transfusion reactions
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Hazards of Transfusion
Muhammad Asif Zeb
Lecturer-Hematology
Khyber medical university
Peshawar
Hazards to the Donor
Hazards to Recipient / Patient
Transfusion risks and adverse reactions
Many of the signs and symptoms of transfusion reactions are Similar
All reactions should be taken seriously
The most commonly encountered reactions are
– Allergic – not life-threatening
– Febrile – respond to treatment
Reactions that cause the most concern are
– Transfusion related acute lung injury (TRALI),
– ABO mismatch,
– TA-GvHD
– Sepsis
Introduction
Introduction
ABO incompatible blood can lead to serious consequences.
Precautions should be taken during:
– Collection of specimen of blood
– Cross matching procedures
– At the time of issue
– At the time infusion of the crossmatched unit of blood
ensure that no error in patient identification is made.
Haemolytic reactions
When transfused red cells are destroyed in the recipient, this is
classified as a haemolytic transfusion reaction.
These reactions are either acute or delayed,
& cell destruction is either intra- or extravascular.
Acute reactions
Reactions that occur shortly after the start of the transfusion are
termed acute.
Although there are many reasons why a recipient could react
immediately – it may be an indication of ABO incompatibility.
Haemolytic reactions
Delayed reactions
Occur due to red cell incompatibility - becomes apparent > 24
hours after transfusion.
Recipient red cell antibodies – too weak for detection during crossmatching or antibody screening
Immune response occurs in the recipient – transfused cells are removed from the circulation.
No reaction occurs immediately after transfusion – reaction is suspected when the Hb fails to increase after transfusion.
Kidd antibodies are sometimes implicated in delayed reactions .
Extravascular haemolytic reactions
Extravascular reactions – antibodies - that do not activate complement – Rh, Duffy or Kell etc.
Incompatible - sensitized red cells – removed from by RE systems of liver or spleen.
Hyperbilirubinaemia is seen
The severity of a haemolytic reaction depends
– Immunoglobulin class of antibody
– Specificity of antibody
– Thermal range of antibody
– Activation of complement
– Titre and strength or potency of antibody responsible and
– Volume of red cells (with the corresponding antigen)
transfused.
Major incompatibility
Serious haemolytic transfusion reactions may occur when a patient receives blood of the incorrect ABO group, usually as a result of misidentification.
patient Such errors mostly occur
– In emergency situations when personnel are under extreme pressure
– During quiet times when there is lack of concentration on the job at hand.
The reactions usually involve antibodies in the recipient that react with antigens on the incoming red cells.
Minor incompatibilities
An adverse reaction seen
– Plasma high titre or haemolysing ABO antibodies – transfused
into a compatible but ABO non-identical group
– Example : donor group O plasma with high titre or haemolysing
anti- A – transfused to group A recipient.
– Donor plasma contains strong, irregular antibodies of
other specificities – in recipient with corresponding
antigen
These adverse reactions are termed minor
incompatibilities – occur rarely
Haemolytic transfusion reaction
Signs and symptoms
– Urticaria/rash
– Pruritus (itching)
– Headache
– Restlessness
– Unexplained bleeding
– Lower back and joint pain
– Tachycardia and chest pain
– Sudden change in blood pressure
CLASSIFICATION
Transfusion reaction
acute delayed
Immunologic Nonimmunologic Immunologic Nonimmunologic
Haemolytic transfusion reaction
Indication when recipient is anaesthetize
Haemoglobinuria
Oliguria and / or anuria
Shock.
ABO hemolytic transfusion reaction
ABO mismatch blood administration
Activation of complement system lead to lysis of RBC,s
C3a, C5a are anaphylotoxin and cause activation and
attraction of Monocytes and neutrophils, endothelial cells,
macrophages, platelets.
Activation leads to release of interleukin and cytokines, e.g
IL 6,8,1, TNFα,
Interleukin 8 (IL-8), which activates neutrophils, and
tumor necrosis factor alpha (TNFα), which activates the
coagulation cascade.
C3a and C5a also activates mast cells and basophiles releasing histamine and serotinin leading to vasodilatation, smooth muscles constriction espicialy bronchial and GIT
Hypotension may be due to vasodilation of blood vessels.
DIC
may lead to bleeding from different site
Intrinsic pathway of coagulation activation due to Ag Ab comlex
Extrinsic due to Activated complement, as
well as TNFα and IL-1 which cause
increase expression of Tissue factor.
Shock may be a component of DIC
Renal failure
Due to free hb
Thrombus formation
Ag Ab complexes
vasoconstraction
Nonimmune-Mediated Hemolysis Transfusion-associated hemolysis can also occur from several
nonimmune-mediated causes.
Before issue, improper shipping or storage temperatures as
well as incomplete deglycerolization of frozen red cells can
lead to hemolysis.
At the time of transfusion, using a needle with an
inappropriately small bore size or employing a rapid pressure
infuser can cause mechanical hemolysis, which may be seen
with the use of roller pumps as well.
Improper use of blood warmers or the use of microwave ovens
and hot water baths can cause temperature-related hemolysis.
Febrile Nonhemolytic
Transfusion Reactions
Studies found that as few as 0.25 × 109 leukocytes could produce a
temperature elevation in the recipient.
FNHTRs may also be the result of accumulated cytokines in a cellular
blood component.
This mechanism may be particularly relevant in reactions seen after the
transfusion of platelets.
Some FNHTRs are attributable to recipient antibodies, particularly HLA
anti- bodies, that react with antigens on transfused lymphocytes,
granulocytes, or platelets.
Cytokine release in the recipient in response to these antigen-antibody
reactions may con- tribute to the severity of the reaction
Pathogenesis Fibrile non hemolytic transfusion reaction
• ?? Previous Transfusion &/Or Preganancies
• Temprature↑ α No: of Leucocytes Transfused
• ?Reacting - Antibodies to HLA reacting with donor leucocytes
Recipient Abs bind to Donor leucocyte Ags
↓
Fix Complements
↓
Activate recipients Monocytes, Lymphocytes & Endothelial cells
↓
secrete Pyrogens Mainly IL-1
Platelet Transfusion
?? Without prior sensitization
• Due to presence of Pyrogenic Cytokines
IL-1β, IL-6 & TNF-α released from leucocytes during the 5
day platelets storage
Theory supported by
a. Very high levels of Cytokines during storage
b. Reaction associated with the plasma portion
c. Not prevented by bedside filteration
d. No ↑ of Cytokines if pre-storage leucocyte filtered
Signs and symptoms
Chills or rigors and fever are noted after
transfusion.
Allergic Reactions
Most allergic transfusion reactions are
mild, but the spectrum can range from a
simple allergic reaction (urticaria) to
anaphylaxis.
Symptoms generally occur within
seconds or minutes of the start of the
transfusion.
Pathophysiology
Allergic reactions are hypersensitivity reactions to allergens in the component and are less commonly caused by antibodies from an allergic donor.
Preformed IgE antibody in the patient or recipient interacts with the allergen, usually a plasma protein in the component.
Mast cells are activated by the binding of allergen to the IgE bound to the mast cells (type I hypersensitivity).
Activation results in degranulation, with the release of preformed histamine, chemotactic factors, proteases, and proteoglycans.
Secondary mediators, including cytokines and lipid mediators such as arachadonic acid metabolites, leukotrienes, and prostaglandin D2, as well as platelet-activating factor, are generated and released in response to mast cell activation
Signs and symptoms
Simple allergic reactions – cause a diffuse rash (urticaria) &
itchy, swollen red areas on the skin
Immune complexes of antigen–antibody in recipient or the donor - stimulate tissue mast cells to release histamine
it results in
– Vasodilatation
– Raised red marks on the skin
occur during the transfusion or within an hour
Oedema (swelling) of the face, lips or mouth - occasionally
Difficulty in breathing occur sometimes
Transfusion associated acute lung injury
TRALI is caused by anti-HLA or anti-granulocyte antibodies in donor
plasma.
Antibodies formed - sensitization of donors
– With a history of pregnancy - multiparous female
– Previous blood transfusion.
Plasma containing these antibodies may activate complement in vivo
WhenTransfused,cause lung injury in the recipient.
When large volumes of components containing plasma are transfused
-TRALI is more likely
Small volumes of plasma may also cause a reaction.
Transfusion associated acute lung injury
Signs and symptoms
Dyspnoea
Hypotension
Fever and rigors soon after the onset of reaction
Pulmonary oedema
Hypovolaemia
Hypotension
This is quickly followed by severe hypoxia – with frothy fluid in the trachea
Sepsis – bacterial contamination of
products transfused
Blood is an ideal medium for growth of harmful bacteria.
It is important to:
– Clean the venepuncture site thoroughly prior to donation
– Maintain the cold chain for storage & transportation of
blood components
Platelet concentrate is at the greatest risk of bacterial
contamination – stored at the higher temperature of
22°C ± 2°C.
Reasons of Bacterial Contamination of blood
donation
• Introduction of micro-organisms – time of donation
– Inadequately cleaned venepuncture site
– Contamination of needle
• Introduction of micro-organisms – component preparation and storage
– Faulty equipment or blood bags
– Introduction of air into the container of blood
• Storage and transportation of blood – at high temperatures
• Bacteraemia in an apparently healthy donor
– Endotoxin-producing Gram-negative bacilli – Yersinia
enterocolitica - present as subclinical infection in donor
– Endotoxins may lead to extremely severe reactions & death of
recipient.
Bacterial contamination of a unit of stored blood may be obvious, with a dark brown or purple appearance.
Heavily infected blood may look normal.
Cloudiness may be a sign of contamination in a unit of platelet concentrate.
Some transfusion services have the facility to screen all platelet concentrates and discard contaminated PC
Signs and symptoms
When infected blood is transfused, symptoms usually appear
within 30 minutes.
These are
– Chills
– Headache
– Vomiting
– Muscular pain
– Diarrhoea
– High fever
– Hypotension (low blood pressure)
– Shock.
There is marked erythema (redness) of the skin – in contrast to the pale, cold skin of haematogenic shock (through blood loss).
Delayed Hemolytic Transfusion Reaction (DHTR)
Mechanism
– Antibodies that exist in low titers prior to the transfusion
– Typically to the Kidd, Duffy or Kell system
– Upon re-exposure, titer increases from memory B-cells
– Resulting Extra vascular red cell distruction
– Usually occur 5-10 days after Tx
Delayed HTRs are defined as fever and other symptoms / signs of haemolysis more than 24 hours after transfusion; confirmed by one or more of: a fall in Hb or failure of increment, rise in bilirubin, positive DAT and positive cross-match not detectable pre-transfusion.
Pathophysiology A patient may make an antibody to a red cell antigen he or
she lacks after transfusion, transplantation, or, as seen in hemolytic dis- ease of the fetus and newborn, after pregnancy.
Red cell antibodies may cause a delayed transfusion reaction if the patient subsequently receives a unit of blood that expresses the corresponding red cell antigen.
Primary alloimmunization may occur any- where from days to months after transfusion of antigen-positive red cells depending on the immunogenicity and dose of the antigen.
D-negative blood is usually transfused to D-negative patients, so
although anti-D is capable of causing DHTRs, the frequency
attributable to anti-D is relatively low.
Newly formed alloantibodies are routinely detected during
pretransfusion screening.
Recently transfused or pregnant patients must have samples
drawn for compatibility testing within 3 days of the scheduled
transfusion to ensure identification of any potential new
alloantibodies
Transfusion-Associated Graft-vs-Host
Disease Presentation
The clinical manifestations of transfusion- associated GVHD
(TA-GVHD) typically begin 8 to 10 days after transfusion.
Symptoms can occur as early as 3 days and as late as 30 days
after transfusion.
Signs and symptoms include a maculopapular rash, fever,
enterocolitis with watery diarrhea, elevated liver function tests,
and pancytopenia.
The rash begins on the trunk and progresses to involve the
extremities. In severe cases, bullae may develop
Pathophysiology
Commonly in severely immunocompromised
patient
Donor lymphocytes engrafted in recipient &
multiply
Engrafted lymphocytes react with host tissues
AIDS patients – HIV infects even donor
lymphocytes
Fresh blood – lymphocytes are more active and
hence chance of engraftment is more
Implicated blood products Reported after transfusion of non irradiated
• whole blood
• packed red cells
• platelets
• granulocytes
• fresh, non‐frozen plasma
No report of TAGvHD after
• frozen, deglycerolized red cells,
• fresh frozen plasma,
• cryoprecipitate.
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