Blood transfusion Flashcards
what are examples of other blood group antigens other than ABO
o Other blood group antigens – Kell (K), M, N, S, Duffy (Fy), Kidd (Jk)
Duffy and Kidd are known for causing delayed transfusion reactions
The level of anti-Duffy and anti-Kidd decline with age
Electronic crossmatching
o Compatibility is determined by an IT system without physical testing of donor cells against plasma
o This is a quick process, requiring fewer staff which allows better stock management
serological crossmatch
o Full Crossmatch (uses IAT): checks blood against the DONOR’s blood specifically
Patient’s plasma is incubated with donor red cells at 37 degrees for 30-40 mins
Detects antibody-antigen reaction that destroys the RBCs leading to extravascular haemolysis
Add antiglobulin reagent to cause cross-linking
IgG antibodies bind to RBCs but do not crosslinking (why the AHG added in an IAT test)
Immediate spin
Incubate patient’s plasma and donor red cells for 5 minutes only and spin
Will only detect ABO incompatibility
IgM anti-A and/or anti-B bind to RBCs, fix complement and lyse the cell
how does group and save work
• GROUP: Testing before transfusion – both of the below are done and included in a “Group and Screen”:
o (1) Use known anti-A, anti-B and anti-D reagents against the patient’s RBCs
o (2) Reverse group: known A and B groups red blood cells are mixed with the patient’s plasma (IgM antibodies)
This group acts as an internal control – if it does not match, this is an anomalous result
New-borns often have a weak reverse group as their ABs have not developed fully yet
o A positive result causes agglutination at the top
o A negative result will mean that the red cells stay suspended at the bottom of the vial
• SCREEN: Antibody screen:
o NOTE: it is impossible to test for all other RBC antigens because there are hundreds of them
o 1-3% of patients have developed antibodies to >1 RBC antigens (i.e. due to previous transfusion or pregnancy)
o Immune antibodies are IgG (these can cause a DELAYED transfusion reaction; extravascular haemolysis)
As opposed to naturally occurring IgM antibodies (that cause an IMMEDIATE intravascular haemolysis)
o A 10-cell panel is used to identify RBC antibodies
o Antibody screen on patient’s plasma – avoid a delayed transfusion reaction with IgG antibodies…
(1) use 2 or 3 reagent RBCs containing all important RBC antigens between them
(2) incubate patient’s plasma and screening cells using the Indirect Antiglobulin Technique (IAT)
• (a) Patient serum containing specific antibody added to reagent RBCs
• (b) Add Anti-Human Globulin (AHG) to promote agglutination
• (c) If +ve, reaction creates bridges between RBCs coated in IgG antibodies visible clumps
why do you need to be careful with platelets
• The reason platelets need to be given more quickly is because they are stored at room temperature and so bacteria can contaminate it quite quickly if patient develops a temperature stop the platelets and take blood cultures
o The platelets should then be sent back to the lab for microbiological testing
MSBOS
Based on negotiation between surgeons and transfusion lab about predictable loss for planned surgery
Some operations rarely need blood whereas others will always need blood (e.g. AAA repair)
For elective surgery, the patient should be group and screened before the operation
If antibodies are not present, a crossmatch is NOT needed but the sample should be saved in the fridge
If unexpected need for blood provided <10 mins (by electronic issue as no antibodies are present)
If antibodies are present, ALWAYS CROSSMATCH
CMV negative blood
Required for intra-uterine and neonatal transfusions
Also used for elective transfusion in pregnant women
irradiated blood
Required for highly immunosuppressed patients
As patients cannot destroy incoming donor lymphocytes
Presence of these lymphocytes fatal transfusion-associated graft-versus-host disease (TA-GvHD)
washed blood
o Washed (i.e. for IgA-deficient patients) RBCs/platelets given to patients who had severe allergic reactions to some donors' plasma proteins This takes 4 hours to happen so needs to be pre-planned
When is platelet transfusion contraindicated
o Heparin-induced thrombocytopaenia and thrombosis
o Thrombotic thrombocytopenic purpura (TTP)
acute reactions to transfusion
o Acute haemolytic (ABO incompatible)
o Allergic/anaphylaxis
o Infection (bacterial)
o Febrile non-haemolytic
o Respiratory
Transfusion associated circulatory overload (TACO)
• Often pre-existing cardiac/respiratory problems
• 1 in 100,000 mortality risk (very preventable)
• MOST COMMON ACUTE REACTION
Acute lung injury (TRALI)
delayed reactions to transfusion
o Delayed haemolytic transfusion reaction (antibodies) – Duffy and Kidd o Infection (viral, malaria, vCJD) o TA-GvHD (week or 2 after transfusion) o Post transfusion purpura o Iron overload
Febrile non haemolytic transfusion reactions
- Occurs during/soon after transfusion (blood or platelets)
- May cause a rise in temperature by around 1 degree, chills and rigors
- Common before blood was leucodepleted (now rarer)
- Tx: transfusion stopped or slowed and may need to be treated with paracetamol
- Caused by the release of cytokines from white cells during storage
allergic transfusion reactions `
- Common, especially with plasma (proteins in plasma)
- Causes a mild urticarial or itchy rash sometimes with a wheeze – caused by allergy to donor plasma proteins
- Can occur during or after (even after patient has left) transfusion transfusion usually stopped or slowed
- Tx: IV antihistamines
- Recipients have a history of atopy
ABO incompatibility
• Symptoms and signs of acute intravascular haemolysis (IgM-mediated):
o General: restless, chest/loin pain, fever, vomiting, flushing, collapse, haemoglobinuria (later)
o Monitoring: Low BP, High HR, High Temperature
• Causes:
o Failure of bedside check
o Wrongly labelled blood sample
o Laboratory error
• In cases where an acute haemolytic reaction may be taking place take samples for:
o FBC Biochemistry Coagulation
o Repeat X-match Direct antiglobulin test (DAT)
bacterial contamination
• Presents similarly to ABO mismatch
o General: restless, fever, vomiting, flushing, collapse
o Monitoring: Low BP, High HR, High Temperature
• Bacterial growth can cause endotoxin production which causes immediate collapse
• The bacteria could have come from the donor (e.g. from low grade GI, dental or skin infection)
• The bacteria could have been introduced during processing (environmental or skin)
• Order of likelihood of contamination:
o Platelets (stored at room temperature) > RBCs > FFP
anaphylaxis
• Severe, life-threatening reaction soon after the start of transfusion
o Shock = Drop in BP + Rise in HR
o Very breathless with wheeze
o Often laryngeal and/or facial oedema
• Mechanism: IgE antibodies in the patient cause mast cell degranulation
• Most allergic reactions are NOT severe, but some can be in the case of IgA deficiency
o IgA deficiency = 1: 600 [COMMON]
o In 25% of these, anti-IgA antibodies develop in response to exposure to IgA in the donor blood
o Only a minority go on to have a severe transfusion reaction
transfusion associated circulatory overload
• VERY COMMON; leads to pulmonary oedema/fluid overload – a TACO checklist exists to help alleviate
• Often caused by lack of attention to fluid balance – especially in…
o Cardiac failure, renal impairment, hypoalbuminaemia, very young/old Clinical fluid overload
• Clinical features: CXR (fluid overload)
o SoB Low O2 saturations Fluid overload
o High HR High BP Cardiac failure
Transfusion related acute lung injury
• Looks at bit like ARDS (more common in FFP or platelet transfusion) No clinical fluid overload
• Clinical features:
o SoB Low O2 saturations Fever
o High HR High BP
• CXR = bilateral pulmonary infiltrates during/within 6 hours of transfusion due to circulatory overload and other causes
• Mechanism:
o Anti-WBC antibodies in donor blood
o These interact with WBCs in the patient
o Aggregates WBCs stick to pulmonary capillaries release neutrophil proteolytic enzymes and toxic O2 metabolites lung damage (however, this mechanism is incompletely understood)
delayed haemolytic transfusion reaction
• 1-3% of all patients transfused will develop an antibody against and RBC antigen that they lack = alloimmunisation
• Further transfusions with RBCs expressing same antigens antibodies will lyse RBCs (extravascular haemolysis)
o This is IgG-mediated so takes 5-10 days
• Haemolysis Tests:
o High bilirubin Low Hb
o High reticulocytes Haemoglobinuria over a few days
• Test U&E because it can cause renal failure
• Repeat the group and screen and look for new antibodies that may have been made against the transfused red cells
transfusion associated graft versus host disease
• Rare but ALWAYS FATAL (can take weeks to months to come on after transfusion)
• Pathophysiology:
o Donor’s blood will contain some lymphocytes that are able to divide
o Normally, the patient’s immune system will recognises these donor lymphocytes as foreign and destroy them
o In susceptible patients (very immunosuppressed), these lymphocytes are NOT destroyed
o Lymphocytes recognise patient’s tissue HLA antigens as foreign and attack (gut, liver, skin and bone marrow)
o Diarrhoea Liver failure Skin desquamation
o Bone marrow failure DEATH
how to prevent graft versus host
• Prevention: irradiate blood components for very immunocompromised patients or have HLA-matched components
post transfusion pupura
- Appears 7-10 days after transfusion of blood or platelets
- Usually resolves in 1-4 weeks but can cause life-threatening bleeding
- Affects Human Platelet Antigen (HPA) 1a -ve patients previously immunised via pregnancy or transfusion (HPA-1a AB)
- Exact mechanism is unknown
- Treatment: IVIG
iron overload
o If someone has lots of transfusions (past thalassaemia patients), iron will accumulate in their body
o There is about 200-250 mg of iron per unit of blood
o This can damage the liver, heart and endocrine organs
o Requires chelation
haemolytic disease of newborn
• Process:
o People lacking an RBC antigen (RhD) can form corresponding antibodies if exposed to the antigen
o This can happen:
By receiving blood transfusions
In pregnancy (foetal red cells enter the mother’s circulation during pregnancy or at delivery)
o In pregnancy, the first RhD-positive foetus will not experience any issues, however, they will stimulate the development of anti-D antibodies in the mother in a subsequent pregnancy, if the mother has another RhD-positive foetus, the antibodies will destroy foetal red cells leading to severe anaemia ± HDN
• Only IgG antibodies can cross the placenta
• Consequences:
o Foetal anaemia (haemolytic)
o Haemolytic disease of the newborn (anaemia, high BR builds up after birth as not removed by placenta)
how does anti D immunoglobulin work
The RhD +ve cells of the foetus will get coated by the exogenous anti-D immunoglobulin
They will then be removed by the mother’s reticuloendothelial system (spleen) before they can sensitise the mother to produce anti-D antibodies
For this to be effective, the anti-D injection must be given within 72 hours of the sensitising event
It does NOT work if the mother has already been sensitised and developed anti-D in the past
how does anti D immunoglobulin work
The RhD +ve cells of the foetus will get coated by the exogenous anti-D immunoglobulin
They will then be removed by the mother’s reticuloendothelial system (spleen) before they can sensitise the mother to produce anti-D antibodies
For this to be effective, the anti-D injection must be given within 72 hours of the sensitising event
It does NOT work if the mother has already been sensitised and developed anti-D in the past
