Blood products Flashcards
List potential adverse reactions to blood transfusion
Class 1 - universal
- Overload
- Hyperkalaemia
- Iron overload
- Hypocalcaemia - citrate load
- Diltuional coagulopathy
- Hypothermia
Class 2 - Immunological
- Acute - haemolytic, non haemolytic, TRALI
- Delayed - haemolytic, non haemolytic, GVHD
Class 3 - Infection
- Viral
- Bacterial
What is the risk of TACO
1/100
What are the 3 electrolytes that are often deranged by transfusion
◦ Citrate overload - due to citrate use in packed red blood cells to avoid clotting
◦ Hyperkalaemia - due to haemolysis associated with storage lesion, rises with aging blood
◦ Iron overload - chronic transfusion occurrence
massive transfusion non immunological problems can include
TACO
* Trasnfusion associated electrolyte disturbance
◦ Citrate overload - due to citrate use in packed red blood cells to avoid clotting
◦ Hyperkalaemia - due to haemolysis associated with storage lesion, rises with aging blood
◦ Iron overload - chronic transfusion occurrence
* Transfusion associated hypothermia - blood prodocts apart from platelets are cooled
* Transfusion associated dilutional coagulopathy
TRALI mechanism
- Transfusion related acute lung injury - acute respiratory, non cardiac pulmonary oedema - pathogenesis uncertain but donor plasma antibodies reacting with patient leukocytes producing neutrophilic activation in lung micro circulation
Transfusin assocaited non haemolytic reaction occur how often? Why?
- Transfusion associated mild allergic/febrile reactions
◦ 1:100 - 1:1000 - febrile non haemolytic
◦ Febrile non haemolytic due to donor white cells reacting with alloantibodies induced by previous transfsion or pregnancy
Why do haemolytic transfusion reaciotns occur
immediate and delayed - causing urticaria, chest pain/dyspnoea, rigors, shock, bleeding/DIC and renal shutdown due to massive haemolysis
◦ massive intravascular haemolysis associated with complement activating IgM or IgG antibodies e.g. ABO or rhesus reaction generally but may occur after multiple transfusions in other antibodies. Coating of red cells with IgG e.g. rhesus generally less severe
Anaphylaxis in transfusion usually due to
IgA deficiency
GVHD in transfusion when
- Transfusion associated graft versus host disease - deposition of donor lymphocytes in recipients skin, liver or GIT leading to rash, heptatitis or diarrheoa
What infectionissues are there with transfusion
- Infection - due to host disease transferance, infection of stored blood or acquired infection through methods of blood administration such as breach of aseptic technique
◦ Bacterial sepsis - PLT/RBC - 3:1000
◦ Hepatitis B/C
◦ CMV - newborns, transplants and cardiac patients can be adversely effected
◦ HIV
◦ HTLV1
◦ Malaria
◦ Toxoplasmosis
◦ Sphillis
◦ CJD
How doe we prevent problems with blood transfusion (non immunological)
- Trasnfusion associated electrolyte disturbance
◦ Citrate overload - ionised calcium monitoring in massive transfusion
◦ Hyperkalaemia - electrolyte monitoring in massive transfusion, ECG monitoring during trasnfusion
◦ Iron overload - chronic transfusion occurrence, iron chelations can be used for those requiring many transfusions - Transfusion associated hypothermia
◦ Warming of blood products especially in the use of multiple products and trauma - Transfusion associated dilutional coagulopathy
◦ 1:1:1 transfusion when in massive transfusion
Don’t give them too much, examine respiratory status
How is TRALI prevented
donor plasma antibodies reacting with patient leukocytes producing neutrophilic activation in lung micro circulation
◦ Male only plasma to reduce the risk of donor serum containing antibodies (e.g. generated in pregnancy) in plasma products
◦ Those who have a history of transfusion generally do not donate plasma or platelets; and platelets from nulligravida or male donors
How do we prevent transfusion non haemolytic febrile reactions
◦ Pretreatment of susceptible patients, leukocyte depletion of blood products as a standard practice and pre-treatment with antipyretic in those susceptible to febrile non haemolytic reactions
How do we prevent haemolytic reactions from occuring?
◦ Questionnaires to identify at risk transfusions - multiple transfusions, previous pregnancy
◦ ABO, Rhesus typing and major cross match prior to non emergency transfusion
◦ Using O negative blood (universal donor) as emergency blood transfusion
◦ Rigorous clerical checks of patient identification prior to transfusion with multiple witnesses
How do you prevent GVHD
◦ Irradiation of blood prior to transfusion for those who are high risk, universal leucodepletion has made this less common
How does citrate toxicity present?
◦ Presenting as muscle tremors, bradycardia, ST prolongation and QT prolongation
What factors is stored blood in particular low in?
- Transfusion associated dilutional coagulopathy
◦ Stored blood has low levels of factor VIII, V and XI dilutional coagulopathy occurs
◦ Platelets are reduced in number and dysfunctional
What re ABO blood groups
Blood group si defined by the antigens found on the surface of RBC
* ABO blood groups - Limited specific variation in a group of oligosaccharides antigens present on the surface of red blood cells produce highly antigenic naturally occurring antibodies to variations not present in host blood.
* This has led to defining these incompatible oligosaccharide variations into ‘blood groups’ referred to as A, B and O which with Rhesus groups are the most important antigens in haemolytic transfusion reactions.
Describe what A and B antigens actually are?
◦ The A and B genes control synthesis of enzymes required for the addition of specific carbohydrate residues to the basic oligosaccharide - the H antigen - (precursor with L fucose as the terminal sugar)
‣ A - N-acetyl galactoseamine added to the terminal group of the h antigen
‣ B - D-galactose is added to the H antigen
What does group O mena
Lack both A and B antigens, still have H antigens
How common is AB
3%
How common is A blood type
45%
How common is B blodo type
9%
How common is O blood type
43%
How common is rhesus +
85%
How common is rhesus negative
15%
Where do you find the A and B antigens
On WCC and many other blood cells, 80% of body fluids will have the antigen
When do natural antibodies to A and B develop in O type blood
First few months of life
What is blood grouping? What 2 stages does it contain?
Performed on recipient and donor cells - both must agree
Forward grouping - testing patients red cells against antisera containing IgM anti A and Anti B and anti AB
Reverse grouping si testing the patient plasma against red cells of known groups
Red cells are also tested using antiserum containing IgG sufficiently potent to agglutinate RH D positive cells in saline
How is Rhesus status tested
Red cells are also tested using antiserum containing IgG sufficiently potent to agglutinate RH D positive cells in saline
How is blood compatability tested?
electronic if no issues with group or screen
Saline agglutination or Major cross match - demonstrate compatability of patients serum and donor red cells in 10 minute centriguge at 37 degrees
What is actually routinely tested when doing a group and hold
ABO and RhD typing
Antibody screen for IgG non ABO red cell antigens doing a indirect antiglobulin test
Red cell cross match
What is an antibody screen for IgG non-ABO red cell antigens
Patients plasma incubated with donor red cells with known anitgen profile - only necessary if clinical suspicion of Anti IgG antibodies
What is a minor cross match
Test patients red cells against donated blood antisera - rarely done
What type fo antibodies are Anti A and Anti B
◦ Anti A and Anti B antibodies are usually IgM and reactive at 37 degrees but more potent at 4 degrees
Who can you give a group A patient blood from? Who can you give it to?
Can give it to A and AB
Can received from A and O
Who can you receive platelets from
Same blood type
Type O
If you have neither of these then from type A rather than type B
If you are going to receive FFP from someone what general charactersitics of donation do you want?
Same type as your blood type
If not then AB if you are type A or B; A if you are blood group AB; or anything if O
Why is there a Hb 70 theshold
Hb 70 with normal cardiac output gets you to a DO2 of 2x VO2 leaving a minimal buffer range (at baseline you have a 4x requirement reserve)
What is washing in the context of donation preparation of product? Who would you do it in?
Removes plasma protein, electrolytes and antibodies
Reduces the shelf life
More important for IgA defiicency, multitransfused patients commonly having minor reactions, paroxysmal nocturanl haemoglobinuria, severe autoimmune haemolytic anaemia
Leucodepletion is done how> Why is it done? Who is it important for?
Via special filters at time of collection or within 48 houyrs
Reduces risk of febrile non haemolytic reactions, immunomodulatory effects or GVHD
Reduces platelet refracoriness, reduced CMV and CJD
reduces storage lsion
Irradation of product is done why?
Prevents transfusion GVHD by preventing proliferation of donor T cells in recipient bone marrow
What are non ABO antibodies of concern
Non ABO antibodies that can cause intravascular haemolysis - 1% of all patients, 5-20% of large transfusion patients
* Rh
* Kell
* Kidd
* Duffy
* Non ABO - other
What is an antiglobulin or Combs test looking for?
Detecting of incomplete IgG and IgM antibodies
What is the principle of a Combs test
‣ Anti-human globulin is produced by rabbits and sheep after injection of human globulin, complement or specific immunoglobulin (IgM or IgG)
‣ When antihuman globulin AHG is added to RBC coated with immunoglobulin,or complement agglutination of red cells indicates a positive test - poly specific and mono specific immunoglobulins can be used to help distinguish the cause of the autoimmune haemolytic anaemia
How does a direct antiglobulin test work
detection of antibody or complement on the RBC that have been sensitised in the patients body - ADH is added to washed RBC and agglutination = positive test
* Detects red cells coated in antibodies or complement - as normally red cells are not coated in this
* By adding a Coombs reagant any red cells with antibodies will bind to the reagant, and reagant can bind to multiple antibodies causing clumpting
* Positive DAT can occur in 1-5% of healthy people with no haemolysis - icnreases with age. Penicillin concurrent therapy can cause DAT positive in 3% or IVIG
* Only performed on blood donation if unusual ABO testing or crossmatch issues
* POsitive in haemolytic disease of newborn (Rh), autoimmune haemolytic anaemia, drug induced immune haemolysis and haemolytic transfusion reactions
What is an indirect antiglobulin test
‣ Indirect antiglobulin test - tests for IgG antibodies in recipient serum directed against donor RBC antigens - 2 stage test used to detect antibodies that have coated the red cells during the test (in vitro)
* Test red cells incubated at 37 degrees with serum
* Second stage red cells washed with saline to remove globulins loosely attached
* AHG (anti human globulin) is then added —> agglutination means original serum contained an antibody that coated the red cells
* Purpose is to find atypical IgG antibodies in the patients serum against donor red cells e.g. atypical blood group antibodies, Rh antibodies in pregnant women, serum antibodies in autoimmune haemolytic anaemia
What type of antibodies are those against ABO groups?
IgM
What is the breakdown of frequency for ABO blood types
O = 46%
A = 42%
B = 9%
AB = 3%
What flaw is there to blood group testing infants?
Anti D onl develops after exposure
What does the screen part of a group and screen refer to?
Antibody screen for minor non ABO antigens e.g. Duffy, Kell
Indirect antiglobulin test
Patients plasma IgG is added to group O RBCs and they are incubated at 37 degrees following which anti human globulin is added. Agglutination indicates a positive test and the presence of antibodies in patient serum
98% sensitive
2-3% may have an antoibody NOT on the screen cells
What does a crossmatch mean? When is a fast cross match done?
Recipient/patient PLASMA and donor red cells
Only for RBC
If the antibody scren is negative then crossmatch is fast
Immediate spin of cells for 5 minutes with donor red cells and platient plasma to check ABO compatable
Recipient ABO is double checked adn computer validated to detect ABO incompatibility (electronic cross match)
What is a slow or full crossmatch?
When the patient has a positive antibody
Antibody needs to be identified
Antigen negative unit is found by label or by phenotyping
A more prolonged check of patient plasma and donor RBC are incubated at 37 degrees wtih Anti IgG to check for agglutination –> tales 45 minutes not accounting for antibody identification and antigen negative unit acquisition
