Transfusion quiz Part 1

FFP and cryoprecipitate require only ABO group matching and PCC does not require any matching. (link)

The prevalence of clinically significant antibodies  is 2% in ED patients, 1.7% in trauma patients, 5% in haematology/oncology patients and 7.5% in the group aged 40-49 years. It increases with age and is more common in women of post child bearing age. RBC transfusion is by far the most important independent risk factor for non-RhD immunisation.  The incidence of these events ranges between 1%–6% in single transfused and up to 30% in polytransfused patients (eg, sickle cell disease, thalassaemia and myelodysplasia).  Risk is about 1•0% at 5 units, 2•4% at 10 units, 3•4% at 20 units and 6•5% at 40 units of red-blood-cells transfused.

The slow rate is to reduce the risk of a severe reaction to the blood product. As little as 10mL of incompatible blood can cause a severe reaction. Transfusing at too slow a rate may result in clotting of the line and increases the risk from bacterial contamination.

The calcium content in Hartmann’s solution makes it incompatible with red cells.(link)

The frequency of blood types in Australia is approximately: O  46% ,A  39%, B  11%  and AB  3.5%.

About 80% of Australians are Rh +ve. (link)

The estimated compatibility of a unit of blood is as follows: ABO matched  99.4%, ABO & Rh  99.8%, ABO, Rh & Ab  99.94%, XMatched  99.95%; Autologous  100%. The increase in risk of transfusion reaction between group specific and cross matched blood is small, hence delaying transfusion for group specific blood is usually inappropriate in significant haemorrhage. (link)

The risk of reaction is increased by only 0.15% when ABO and Rh matched blood is used instead of fully cross matched blood is used. (link)

The hepatic metabolism of citrate is normally rapid, but is impaired by hypotension, hypothermia and liver disease. An infusion rate of > 100mL/min is usually required to produce citrate toxicity in patients without these risk factors. Citrate contributes to metabolic acidosis and can decrease ionised calcium (cofactor in coagulation cascade), although the significance of this is debated as hypocalcaemia severe enough to impair coagulation is incompatible with life. Citrate toxicity can also cause a metallic taste or perioral paraesthesia. (link)

Cooled blood shifts the haemoglobin oxygen dissociation curve to the left, hence cool red cells have a higher affinity for O2 and release it less. Cool red cells also have impaired red cell deformability. Potassium moves out of the red cell when cooled, but is taken back up as the blood is warmed. Bacterial infection rates are increased by blood warming, due to higher replication rates of organisms at higher temperatures (the reason RBCs are cooled in the first place and platelets only have a 5 day shelf life). (link)

A febrile non haemolytic reaction is seen frequently multiparous women or in multiply transfused patients and is due to recipient antibodies to donor white cells. It is dose related and often occurs towards the end of the transfusion (30 – 120 min after starting transfusion) and can occur 1-2 hours after the transfusion has finished. The temperature rise is usually ≤ 1C above baseline.
A haemolytic reaction usually occurs at the start of the transfusion and is characterised by pain at the injection site as well as headache, chest or back pain +/- hypotension or other evidence of haemolysis. A mild haemolytic reaction can also cause a temperature rise of ≤ 1C above baseline, so is the least useful of the features listed. (link)

Whilst the ARCBS only specifies that a unit of RBCs is > 220mL, the average unit is probably closer to 250mL than 350mL. There is a strange absence of relevant information about this. (link)

4 hours is the maximum transfusion time for a single unit. (link)

FFP should usually be administered at 10 mL/min (i.e. within 30 min), but not over longer than 1 hour for stable patients. It should be given as rapidly as possible in the presence of severe bleeding. (link)

A change in clotting factor concentrations of at least 10% is considered clinically significant. Usually there is an ample oversupply of clotting factors in the blood for normal functioning. (link)