglobinemia

Direct antiglobulin test(DAT) may be positive ornegative

Incompatible blood administrationresults in an antigen/antibodyresponse with activation ofcomplement and subsequentintravascular hemolysis. Acutehemolytic reactions usually involvethe ABO blood system.Misadministration of blood oftenresults from improper identificationof transfusion recipients, either at

the time of phlebotomy for the typeand screen specimen or at the timeof transfusion. Occasionally, acutehemolysis may occur from mixing ofblood with a fluid other than normalsaline or from improper warming orfreezing of blood.

Maintain airway; provide oxygenand ventilatory support ifnecessary

Diuretics to promote renalperfusion

Cardiovascular support withpressor agents, as indicated(pressor agents that decreaserenal blood flow arecontraindicated)

Hydration to maintain urinaryoutput

Treatment of DIC

Initiate transfusion reaction work-up; send unit and administrationset with attached solutions to thelaboratory, in addition to blood andfirst posttransfusion urinespecimens

Do not initiate another transfusionwithout Blood Bank consultation

If patient is hemodynamicallyunstable, invasive monitoring ofpulmonary artery occlusionpressure can guide fluid therapy

Red cell exchange may beconsidered in patients with asignificant load of circulatingincompatible red cells

Document reaction in patientschart as per institution policy

Prevention:

ABO mistransfusions may beavoided by proper patientidentification

Administer blood only with normalsaline

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Sepsis/Bacterial Contamination


Fever, often > 2C/4Fabove baseline

Chills

Rigors

Hypotension

Shock

Renal failure

Unexplained bleedingfrom mucous membranesor infusion sites

Sepsis is the result of transfusion ofbacterially contaminated bloodcomponents. The bacteria usuallyoriginate from the blood donor,either from venipuncture (e.g.,Staphylococcus, Streptococcus) orfrom unsuspected bacteremia (e.g.,Yersinia), but may also result fromdonor unit processing. Bacterialmultiplication is more likely to occurin components stored at roomtemperature (e.g., platelets) than incomponents stored at refrigeratortemperatures (e.g., red cells).


Cardiovascular support withpressor agents, as indicated

Hydration to maintain urinaryoutput

Treatment of DIC

Initiate transfusion reaction work-up; send unit and administrationset with attached solutions to thelaboratory, in addition to bloodand first posttransfusion urine

specimens Do not initiate anothertransfusion without Blood Bankconsultation

Gram stain and culture theimplicated blood component;draw blood culture from patient

Prompt initiation of IV antibioticsif indicated by the Gram stainresults


Prevention:

Visual inspection of units forcolor changes, hemolysis, clots

Blood and components shouldbe transfused within 4 hours afterissuance

Tubing should be changedbetween blood units as perinstitutional policy

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Transfusion-Related Acute Lung Injury (TRALI)


Acute respiratory distressor failure during or within 6hours after transfusion;often dramatic onset

Dyspnea

Cyanosis

Bilateral pulmonaryinfiltrates on chest x-ray

Hypoxemia (O2 sat 90%on room air or PaO2 300mm Hg)

No evidence of circulatoryoverload (pulmonary

artery occlusion pressure< 18 mm Hg, if available)

Hypotension or, in somecases, hypertension

Fever

Tachycardia

Transient leukopenia

Most patients improveover 2-3 days

Mortality rate about 10%

TRALI most commonly results fromthe infusion of donor antibodies

directed against recipient HLAclass I or II antigens or neutrophilantigens. The antigen/antibodycomplex activates complement withresultant neutrophil influx into thelungs. Neutrophil activation causescapillary leakage and pulmonarydamage. Infrequently, recipientantibodies against cognate donorantigens may be implicated.

In a number of TRALI cases, no

antibody is found. Biologicalresponse modifiers, such asmembrane lipids, whichaccumulate during blood storage,may be implicated in these cases.

TRALI may occur with any bloodproduct, but it occurs morecommonly with productscontaining large volumes of donorplasma. No particular patient riskfactors have been identified.

Donors of implicated units areusually multiparous females whohave been immunized to HLA orneutrophil antigens via pregnancy.

Maintain airway; provide oxygenand ventilatory support if necessary

Treat hypotension

Diuretics and steroids aregenerally not helpful and may becontraindicated

Initiate transfusion reaction work-up; send unit and administrationset with attached solutions to thelaboratory, in addition to bloodand first posttransfusion urinespecimens



Additional Testing:

Normal brain natriuretic peptide(BNP) can help distinguish fromtransfusion-associated circulatoryoverload (TACO)

Patient serum should be tested forantibodies against HLA orneutrophil-specific antigens and

the patients HLA type should bedetermined

The blood collection facility willtest involved donors for antibodiesto HLA and neutrophil-specificantigens. If found, they will becompared with the patientsphenotype

Future Transfusion:

Implicated donors are deferredfrom further blood donation

Patients are not generally at riskfor recurrence

Because HLA antibodies are morecommon in female donors, manycenters are providing plasma fromdonors who are male or who havebeen screened.

8B
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7/13

Allergic (Severe) Anaphylactic or Anaphylactoid Reactions


Anxiety

Wheezing, stridor,dyspnea

Throat fullness/tightness

Cyanosis

Hypotension

Tachycardia

Urticaria

Flushing

Gastrointestinal distress

Shock

Patient is afebrile

Loss of consciousness

Cardiac arrest (rare)

The transfusion recipient has anantibody which may be an IgEdirected against an antigen in donor

plasma, such as an IgA-deficientpatient who possesses antibodiesto IgA. The cause, however, is oftennot identified.


Treat hypotension -Trendelenberg position andfluids; dopamine if unresponsive

Epinephrine if necessary

Intubate if significant upperairway obstruction




Additional Testing:

Send a specimen for IgA level, ifclinically indicated

Future Transfusion: Patient may be given

diphenhydramine (Benadryl),steroids, and/or ephedrine prior totransfusion

IgA-deficient patients can begiven washed cellularcomponents or components fromIgA-deficient donors, althoughsuch donors are rare andcomponents may be difficult toobtain

Use washed or deglycerolizedRBCs (or washed platelets) forpatients experiencing severereactions not caused by anti-IgA

Consider storing autogeneic unitsfor future transfusions

9B
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8/13

Transfusion-Associated Circulatory Overload (TACO)


Dyspnea

Orthopnea

Cough

Rales on auscultation

Cyanosis

Headache (severe)

Tachycardia

Hypertension

Congestive heart failure

Bilateral pulmonaryedema on CXR

Pulmonary arteryocclusion pressure

TACO is a life-threatening conditiondue to rapid increases in bloodvolume in patients withcompromised cardiac or pulmonaryfunction and/or in patients withchronic anemia and expandedplasma volumes.

It may also be caused by infusionof 25% albumin (oncotic pressurecauses shift of fluid fromextravascular to intravascularspace).

Upright posture


Diuretics (e.g., furosemide)


Do not initiate another transfusionwithout Blood Bank consultation.

Circulatory overload must beaddressed prior to initiation ofadditional blood components orvolume expanders

Phlebotomy (250 mL increments)to reduce blood volume


Additional Testing:

brain natriuretic peptide (BNP)

can help distinguish from TRALI

Future Transfusion:

Except in conditions of ongoingrapid blood loss, bloodcomponents should beadministered to at-risk patientsslowly (1mL/kg/h) with attention tototal fluid input and output; ifextended periods of transfusionare required, request split units

Diuretics may be given prior to orduring the transfusion

10B
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9/13

Febrile Nonhemolytic Reactions


Temperature rise of> 1C/2F or atemperature of 38Cduring or within 4 hours oftransfusion, without anyother obvious cause

Chills/rigors with orwithout fever

Headache

Nausea/vomiting

Tachycardia, palpitations,and cough may also occur

Preformed anti-HLA antibodies inthe recipient (from pregnancy or

previous transfusion) react withcorresponding antigens ontransfused white blood cells orplatelets and trigger cytokinerelease.

Alternatively, preformed cytokinesfrom white blood cell breakdownin the donor units may be directlyinfused.

Most febrile nonhemolytic reactionsare benign, although some may

cause significant discomfort andhemodynamic or respiratorychanges.

Non-salicylate antipyretic(acetaminophen)

Meperidine (injection) may beuseful in patients with rigors




Future Transfusion:

Leukocyte-reduced (pre-storage)blood components may beindicated in patients with a historyof febrile non-hemolytictransfusion reaction or who arechronically transfused

Platelets that are not leukocyte-reduced should be 3 days old to

reduce cytokine-mediatedreactions

Plasma removal may decreasefrequency of febrile reactions

Premedication withacetaminophen has not beenshown to be of benefit whenleukocyte-reduced componentsare given

11B
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10/13

Allergic (Mild) Reactions


Skin

Urticaria

Itching

Flushing

Erythema

Localized angioedema

Respiratory tract

Cough

Hoarseness

Stridor

Wheezing

Chest tightness or pain Dyspnea

Gastrointestinal tract

Cramps

Nausea

Vomiting

Diarrhea

Cardiovascular system

Tachycardia

Other arrhythmias

Cardiac arrest

The transfusion recipient usuallyhas an IgE antibody on mast cellsdirected against an antigen indonor plasma resulting inactivation and release ofhistamine.

Diphenhydramine (Benadryl) ifurticaria is only symptom

In the case of mild reactions, thetransfusion may be restarted aftertreatment, provided unit can becompleted within 4 hours ofissuance

Do not restart unit if urticariasevere or patient developssignificant local swelling,respiratory or gastrointestinalsymptoms, or hypotension

Monitor closely for any othersigns or symptoms


Future Transfusion:

Patient may be givenantihistamine (diphenhydramine)prior to transfusion

If antihistamine is insufficient,hydrocortisone one hour prior to

transfusion may be helpful In cases of recurrent or severe

reactions, washed ordeglycerolized frozen red cellsmay be useful

12B
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11/13

Delayed Reactions

Graft-vs-Host Disease (GVHD)


Fever

Watery diarrhea (profuse) Vomiting

Rash (maculopapular)

Hepatitis (elevated liverfunction tests)

Refractory pancytopeniawith bleeding andinfectious complications

Symptoms typicallyappear 8-10 daysfollowing transfusion(range 3-30 days)

Rapid progression withvirtually 100% mortality

GVHD can occur when, following

successful engraftment of donorT-lymphocytes, the transfusedforeign lymphocytes, if HLA-incompatible with the transfusionrecipient, mount an attack againstthe recipients tissues, causingenterocolitis, rash, andpancytopenia. Because ofresultant marrow aplasia, patientssuccumb, primarily from sepsis.

GVHD is rare in U.S. transfusionrecipients and is observed almost

exclusively in immunocom-promised patients.

The diagnosis is proven bydemonstration of donor-derivedlymphocytes in recipientsperipheral blood or tissues (by HLAtyping).

Immunosuppressive agents

(corticosteroids, cytotoxic agents,intravenous immune globulin)

Treatment is usually not successful

Only stem cell transplant iscurative

Prevention:

Patients at increased risk shouldreceive irradiated cellularcomponents (see Guidelines forIrradiation of Blood and BloodComponents)

Directed blood donations (cellularcomponents) from blood relativesand cellular components fromdonors selected for HLAcompatibility should be irradiated

13B
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12/13

Delayed Hemolytic Reactions (> 24 Hours)


Fall in hemoglobin and

hematocrit Fever

Jaundice

Lactate dehydrogenase(LDH)

Leukocytosis may occur

Reaction typically occurs3-7 days aftertransfusion, but mayoccur 14 days aftertransfusion or later

Patient may be

asymptomatic Direct antiglobulin test

(DAT) may be positiveand an antibody, notdetected prior to thetransfusion, may beidentified

A patient has made an antibody

against a red cell antigen in theremote past. Over time, the titer ofthis antibody has decreased tobelow detectable levels, so theantibody screen performed prior tothe current transfusion does notdetect the antibody. Administrationof antigen-positive blood presentsa second challenge to the immunesystem and provokes a subse-quent anamnestic response.Hemolysis is usually extravascular;

however, it may be intravascular.

Send a new blood specimen for

antibody screen, antibodyidentification and DAT

Monitor renal function


Future Transfusion:

Transfuse with antigen-negativeblood, as indicated

14B
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13/13

Posttransfusion Purpura (PTP)


Thrombocytopenia, whichmay be severe, occurringwith abrupt onset 1-2weeks after a transfusion

Melena

Hematuria

Vaginal bleeding

Occurs most commonlyin multiparous women

Usually self-limited ( 2weeks), but bleeding maybe severe and can befatal (e.g., intracranial

bleeding)

Thrombocytopenia occurs in apatient who has made an antibodyagainst a foreign platelet antigen asa result of pregnancy or a previoustransfusion. After a transfusion ofred cells or platelets, antibodiesattach to surface antigen sites onplatelets, resulting in theirdestruction by splenic and livermacrophages. Most commonly theimplicated antibody is against theHPA-1a (PLA1) antigen (60% ofcases). Through a mechanism notclearly elucidated, likely auto-

immune, the patients own antigen-negative platelets are alsodestroyed.

Intravenous immune globulin (IVIG)

Plasmapheresis with FFPreplacement, if refractory to IVIG

Steroids, although their benefithas not been documented

Send blood specimen tolaboratory for platelet antibodywork-up


Transfusion of antigen-negativeplatelets is generally ineffective

Future Transfusion:

Repeat reactions are rare, butpatients with a documentedhistory of PTP should receiveantigen-negative bloodcomponents, if available

Platelet typing of family membersmay help identify potentialantigen-negative donors

15B
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