Blood transfusion Flashcards
how does group and screen work
group - test patients antigens vs known A, B group RBCs (reverse group) and test patients RBCs vs known anti A (forward group)
screen -Use 2 or 3 reagent red cells containing all the important red cell
antigens between them
• Screen by incubating the patient’s plasma and screening cells
using IAT** technique
**INDIRECT ANTIGLOBULIN TECHNIQUE (bridges red cells coated
by IgG, which can’t themselves bridge 2 red cells – to form a
visible clump. Takes 30 mins’ incubation at 37°C)
how does electronic crossmatch work
Electronic issue (EI) is the selection and issue of red cell units where compatibility is determined by IT system, without physical testing of donor cells against patient plasma
how does serological crossmatch work
1)FULL CROSSMATCH
INDIRECT ANTIGLOBULIN TECHNIQUE
Patient plasma incubated with donor red cells at 370C for 30-40
mins, will pick up antibody antigen reaction that could destroy the
red cells and cause extravascular haemolysis
ADD ANTIGLOBULIN REAGENT (AHG)
2)
IMMEDIATE SPIN (SALINE, ROOM TEMPERATURE)
Incubate patient plasma and donor red cells for 5 minutes only
and spin, will detect ABO incompatibility only
what are the 3 pillars of patient blood management
optomise haemopoisis, bleeding, tolerance of anaemia
patient information and consent
- ‘Valid’ consent is required for transfusion (verbal & written),
- Alternatives should be considered if appropriate
a) Iron / B12 / EPO / Folate
b) Cell Salvage - If transfused in an emergency, patient must be informed afterwards
- Involve patients in the process to ensure they get the right blood
and the right ‘special requirements’
red cells transfusion
Give ABO/D compatible Group O (negative) in emergency Consider special requirements Stored at 40 C for 35 days. Must be transfused within 4 hours of leaving fridge Transfuse 1 unit RBC over 2-3 hours
Platelets
ABO/D antigens weakly expressed Should be D compatible Consider special requirements If group O given to A, B or AB patients select ‘high-titre’ negative (anti-A/B antibodies) Stored at 20 0 C for 7days Transfuse 1 unit of platelets over 20-30 minute
FFP
Give ABO compatible (D group does not matter) AB plasma can be given to all groups as it has no anti-A/B antibodies but it is in short supply No need to cross match but does take 30-40 minutes to thaw Once thawed can be kept at 4 0C for 24 hours Transfuse 1 unit over 20-30 minutes
Cryoprecipitate
Give ABO compatible (D group does not matter) AB plasma can be given to all groups as it has no anti-A/B antibodies but it is in short supply No need to cross match but does take 30-40 minutes to thaw
nce thawed has to kept at room temperature and use within 4 hours Transfuse 1 unit over 20-30 minutes
what is maximum surgical blood ordering schedule
MSBOSMSBOS is based agreement between surgeons and transfusion lab about
predictable blood loss for ‘routine’ planned surgery.
Junior doctors / nurses doing pre-admission clinics have some idea what is
normal
what percentage blood loss is major
30%
when is platelet transfusion contraindicated
heparin induced thrombocytopenia thrombosis and TTP
how much does the platelet count go up by in one dose
30-40
platelet indication
massive transfusion, prevent bleeding post chemo, during surgery, platelet dysfunction or immune activebleeding
FFP indication
massive transfution to treat coagulopathy, aim to get PT:APTT <1.5, liver disease, replacement of single coagulation factor deficiency, DIC, TTP,
what does cryoprecipitate contain
fibrinogen mainly, fVIII, vwf, fibronectin, FXIII, IgA, albumin
cryoprecipitate indication
fibronogen low
can u do pre-eperative autologous deposti in the UK
no
whenb would u give CMV negative blood
neonatal, pregnant
when would you give washed blood
severe allergic reaction to plasma proteins
What are the acute adverse reactions to transfusion
Acute haemolytic (ABO incompatible) 2. Allergic/anaphylaxis 3. Infection (bacterial) 4. Febrile non-haemolytic 5. Respiratory • Transfusion associated circulatory overload (TACO) • Acute lung injury (TRALI)
what are the delayed adverse reactions to transfusion
1. Delayed haemolytic transfusion reaction (antibodies) 2. Infection viral, malaria, vCJD 3. TA-GvHD 4. Post transfusion purpura 5. Iron overload
how to detect an acute reaction
Monitoring may be the ONLY way to detect
reaction if patient unconscious
Baseline temp, pulse, respiratory rate, BP
before transfusion starts
Repeat after 15 mins (as most, but not all,
reactions will start within 15 mins)
Ideally repeat hourly and at end of
transfusion (as occasionally reactions start
after transfusion finished
febrile non haemolytic transfusion reaction
During / soon after transfusion (blood or platelets),
rise in temperature of 10C, chills, rigors
Common before blood was leucodepleted, now rarer
Have to stop or slow transfusion; may need to treat with
paracetamol
Cause: White cells can release cytokines during storage
allergic transfusion reactions
Common especially with plasma
Mild urticarial or itchy rash sometimes with a wheeze
During or after transfusion
Usually have to stop or slow transfusion
IV antihistamines to treat (and prevent in future if recurrent)
Cause:
• Allergy to a plasma protein in donor so may not recur again,
depending on how common the allergen is
• Commoner in recipients with other allergies and atop
wrong blood abo reaction
Symptoms and signs of acute intravascular haemolysis- IgM
• Restless, chest/ loin pain, fever, vomiting, flushing, collapse,
haemoglobinuria (later);
• ↓BP & ↑HR (shock), ↑Temp
Stop transfusion – check patient / component
Take samples for FBC, biochemistry, coagulation,
Repeat x-match and Direct Antiglobulin Test (DAT)
Discuss with haematology doctor ASAP
bacterial contamination
Restless, fever, vomiting, flushing, collapse.
↓BP & ↑HR (shock), ↑Temp
•Bacterial growth can cause endotoxin production which causes immediate
collapse
•From the donor (low grade GI, dental, skin infection)
•Introduced during processing (environmental or skin)
•Platelets >red cells > frozen components (storage temp)
anaphylaxis
“Severe, life-threatening reaction soon after start of transfusion”
• ↓BP & ↑HR (shock),
• very breathless with wheeze,
• often laryngeal &/or facial oedema
Mechanism:
IgE antibodies in patient cause mast cell release of granules & vasoactive substances
Most allergic reactions are not severe, but few are e.g. in IgA deficiency
IgA deficiency
• 1:300 - 1:700 (common); where in 25%, anti-IgA antibodies develop in response to
exposure to IgA (transfusion – especially with plasma);
• But only minority ever have transfusion reactions- frequency is 1:20,000 - 1:47,000
Transfusion associated circulatory overload
Pulmonary oedema / fluid overload;
• Often lack of attention to fluid balance, especially in
cardiac failure, renal impairment, hypo-albuminaemia,
those on fluid replacement, very young, very small and very
old.
• Clinical features: SOB, ↓SAO2 , ↑HR, ↑BP
• CXR: fluid overload / cardiac failure
Transfusion associated lung injury
acute lung injury/ARDS
• SOB, ↓O2, ↑HR, ↑BP; (similar to TACO)
• CXR: bilateral pulmonary infiltrates during/within 6 hr of transfusion, not due to circulatory
overload or other likely causes
Mechanism
• Anti-wbc antibodies (HLA or neutrophil Abs) in donor
• Interact with corresponding ag on patient’s wbc’s
• Aggregates of wbc’s get stuck in pulmonary capillaries → release neutrophil proteolytic enzymes
& toxic O2 metabolites → lung damage
Mechanism not fully understood, antibodies don’t always cause problems
• Prevention - male donors for plasma & platelets (no pregnancy or transfusion, so no HLA/HNA
antibodies
Transfusion associated graft versus host disease
• Rare, but always fatal (death weeks to months post transfusion)
• Donor’s blood contains some lymphocytes (able to divide)
• Normally, patient’s immune system recognises donor’s lymphocytes as ‘foreign’ and
destroys them
• In ‘susceptible’ patients (e.g… very IS) - lymphocytes not destroyed
• Lymphocytes recognise patient’s tissue HLA antigens as ‘foreign’ – so attack patient’s
gut, liver, skin and bone marrow -
• Prevent: irradiate blood components for very immunosuppressed; or patients having
HLA matched components.
• Clinical features - severe diarrhoea, liver failure, skin desquamation,
bone marrow failure
Post transfusion purpura
• Purpura appears 7-10 days after transfusion of blood or platelets and
usually resolves in 1 to 4 weeks but can cause life threatening bleeding
• Affects HPA -1a negative patients - previously immunised by pregnancy or
transfusion (anti-HPA-1a antibody)
• ?exact mechanism of own platelet destruction, as HPA-1a negative!
?innocent bystander mechanism
• Treatment – infusion of IVIG
Iron overload
If lots of transfusion (e.g. >50) over time accumulate iron (not
excreted); 200-250mg of iron per unit of blood
• Can cause organ damage - liver, heart, endocrine etc
• Prevent by iron chelation (Exjade) with transfusions once
ferritin >1000 e.g. used in Thalassaemia / Sickle cell disease -
regular transfusions
Treatment of rhesus disease
All pregnant women have G&S at around 12 weeks
(booking) and again at 28 weeks to check for RBC
Antibodies. If antibody present:
check if father has the antigen (so baby could inherit it)
monitor level of antibody (high or rising - more likely to affect fetus)
Check ffDNA sample
Monitor fetus for anaemia – MCA Doppler ultrasound
Deliver baby early, as HDN gets a lot worse in last few weeks of pregnancyIf necessary, intra-uterine transfusion can be given
to fetus
Specialised centres, highly skilled - needle in
umbilical vein
At delivery - monitor baby’s Hb and bilirubin for
several days as HDN can get worse for few days
Can give exchange transfusion to baby if needed
to bilirubin and Hb; plus phototherapy to
bilirubin
what is non invasive fetal genotyping
NHSBT offers fetal genotyping - support for routine maternity and transfusion services
both nationally and internationally.
• A rapid, non-invasive, convenient and reliable service for prediction of fetal D, C, c, E
and K status, using cell-free fetal DNA in maternal blood for women who have alloantibodies.
• Upon identification, mothers can then be informed and prepared for further careful
monitoring during their pregnancy.
• Also identifies pregnant women who have antigen-negative fetuses and who therefore
are not at danger from HDF
what are the clinical features of haemolytic disease of the newborn
Only IgG antibodies can cross the placenta.
If mother has high levels of IgG antibody - it can destroy
fetal red cells, if they are positive for the corresponding
antigen
Fetal anaemia (haemolytic)
Haemolytic disease of newborn (anaemia
plus high bilirubin - which builds up after
birth as no longer removed by placenta, hydrops fetalis, kernicterus
