transfusion reaction- drgsp

7/31/2019 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.

transfusion reaction- drgsp

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