transfusion reaction- drgsp
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Transfusion
ReactionsDr Gaurav Pawar
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Transfusion reactions
Transfusion of blood and its product isordinarily safe and effective way ofcorrecting hematogical defects but adverse
effects do occur during or after transfusion
and they are commonly called Bloodtransfusion reactions.
Non-threatening to fatal
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Categories of
Transfusion Reactions Reaction -- Immune mediated
Acute
rapid onset within < 24 hrs
Delayed days to weeks
Reactions may involve antigen-antibodyinteractions
May involve infectious agents
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Hemolytic Transfusion
Reactions (Immune-
HTR) IHTRs occur very soon after the transfusion of immunological incompatible
whole blood or red cells to a recipient.Commonly red cells AB e.g anti A ,
anti B, Anti -kell, anti- Jka, Fyb cause IHTR. IHTR can destroy red cells by
both Intravascular and Extravascular hemolysis.
Causes- Clerical and Technical
Clerical Errors- Inadequate or incorrect labelling of blood bag
Confusion in the identity of patient at time of collection
Improper identification of patient blood sample
Wrong blood issued
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Technical Error-
Error in blood grouping and cross matching
Weak Ab not detected by routine test
Incompatibility not detected due to improper method
Destruction of recipients by donor Ab
Incorrect interpretation of test result
The interaction of AB-Ag on a red cell membrane can initiateneuroendocrine responses , complement activation,cytokine effect
,coagulation effects.
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Signs and Symptoms
Chills and Fever >1or 2 C , with or without chills
Acute renal failure
Early signs-
Anxiety
Pain at infusion site
Back/chest pain
Oozing of blood from intravenous line site
Oliguria and anuria
Shock
Haemoglobinuria, Haematuria
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Non immunological-HTR
Bacterial contamination reactions.
Circulatory overload.
Transfusion haemosiderosis.
Complications of massive transfusion.
Non immune hemolytic reaction
Disease transmission.
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Bacterial contamination
reaction Although uncommon,but this type of specific reaction can have a rapid onset
and high mortality in recipients.
The presence of bacteria in transfused blood may lead either to febrilereactions in the recipient ( due to pyrogens ) or serious manifestations of
septic or endotoxic shock.
Commonly caused by endotoxin produced by bacteria capable of growing incold temperatures such as Pseudomonas species, E. coli, Yersinia
enterocolitica.
Infection of stored blood is extremely rare.
Skin contaminants are not infrequently present in freshly donated blood butthese organisms ( predominantly staphylococci ) do not survive storage at 4 C although they will grow profusely in platelet concentrates stored at 20- 24 c
Healthy donor who are bacteremic at the time of donation. The majority aredue to Yersinia enterocolitica, which grows well in red cell components due to
its dependence on citrate and Iron.
Gram negative, endotoxin producing contaminants found in dirt, soil and
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Clinical manifestation Usually appear rapidly during transfusion or within about 30 minutes
after transfusion with dryness, flushing of skin.
Fever, Hypotension, Chills, Muscle pain, vomiting, Abdominal cramps,Bloody diarrhoea, Hemoglobinuria, Shock, Renal failure, DIC.
Management- Rapid recognition is essential Immediately stop the transfusion.
Therapy of shock, steroids, vassopressors, fluid support, respiratoryventilation and maintenance of renal function.
Broad spectrum IV antibiotics
The blood component unit and any associated fluids and transfusion
equipment should be sent immediatelyto blood bank for investigationie: gram stain and culture.
Blood C & S from the recepient.
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Circulatory overload
All patient will experience a temporary rise in blood volume and venouspressure following the transfusion of blood or plasma except for those who
are actively bleeding. However, young people with normal cardiovascularfunction will tolerate this changes provided it is not excessive.
Pregnant women, patient with severe anaemia, elderly with compromisedcardiovascular function will not tolerate the increase in plasma volume and
acute pulmonary edema may develop,Acute Renal Failure.
Frequently due to transfusion of a unit at too fast rate,multiple transfusion inshort duration.
Signs of cardiac failure raised JVP, basal crepitations in both lungs, drycough, breathlessness.
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Management-Stop the transfusion immediately.
Prop up the patient
Oxygen therapy
Intravenous diuretics should be used appropriately.
If more rapid volume reduction is needed, therapeutic phlebotomy can be used.
Prevention-Packed cell should be used instead of whole blood.
Packed cells should be given slowly over 4 hours. Patient at risk, rate should be
100 ml per hour or less are appropriate.
Diuretics should be given at the start of the transfusion and only one or two units ofconcentrated red cells should be transfused in any 24 hour period.
Blood transfusion should be given during the daytime, Overnight transfusionshould be avoided wherever possible.
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Complication of massive
transfusion Massive transfusion is defined as the replacement of total bloodvolume within a 24 hour period.
This will inevitably lead to-
1. Dilution of platelets.
Blood effectively has no functional platelets after 48 hours storage,after 8 to 10 units of blood transfusion, thrombocytopenia will usually
seen.
Bleeding due to a slightly low platelet is uncommon, therefore routineadministration of platelet after certain amount of blood transfusion is
unnecessary.
Regular monitoring of platelet count is more important.
Platelet transfusion may be recquired if platelet count
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2. Dilution of coagulation factors -Stored Whole blood < 14 days hasadequate levels atmost coagulation factors for haemostasis. If stored
blood of more than 14 days, or plasma reduced blood or red cells in
optimal additive solution is used, replacement of coagulation factors with
FFP is necessary
3.Hypothermia -( defined as core body temperature less than 35 c ) is
associated with large volumes of cold fluid transfusion. This may resultsin cardiac irregularities in particular VF. Therefore the use of blood
warmer is important.
4.Excess citrate can act on the patients plasma free ionized calcium andresults in hypocalcaemia ( transient )Citrate toxicity occur with extremely
rapid transfusion ( one unit every 5 minute ), in premature infant havingET with blood stored in citrate for longer than 5 days.
5.Hyperkalemia-Can be caused by intracellular loss of potassium fromRBC during storage or infusion of intracellular potassium depleted RBC
blood components such as washed RBC or frozen washed RBC .
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The most important consideration in
massive blood transfusion is to replaceblood loss quickly and adequately. Too little
blood , too late has more serious
consequences than massive blood
transfusion itself.
L b I i i
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Lab Investigations
Check identity of patient ,donor blood
Compare the color of plasma of patients pre and post-transfusion blood
specimen1) Pink red discoloration in post transfusion sample indicatesthe presence of free Hb due to destruction 11) Yellow to brown
discoloration after 4 to 10 hrs after transfusion indicates bilirubin.
Check the color of bag - 1) Greenish-Purple color and clots in bag maybe due to bacterial contamination 11) Change in color both in bag and
tubing of bag may be due to hemolysed blood
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Repeat ABO, RH(D),testing in pre and post transfusion both from bagand tubes
Perform DCT test on patients blood --- 1) If DCT is negative, then redcells not coated with IgG Ab and their is no incompatibility. 11) If Ab
coated donor incompatible cells are not immediately destroyed, theDCT on the post -reaction blood sample will be positive 111) If the
patients blood sample is drawn several hrs later then the Ab coated
donor cells destroyed ,so DCT will be negative.
Bacteriological smear and culture of donor
s blood is done to rule outbacterial contamination.
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Nonhemolytic
TransfusionReactions(FNHTR) It is often described as increase of 1c or more temperature,above the
patients base line during or within 24 hrs of transfusion without any
other medical explanation.
These are self limiting and are usually seen in multi-transfusedpatients or multiparous women who have an Ab directed against
donor leucocytes.Such Ag-Ab reaction can activate compliment and
cytokines production,so releasing endogenous pyrogens.
Symptoms and signs- Raises temperature >1C (fever)
Chills with fever Shaking Hypotension Cyanosis Tachycardia Leukopenia
Cough
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Management- Antipyretics are used to treat fever or aregiven as a preventive measure
Aspirin not used because of its effect on platelet function
Leukocyte reduced units should also be given
Antihistamines i.m e.g chlorpheniramine
Routine use of prophylactic antipyretics is not recommended becausethey mask symptoms of acute hemolysis.
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Allergic Transfusion
Reactions These are attributed to foreign protein (allergens ) in donor plasma that
react with IgE in the patient attach to mast cell and basophil.
A mild transfusion reaction causes: Urticarial Reaction: hives,itching,rarely laryngeal edema
Erythema: redness of the skin
Dyspnea: shortness of breath
The patient should be treated with an antihistamine to ease discomfort.
Transfusing saline wash RBC may help patients with frequent severeallergic reactions.
Corticosteroids are indicated only in severe repetitive cases.
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Anaphylactic ReactionsAnaphylactic and anaphylactoid reactions are due to immediate
hypersensitivity of immune system.
May begin after infusion of only a few ml of plasma or plasma containingblood producsts
Symptoms may involve one or several systems
Respiratory tract (cough ,bronchospasm, dyspnea)
Gastrointestinal tract nausea,vomiting, diarrhoea
Circulatory system-arrhythmia,hypotension,syncope
Skin-flushing ,urticaria
Good transfusion practice calls for close observation duringthe first quarter hour of infusion and less intensive afterwards
but nonetheless continuing surveillance is kept.
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Causes Anaphylactic and Anaphylactoid reactions are generally caused in patients who
are congenitally IgA deficient and have developed anti- IgA deficient Ab by
sensitization from tranfusion or pregnancy.
IgA is most common immune deficiency 1 in 700-800 persons .
Management- Stop transfusion .keep i.v line open with normal saline
Inject epinephrine (adrenaline) S.C /I.M usually about 0.5 ml 1:1000 sol
Inject antihistamines
If hypoxia develops give oxygen by catheter or nasal mask
For RBC transfusion this can be done by using saline washed or frozenthawed RBCs
If plasma needed it should be from a known IgA deficient donor.
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TRALI(Transfusion-
related acute lung injury) Also known as non-cardiogenic pulmonary edema, this unusual life
threatening complication is associated with altered permeability of the
pulmonary capillary bed from activation of compliment ,histaminemediated events ,PGs ,which leads to fluids accumulation, inadequate
oxygenation and reduced cardiac return.
Reaction of anti-leukocyte antibodies in donor or patient plasma thatreact with leukocyte in pulmonary microvasculature ,leading to
leukocyte emboli aggregating in the lung capillaries.
Other cause cytokines in the donor units
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Manifestations 1 in 5,000 transfusions
Symptoms occur within 2 hours and may end in 2-4 days if treated (Average =6 hrs)
Acute onset of Respiratory distress, dyspnea ,cyanosis, fever,chill,X-Ray willshow b/l pulmonary infiltrates but no left lung failure signs.
Potentially fatal hypoxia may occur and persist for 24-28 hrs
Treatment The cornerstone of therapy is effective supportive care forrespiratory insufficiency .
Oxygen therapy and ventilatory assistance i.e intubation
II.V steroids are used imparically but no improvement seen till now
If TRALI caused by patients anti-leukocytes Ab the leukocyte-poor componentsshould be used.
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TRALI case
Before After
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Delayed Hemolytic
Transfusion Reactions DHTRs occur at least 24 hrs after transfusion
Mediated by IgG antibodies,the initial level of AB in the recipient is low but thetransfusion provokes an anamnestic response.
Patient previously exposed to RBC antigen and has low antibody titer until exposed
again,so resulting in haemolysis
Rh, Kidd, Duffy, and Kell ,anti-Fy, anti Jk
Clinical Features- Maximum rate of destruction is 4-13 days after transfusion.
Jaundice occurs 5-7 days afterwards
Haemoglobinuria is not uncommon and is seen with antibodies ofdifferent specificities
DHTR s may result occasionally be followed by renal failure
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Lab features
A fall in haemoglobin not attributed to any other cause
Appearance of new Alloantibody
Sphrerocytes in peripheral blood smear may be the only indicator
Positive DAT test ,becomes positive after a few days after transfusion andremains so until incompatible cells been eliminated
The Ab responsible for this reaction can be detected by preparing aneluate from the patients red cells
The Ab is detected 4-7 days after transfusion and peaks after 10-15 days .
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Graft-versus-Host Disease
(Transfusion Related) Rare but fatal condition that has a 90% mortality rate
Symptoms appear after about 12 days
May be caused by donor lymphocytes transfused into animmunocompromised recipient, patients on chemotherapy ,irradiation
Pancytopenia occurs as a result of the immunologic response
Pathogenesis of GVHD ,the donor lymphocytes engraft and multiply in therecipients .The engrafted cells react with the host tissues to cause the clinical
manifestations ,the donor lymphocytes are not destroyed as the host isimmunocompromised.
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Clinical features- fever , diffuse erythematous rash, diarrhoea,bone marrow suppression, infection
Prevention can be done by use of irradiated blood and bloodcomponents .A radiation dose of 1500-5000 rad for 10 min
renders 85-95% of lymphocytes incapable of replication.
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Post transfusion Purpura
About 5-10 days after being transfused with platelets, the platelet countdrops
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Alloimmunization-Blood transfusion exposes a patient toseveral foreign antigens.If the recipient does not possess
these Ag ,antibodies will be formed against them.
Immunomodulation- Transfusion of blood is associated withchanges in immune function. The effect is apparent with
multitranfused patients.There is decreased lymphocyte
responsiveness to phytohaemagglutinatinin and in mixed
lymphocyte culture with pooled mormal lymphocytes as
stimulator cells.
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Disease transmission
Hepatitis
Syphilis
Malaria
Cytomegalovirus
Human immunodeficiency virus
Human T cell leukaemia viruses.
Donor selection criteria and subsequent screening of all donations are
designed to prevent disease transmission, but these do not completelyeliminate the hazards.
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Hepatitis
Hepatitis A is rarely transmitted by transfusion. Any donor who hasbeen in close contact with Hepatitis A patient or develops hepatitis A isdeffered for 12 months.
Hepatitis Bis a frequent sequel to blood transfusion. Currently allblood donations are tested for HBsAg by very sensitive third generationtechniques ( eg; ELISA ), able to detect at least 0.5 iu of HBsAg per ml ofserum.
EIA method is used with 99.9 % sensitivity.
HBsAg positive subjects are permanently excluded from donations.
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Syphilis
The organism is more likely to be transmitted in platelet concentrate dueto their room temperature storage and short shelf life.
Treponema pallidum does not survive well at 4 c and red cellpreparation are likely to be non infective after 4 days refrigeration.Passive transmission of the antibody to the recepient may causediagnostic confusion.
Any donations with positive result is discarded, any subjects withpositive tests are permanently deferred, even after effective therapy.
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Malaria
Malarial parasites remain viable in blood stored at 4 C and easily transmitted byblood transfusion.
In some endemic areas, all recipients are treated with antimalarial drugs.
Donors who come from endemic area or have had an attack of malaria can beaccepted, their plasma can be used for fractionation but red cells must bediscarded.
BFMP should be tested for certain group of donors ie : army, donors from
endemic area.
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Cytomegalovirus
Post transfusion CMV infection is not uncommon.
The infection is characterised by fever spleenomegaly, and atypical lymphoidcells in the peripheral blood.
Due to its benign course, screening for past infection among donors are notnecessary.
However, there are patient at risk of developing fatal pneumonitis or disseminatedCMV infection : prem baby < 1500g, BM or and other organ transplant recipient,pregnant women ( risk to fetus ).
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For them, anti
CMV free blood & components should be
provided.
In UK, incidence of CMV antibodies in adult population is
50 to 60 %.
As an alternative, since CMV is cell associated,leukodepleted blood may be used.
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Human
immunodeficiency virus
HIV can be transmitted both in cellular and plasma components.
The majority of recipient of blood or blood products who have beeninfected in the past were transfused before 1985 with unheated, nonpasteurized pooled plasma products, Factor VIII and IX.
HIV is heat labile, therefore prolonged heat treatment of Factor VIII forheomophiliacs is effective.
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Human
immunodeficiency virus Routine screening of all donated blood started in October 1985 in UK.
This in combination with donor education, and self deferral has reducedthe risk of HIV transmission through contaminated blood. There were 2
documented cases in the UK since screening program introduced.
With screening programe, HIV transmission still occur through donationsgiven in the window period of infectivity.
With current antibody screening technique, the estimated window periodis about 3 weeks.
PCR for HIV RNA is able to reduce the window period to approximately1 week.
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Human T- cell leukaemia
viruses. HTLV 1 and II are related retroviruses.
HTLV 1 is endemic in the caribbean, parts of Africa and in Japan, 3 6% of the population are seropositive.
HTLV 1 is associated with tropical spastic paraparesis and adult T cell leukaemia.
Importance of HTLV II is not clear.
Both HTLV 1 and II are cell associated and not transmitted in plasma.
Currently available test include ELISA and gelatin particle assay, butconfirmation of positive result are difficult due to cross reactivity withother retroviruses.
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THE END
Thank you for your attention.