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%
