blood transfusion Flashcards
why do we transfuse blood
low levels of blood
- bleeding
- failure of production
- XS rate of destruction
how do different blood groups arise
from surface antigens on red blood cells (mic of proteins and sugars)
surface antigens can provoke antibodies and therefore immune response
what does the ABO gene encode for
glycosyltransferase
glycans added to proteins or lipids on red cells
what do A and B genes code for
transferase enzymes
what are the A and B antigens
A - N-acetyl-galactosamine
B - galactose
what is the O gene
non-functional allele
A and B are co-dominant and O is recessive
antibodies against different blood groups
blood group A = antibodies against B
blood group B = antibodies against A
blood group O = antibodies against A and B
blood group AB = NO antibodies against A and B
prevalence of different blood groups in UK
A 42%
B 9%
AB 3%
O 46%
how do we encounter the ABO entigens
encoded by many bacteria in the bowels
- anti-A/B naturally occurring
because they are sugars you form an IgM
thermal range of IgM antibodies
most only react to cold temps e.g. 20 degrees
ABO antigens are particularly strong and thermal range often goes up to 37 degrees - why there are such catastrophic reactions irl
red cell donor/recipient compatibility
O. = universal donor AB = universal recipient
x combinations can cause a severe ABO reaction and you should never transfuse these combinations
red cell vs FFP donor/recipient compatibility
plasma contains antibodies
e.g. B donor will have anti-A in their plasma so can’t donate to A patient
reactions to plasma are usually much less severe than red cells
RhD blood group system
protein antigen which crosses the membrane
very immunogenic protein - if you are an RhD individual and you are exposed to all the epitopes in the RhD gene, you are highly likely to make an antibody against it (?)
varies between racial groups
RhD nomenclature
DD - +ve for RhD gene
dd - -ve
anti RhD
RhD -ve individuals can make anti-D if exposed to RhD +ve cells (transfusion or pregnancy)
anti-D can cause transfusion reactions or haemolytic disease of the newborn
screening in blood donors
medical hx, prev transfusion
sex, age, travel, tattoos etc
tested for ABO and Rh blood groups
screened for hepB/C/E, HIV, syphilis
variably screened for: HTLV1, malaria, west nile virus, zika virus (depending on travel hx etc)
indications for red cell transfusion
- correct severe acute anaemia, which might otherwise cause organ damage
- improve QOL in pt w/ otherwise uncorrectable anaemia
- prepare a pt for surgery or speed up recovery
- reverse damage caused by pts own red cells e.g. sickle cell disease
red cell transfusion
red cells stored at 4 degrees
transfuse over 2-4hrs
1 unit increments ~5g/L
platelet transfusion
1 dose platelets = 4 pooled/1 apheresis donor
increments ~30.10^9/L
stored at ~22C, shelf life 7 days
transfuse over 20-30 mins
indications for platelet transfusion
massive haemorrhage - keep platelet count above 75.10^9/L
BONE MARROW FAILURE (platelet count < 10-15.10^9/L OR <20.10^9/L if additional risk e.g. sepsis)
prophylaxis for surgery - minor procedures 50.10^9/L, more major surgery 80.10^9/L, CNS/eye surgery 100.10^9/L
CP bypass - use only if bleeding
fresh frozen plasma
1 unit from 1 unit of blood
stored frozen, allow 30 mins to thaw
lab test - PT and APTT
indications for fresh frozen plasma
massive haemorrhage (use in 1:1 ratio)
DIC w/ bleeding
prophylactic - pts expected to bleed e.g. liver failure
cryoprecipitate
1-2 pools if fib <1.0g/dl (1.5g/dl)
stored frozen, allow 20 mins to thaw
lab test: fibrinogen
used when you want to give lots of fibrinogen to someone and you haven’t got much intravascular volume to give it in
how to choose compatible blood
blood sample (EDTA)
2 sample policy
group and screen/save
cross matching
what is group and screening
ABO and RhD type
checked against historical records for any discrepancy
screen for allo-antibodies in serum
Coombs test
trying to detect the antibody on the surface of red cells
can pick up IgG on the surface of red cells by using anti-human globulin
Coombs test: direct vs indirect
direct:
- AI haemolytic anaemia
- passive anti-D
- haemolytic transfusion reactions
indirect:
- cross matching
e.g. pt w/ AI haeomolytic anaemia, send for direct Coombs test, +ve = shows antibody on the surface of the red cell
what is an indirect Coombs test
adding an external antibody to see if it binds the red cells which you then cross link
allo-antibody screening
~1% of pop have antibodies
usually due to previous transfusion or pregnancy
10% of transfusion pts have had one before
clinical significance of antibodies reactive at 37degrees
> 21 blood group systems: ABO, Rh, Kell, Duffy, MN, P
development of maternal anti-D antibodies (sensitisation)
mothers can develop antibodies against antigens carried by their babies
~15% of mothers are RhD- and if the father is RhD+ they are at risk of developing the disease
red cells leak across the placenta (pregnancy/birth) - mother forms antibodies (IgG)
IgG can cross the placenta in subsequent pregnancies and cause alloimmune haemolysis in the baby
baby becomes profoundly anaemia, can develop cardiac failure and die
I
haemolytic disease of the newborn
RhD most immunogenic (also c, K; other Rh antigens (JKA, ABO) less immunogenic)
+ve DAT at birth, anaemia, jaundice (profound haemolysis)
brain damage
how to prevent HDN
give anti-D to RhD- mother
~28wks
RhD- w/ RhD+ baby should be given further anti-D at birth to prevent problems in future pregnancies
also given if any form of trauma during pregnancy (sensitising events)
treatment of HDN
careful monitoring:
- antibody titres
- doppler US
- intrauterine transfusions
what is NAIT
neonatal alloimmune thrombocytopenia
similar process to HDN but for platelets
cellular therapies
leucapheresis
- stem cells for transplantation
- lymphocytes for immunotherapy, CAR-T cells
other banks: bone, milk, tendons, heart valves, faecal; islet cells, mesenchymal stem cells
gene therapies
