Adverse reactions of blood transfusion


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medical- pathology-transfusion medicine


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ADVERSE EFFECTS OF BLOOD TRANSFUSION Dr. Sonal Sharma Dept of Pathology BARC Hospital

Catagories of transfusion reactions:

Catagories of transfusion reactions Reactions Immune mediated Non immune mediated Acute Delayed Hemolytic Alloimmunisation Febrile non hemolytic Post transfusion purpura Allergic GVHD Anaphylactic TRALI ( contd )

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Non immune mediated Acute Delayed Bacterial contamination Infections Circulatory overload 1. HIV1&2 Physical/chemical 2 . HBV hyperkalemia 3. Syphilis 4. Malaria Iron overload

Immediate immune-mediated transfusion reactions:

Immediate immune-mediated transfusion reactions Occurs very soon after transfusion The common Ab are – Anti-A, Anti-B, Anti- Kell , Anti- Jk a , Fy b Mechanism of action – Ag- Ab complexes Complement activation ( hemolysis ) Neuroendocrine responses Coagulation effects Cytokine effects Immune mediated red cell lysis is either intravascular/ extravascular When intravascular there will be intravascular circulation of the stroma of lysed RBCs


Causes Clerical errors Inadequate, incorrect labelling Confusion in the identity of the patient Improper identification of patients sample by the blood bank technician Wrong blood issue Technical errors Grouping and cross matching errors Improper methods Weak Ab Destruction of recipient cells by donor Ab (mostly if gp O to gps A,B /AB) Incorrect interpretation of the results

Signs and symptoms:

Signs and symptoms Fever >1 o C or 2 o C + chills, rigors Pain at the infusion site, chest, flank Tachycardia Hypotension Respiratory distress – dyspnea, tachypnea, hypoxemia Oozing from IV line site Hemoglobinuria Oliguria Anuria Shock

Immediate non immune mediated reactions:

Immediate non immune mediated reactions Causes Bacterial contamination (during phlebotomy) Endotoxins of E.coli, Pseudomonas, Y.enterocolitica Platelet transfusion Damage to the RBCs Physical hemolysis Roller pump like used in cardiac surgery Infusion under pressure through small bore needles Blood pumps

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Chemical hemolysis Concomitant administration of either D5/hypotonic saline, drugs etc through a common infusion set Thermal hemolysis Cooled below -3 O C or >42 o C S/S Usually appear within 30min of transfusion Severe hypotension Fever and chills Vomitting Abdominal cramps Muscular pain Hemoglobinuria Shock DIC Renal failure


Hyperkalemia It usually occurs after massive transfusion A life threatening load of K+ may be released into the circulating plasma Plasma levels of potassium must be montiored periodically Periodic cardiac evaluation for arrhythmias If needed, dialysis must be done


Anaphylaxis Begins after infusion of few mL of plasma/plasma containing blood products Causes Immediate hypersensitivity Congenital IgA deficient It is the most common congenital immune deficiency, affecting 1 in 700-800 As many as 30% of these have anti IgA from transfusion/pregnancy

Signs and symptoms:

Signs and symptoms Respiratory system – bronchospasm , cough, dyspnea GIT – nausea , vomiting, diarrhea Circulatory system – hypotension, arrhythmias, syncope Skin – flushing, urticaria


TRALI Non cardiogenic pulmonary edema Unusual but life threatening Associate with altered permeability of pulmonary capillary bed due to Activation of complement Histamine/PG mediated events Leads to fluid accumulation, inadequate oxygenation and reduced cardiac return Anti-leukocyte Ab in donor plasma + leukocytes in pulmonary vasculature – leucocyte emboli. Acute onset of cough, dyspnea, cyanosis, fever and chills

Circulatory overload:

Circulatory overload Very young or very old patients Having underlying CCF/chronic normovolumic anemia Large volume transfused within a short time Signs & symptoms Cyanosis Dyspnea Tachycardia Peripheral edema Hypertension CCF


Management In the ward maintain airway – O2 by mask,nasal catheter, intubation Stop transfusion, disconnect i.v line, start NS with a new infusion set Drugs Adrenaline – 0.01mg/kg i.m Corticosteroids and bronchodilators Diuretics like frusemide Antihistaminics Antipyretics Suspected DIC should be treated with cryprecipitate, FFP and platelets


contd hourly monitoring of the patient for vital signs, urine output, bleeding, ECG If still febrile – higher doses of antipyretics If hypotension persists Continue giving NS Inotropes – dopamine Urine output falling or any other e/o renal failure i.v fluids Frusemide Dopamine infusion dialysis\

Management of immediate HTRs:

Management of immediate HTRs Check the label, cross-matching report and identify patient, confirm whether patient has received the correct blood unit/component Notify the blood bank and describe the s/s Post transfusion blood sample 10ml in plain and 2 ml in EDTA from another vein should be sent to the blood bank along with the blood bag, transfusion set and transfusions reaction report First voided urine should be sent for analysis of free hemoglobin

Laboratory investigations:

Laboratory investigations Check identity of the patient, donor blood and all relevant papers to ensure that there was no clerical error color of plasma of patient’s pre & post transfusion blood samples Pink /red - free Hb present Yellow/brown colour ,about 4-10 hrs after transfusion-increased bilirubin Colour of bag Purple – bacterial contamination Red – hemolysis

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Repeat ABO, Rh testing in patient’s pre and post samples Sample from the bag Perform DAT on patient’s sample Negative test implies no coating of the red cells by IgG Ab or no incompatibility In a non-immunological reaction DCT will be negative If the sample is drawn several hours later then the Ab coated red cells may be destroyed and DCT will be negative If Ab coated red cells are not immediately destroyed, the DCT will be positive Bacteriological smear and culture of the donor’s blood

Interpretation of the lab findings:

Interpretation of the lab findings If above results are negative, then there has not been an acute hemolytic reaction In case of any positive findings Repeat cross match testing with pre and post transfusion samples Repeat Ab screening If any irregular Ab is detected on screening then it should be identified by panel of cells by saline and IAT

Optional tests for clinical evaluation of patients:

Optional tests for clinical evaluation of patients Serum non-conjugated bilirubin is tested in pre & post transfusion blood samples of the patient Haptoglobin levels in pre and post transfusion samples of the recipient Estimation of free Hb in te patient’s sample – normal

Febrile non hemolytic transfusion reactions:

Febrile non hemolytic transfusion reactions It is described as increase of 1 o C or more of the patient’s base line temperature during or within 24 hrs, without any medical explanation Usually self limiting Seen in multi-transfused patients or multiparous women Mediated by Ag-Ab complexes-activation of complement, cytokine stimulation, release of endogenous pyrogens

Signs and symptoms:

Signs and symptoms Generally symptoms are mild and benign Temperature rise 1 O C or more with/without rigors Hypotension Cyanosis Tachycardia Tachypnea Dyspnea Cough Leukopenia

Allergic reactions:

Allergic reactions Foreign protein (allergen) in donor plasma They react with IgE attached to mast cells and basophils Initiate histamine release s/s Erythema Pruritus Hives Fever +

Delayed transfusion reactions:

Delayed transfusion reactions There are two types of tranfusion reactions Primary alloimmunisation Usuallly occuring several weeks after transfusion Mostly mild Result of primary alloimunization due to incompatibility of other blood group systems – Rh, Kell, Duffy, Kidd s/s Mild fever Fall in Hb Irregular Ab DAT may be positive

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Anamnestic response Due to transfusion of incompatible red cells in a patient, already immunized by previous transfusion Due to incompatibilty of other blood group system Ag The Ab concentration after few days and they destroy the red cells causing hemolytic reactions No reaction at the time of trnasfusion, later on there may be Fall in Hb Rise in bilirubin and mild jaundice (5/7 days later) Rarely renal failure

Platelet incompatibilty:

Platelet incompatibilty Rare complication Anamnestic production of platelet Ab Usually seen in multiparous women Platelet specific allo-Ab anti-P1 A1 This Ab destroys the P1 A1 positive platelets and also causes non specific destruction of P1 A1 negative platelets s/s Post transfusion purpura Febrile reactions – chills, fever, dyspnea Management Steroids Plasmapheresis IVIg

Transfusion associated GVHD :

Transfusion associated GVHD Very rare (0.1-1%) complication seen in Immuno -compromised individuals esp in solid tumor cancer pxts on chemo, but can occur with acute/chronic leukemia, lymphomas, new borne with erythroblastosis fetalis and transplant pxts Different from transplant GVHD by it’s effect on bone marrow (BM aplasia ) It occurs in immuno -compromised recipients of blood products from donors with identical HLA haplotypes . They are heterozygous for a HLA haplotype for which the donor is homozygous .e.g. genetically identical relatives HLA ag are shared by donor and recipient, thus donor lymphocyte are engrafted by recipient because they are the only Ag seen by the host. On the flip side the donor lymphocytes view the recipient’s tissues as foreign leading to immunologic activation and GVHD. Bone marrow aplasia is the primary cause of death

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Clinical presentation Skin : Swollen, erythroderma and bullae formation- most common GI : Diarrhea and abdominal cramps Liver: Elevated LFT and Hyperbilirubinemia Heme : Bone marrow aplasia , persistent thrombocytopenia Skin manifestation of GVHD Generalized swelling, erythroderma and bullous formation

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Implicated products Non Irradiated whole blood PRBC Platelets Granulocytes Fresh non frozen plasma It has not been seen with frozen deglycerolized RBC, FFP or Cryoprecipitate Treatment Poor response to standard immunosuppressive therapies, Thalidomide has been tried with variable success. Prevention Is the Key, since response to treatment is poor Gamma irradiation and leuko -reduction of products Avoid blood products from genetically identical donors

Non-immune delayed complications:

Non-immune delayed complications Hemosiderosis In pts. who require multiple transfusion Storage of iron usually occurs in the reticulo -endothelial sites, but may also occur in the parenchymal cells Iron deposition interferes with functions of heart, liver and endocrine functions Treatment Daily dose of 20-40mg/ Kgwt . Of desferrioxamine administered subcutaneously over 8-10hrs Transfusion of neocytes

Transfusion transmitted diseases:

Transfusion transmitted diseases Three basic conditions that will determine whether the infectious agent is likely to be transmitted by blood Capability of using the blood stream as a route of entry Infected donor otherwise clinically free of signs and shymptoms the ability to exist naturally for a period of time

Mean time between infection and seroconversion:

Mean time between infection and seroconversion Infection Mean time Range HIV 22days 6-38days HCV 98days 56-189days HBsAg 56days 24-128days HTLV 51days 37-72days


HIV The finding of anti-HIV in patients with previously unexplained immunodeficiency is diagnostic of AIDS Ab may be present as early as 14 days of infection or may not be detected even upto 28 days or more after infection The most important Ab are anti-p24 and anti-gp41

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Testing for AntiHIV ELISA/EIA Particle agglutination assays Specialized rapid assays WINDOW PERIOD “window period” is the time period between acquisition of infection and production of Ab During this time the Ag are detected in the sera The Ag detected are p24 and gp41 The length of time for which they are detected is very short, about 1-2weeks

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HIV Ag detection assays Aimed at detecting the viral Ag, nucleic acids They are useful in detecting the HIV infected donor’s blood earlier than the Ab assays Useful in the following conditions Detecting the infection during window period Confirming infection in in neonates of a seropostive mother May help to resolve indeterminate Western blot tests Monitor HIV patients on ART Methods ELISA for p24 Ag PCR Viral isolation

Recommendations for HIV1&2 testing:

Recommendations for HIV1&2 testing Sera of all donor s should be tested for anti-HIV1&2 by ELISA/EIA Sera non reactive on first screening are considered NEGATIVE and are recommended for transfusion If positive on the first screening then it should be repeated in duplicate If both negative then it is HIV NEGATIVE If one or both positive, then WESTERN BLOT is done If positive, then donor should be counselled If negative, then re-evaluate after 3 months


Hepatitis HAV, HBV, HCV & HDV have been associated with post-transfusion hepatitis Hepatitis C Most common cause of non-A, non-B hepatitis in the world Prevalence of anti-HCV in voluntary / replacement donors in India is reported to be 0.6-5.2% 75-80% progress to chronic state ,10-20% of which develop cirrhosis and HCC Avg incubation period is 6-7weeks (2-26weeks)

Hepatitis C:

Hepatitis C anti-HCV EIA assay Initial clone discovered from the NS4 region was 5-1-1 First generation assay recognized c100-3 Ag The second generation added c22 core Ag and c33c from the NS3 region The third generation has added a NS5 protein PCR is useful in HCV detection in Immunosuppressed Recent organ transplant Indetermined Recombinant immunoblot assay Acte infection

Hepatitis B:

Hepatitis B Incubation period is between30-150 days HBsAg First marker, also found in chronic carriers Anti-HBs when HBsAg disappears Core Ab window AntiHBc HBe & Anti-HBc Shortly after infection and before S/S HBe Ag Disappears when patient enters convalscence

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Initially anti-HBc is IgM type later IgG anti-HBc appears Individuals who recover from infection will have anti-HBs and /or anti-HBc In persons who do not develop immunity to HBV, HBsAg, HBeAg and anti-HBc may be present

Hepatitis B:

Hepatitis B Incubation period is b/w 30-150 days Usually the first marker is HBsAg, detectable from few days to several months Also found in some chronic carriers Anti-HBs is detectable once HBsAg disappears “Core-Ab period” – anti-HBc is the only marker of recent infection Shortly after infection and before signs and symptoms - HBe and anti-HBc Initially anti-HBc is IgM type and as the infection progresses IgG anti-HBc appears

Serological markers of HepB and their significance:

Serological markers of HepB and their significance Marker significance HBsAg Active infection, acute or chronic Anti-HBsAg Clinical recovery, infection resolved, immunity developed Anti-HBc(IgM) Early acute infection Anti-HBc(IgG) Active or past infection HBeAg Acute or serious chronic infection Anti-Hbe Resolution of acute infection may be a late sequelae

Other infectious agents transmitted:

Other infectious agents transmitted Bacteria – syphilis Treponema pallidum (spirochaete) Incubation period is b/w 1-4months Incubation period in transfusion syphilis varies from 4-4.5 weeks Its not a major hazard of transfusion as Spirochetes do not survive in citrated blood stored at 4 deg C for 72 hrs Exclusion of sexually promiscuous donors Most recipients receive antibiotics because of their clinical condition

Role of serology:

Role of serology Spirochetaemia is common during the early stages of syphilis Screening tests are often negative during this time Only about 25% of people exhibit a reactive STS Majority are reactive only after about the 4 th week of onset of I syphilis It is yet safe to test blood for donation for syphilis because Possibility of spirochete transmission Exclude donors who are in high risk group for HIV and HBV Low costs of STS

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The tests are of two types Non-specific VDRL test Rapid Plasma Reagin test (RPR) Specific TPHA FTA-ABS TPI Enzyme immunoassay

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Protozoa – Malaria Can also be transmitted by Infected blood It manifests a week to several months after transmission Incubation periods of P.vivax and P.falciparum are the shortest – 1week-1month P.malariae has the longest incubation period – many months The parasite survives for at least one week at 4 O C in whole blood and red cell concentrates and in platelets at room temperature

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Screening tests for malaria Microscopic examination of thick and thin smear Difficult if parasite load is less than 100/uL of blood, but it is the best practical method Tests for Ab to MP IFA ELISA Immunodiagnostic testing by EIA Nucleic acid probe method including PCR

Other viruses:

Other viruses CMV Blood components containing WBCs are more likely to transmit CMV Plasma derived components are not likely to transmit CMV Can cause severe disease in a seronegative premature baby / LBW / immunosuppressed More than 90% of adults in underdevloped and about 50-80% of those in developed nations have Ab to CMV, routine screening is not advisable

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For seronegative / high risk patients , CMV negative or leuko-depleted components preferred Screening tests for CMV Latex agglutination Enzyme immunoassay Complement fixation

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HTLV I & II Retroviruses HTLV I – adult T-cell Leukemia/Lymphoma, neurological conditions. Incubation period is very long and 2-4% of seropositive persons develop the disease HTLV II – importance is not clear, may be associated with HCL

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Transmission Transfusion of cellular components After refrigerated storage for more than 10 days, the red cells are far less likely to undergo seroconversion Donor screening Considered in areas where it is endemic Countries in the western pacific and the Caribbean basin ELISA for HTLV-I Ab Western Blot, Immunoflourescent or Radioimmune precipitation techniques for confirmation PCR to differentiate between HTLV I & II

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Hepatitis A virus transmission by blood is very rare Hepatitis D / Delta virus is dependent on pre-existing / concomittant HBV infection for its propogation Hence routine testing of these is not recommended


Conclusion Transfusion reactions are mostly due to clerical errors and can range from benign reactions to life threatening emergencies Early detection, discontinuation of transfusion and instituting supportive care are key to management. Reporting of all reactions helps to improve standard practices and reduce future occurrences.

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