Blood product transfusion

Question 1

How is blood split INITIALLY once donated? Three groups?

Answer 1

• Split one unit of blood by centrifuging whole bag – red cells bottom, platelets middle and plasma on top.
• Then, each layer is squeezed into satellite bags.
• This is all processed in a closed system to prevent bacteria entering the system – of which blood is a great culture.

Question 2

When are the indications for red cell transfusions needed? (x2)

Answer 2

• When there is massive bleeding and saline is not sufficient.
• If patient is anaemic, but iron/B12/folate therapy is not appropriate/sufficient e.g. if a patient is severely anaemic from iron deficiency, they may be given a pint of blood to lift them off the floor, and then iron infusions after for recovery so their body can start making Hb again.

Question 3

What is the mechanism that causes death when the wrong blood group is transfused?

Answer 3

IgM antibodies form a pentameter structure and are ‘complete’, meaning that they fully activate the complement cascade, causing haemolysis of RBCs. This releases Hb into the blood, which is toxic to the kidneys. Release of bilirubin from Hb breakdown in the liver gives patient jaundice, and activation of the cascade causes a cytokine storm. Cytokine storm results in fall in BP and shock in patients –> death.

Question 4

What blood group is the universal acceptor?

Answer 4

AB is the universal acceptor because they have no antibodies in their plasma for A or B antigens. This is because they already have A and B antigens on their RBCs.

Question 5

What blood group is the universal donor?

Answer 5

O is the universal donor because they have no antigens on their surface, so regardless of the antibodies present in the recipient’s body, it will not cross-link with O blood.

Question 6

What is the RH blood grouping?

Answer 6

Describes patients who are RhD positive or RhD negative. RhD positive means you have the D antigen, while negative means you do not.

Question 7

What are the genetics of the RhD positive or negative groups?

Answer 7

D codes for D antigen on RBC; d codes for no antigen and is recessive. Therefore, DD or Dd = RhD positive; dd = RhD negative.

Question 8

How is the ABO and RH blood groupings shortened?

Answer 8

Patients’ ABO and Rh D groups usually shortened e.g. O positive means ABO group O and RhD positive.

Question 9

Why is RH blood grouping clinical important to understand?

Answer 9

D antigen is the next immunogenic (sets off antibodies) after the AB antigens.

Question 10

Presence of RhD antibodies (anti-D antibodies)? !!!

Answer 10

People who LACK the RhD antigen (RhD negative) CAN make anti-D antibodies only AFTER they have been exposed to the RhD antigen – either by transfusion of RhD positive blood, or in women if they are pregnant with an RhD positive foetus. Those who are RhD positive will have the D antigen and NO anti=D antibodies in their system, even after exposure to RhD-positive blood through transfusion or pregnancy.

Question 11

What class of antibody is produced against the RhD antigen?

Answer 11

IgG.

Question 12

What happens when a patient with anti-D antibodies is transfused with RhD positive blood?

Answer 12

• NOTE: this can only occur after the 2nd RhD positive transfusion. Remember, patient does not have anti-D antibodies from birth; anti-D antibodies are only found in the blood after an initial exposure to RhD positive blood IN RhD NEGATIVE PATIENTS.
• IgG antibodies will cause haemolysis of RBCs, but this is a DELAYED HAEMOLYTIC TRANSFUSION REACTION (takes around 5-10 days).
• IgG antibodies attach to the RBCs but do not activate the complement cascade straight away. Damage occurs as the RBCs pass through the spleen: resident macrophages recognise the RhD positive blood and IgG antibodies and destroy RBCs.
• Results in fall in Hb (anaemia), high bilirubin, jaundice and in some cases renal failure.
• This is all less dramatic and less immediately fatal than incorrect ABO transfusion.

Question 13

What are the implications that should be considered in patients where anti-D antibodies are known? (x2)

Answer 13

• FUTURE TRANSFUSIONS: patient must, in future, have RhD negative blood, otherwise they will develop delayed haemolytic transfusion reaction. In any case, where blood group is known, RhD negative patients should always be given RhD negative blood to avoid EVER making anti-D.
• HAEMOLYTIC DISEASE OF THE NEWBORN (HDN): if RhD negative mother has anti-D and in the next pregnancy, the fetus is RhD positive, mother’s IgG anti-D antibodies can cross the placenta and cause haemolysis of foetal red blood cells.

Question 14

What causes death in haemolytic disease of the newborn? (x2)

Answer 14

• Bilirubin circulates in toxic levels from increased breakdown of Hb in the liver from IgG-mediated haemolysis. Causes brain damage from bilirubin staining of brain stem columns – clinical signs include hyperextension of legs, arms and neck of NEWBORN BABY.
• Hydrops fetalis: FOETUS develops anaemia from IgG-mediated haemolysis of foetal RBCs. The heart therefore pumps a much greater volume of blood to deliver the same amount of oxygen. The increased demand on CO leads to heart failure and corresponding oedema.

Question 15

What are anti-D injections?

Answer 15

Injection of anti-D antibodies, given to RhD neg mothers during pregnancy when exposed to RhD pos blood from their baby (remember, during pregnancy, there is some sharing of blood). Anti-D injections take RhD positive blood out of the mother’s system before the body can amount an immune response and produce anti-D antibodies of their own. Injections given when a small amount of blood has been shared e.g. torn vagina and some sharing of mother and baby blood there.

Question 16

What other red cell antigens are there?

Answer 16

RhC/c/E/e etc.

Question 17

What are the clinical implications of patients who develop antibodies against less common red cell antigens e.g. RhC/c/E/e? How is this screened?

Answer 17

• Once patient forms antibodies against an antigen, they must use antigen-negative blood of the corresponding antigen, or they risk delayed haemolytic transfusion reaction.
• Plasma is screened for red cell antibodies BEFORE transfusion. If, after the ANTIBODY SCREEN, an antibody to one of these antigens is found, antigen-negative blood is given. However, only 8% will form an antibody to one of these antigens, so it is not really an issue.

Question 18

How can plasma be processed once separated from whole blood? (x3 options)

Answer 18

• FRESH FROZEN PLASMA (FFP): Frozen to preserve coagulation factors and stop degeneration.
• Make CRYOPRECIPITATE: This is FFP which is THAWED in a FRIDGE, leaving a liquid component and a cryoprecipitate. The cryoprecipitate is rich in fibrinogen (FI) and F8, so it is useful for patients who need just FI or FVIII.
• Plasma is FRACTIONATED (like in the oil industry): separating plasma into albumin, haemophilia factors (usually FVIII and FIX to treat Haemophilia A and B respectively, and Factor VIII for von Willebrand’s disease), and immunoglobulins.

Question 19

What is the clinical significance of Albumin extracted from fractionation? (x3) Two types?

Answer 19

• 4.5% ALBUMIN: useful in people who are losing a lot of water and proteins because of severe burns. Also used in plasma exchanges.
• 20% ALBUMIN: for certain severe liver and kidney conditions where you are losing proteins in the blood.

Question 20

Why is it important to know blood group of patient before administration of FFP?

Answer 20

Because the plasma is what contains the antibodies of the donor blood. Therefore, must make sure that FFP does not contain antibodies corresponding to any of the recipient’s antigens.

Question 21

When is FFP administered to a patient? (x2)

Answer 21

• If patient is bleeding and has ABNORMAL coagulation test results – both PT and APTT coagulation tests are prolonged –> if both PT and APTT are prolonged, it suggests multiple factors are missing, so FFP should be administered as oppose to individual factors.
• Reversal of anticoagulants e.g. warfarin. Used just before urgent surgery. However, not practical because it’s basically over-kill: Patient should only be given factors that are being suppressed by the anticoagulant. FFP is used when the factors that are deficient are not known, or when there is no preparation available that will replace just the factors lost, so all factors must be given instead.

Question 22

What clotting factors does warfarin inhibit?

Answer 22

Factors II, VII, IX and X.

Question 23

When is cryoprecipitate used? (x2)

Answer 23

• Massive bleeding and fibrinogen is very low.
• Hypofibrinogenemia.

Question 24

If a patient is bleeding post-surgery, their PT and APTT are prolonged, and fibrinogen is low, what components should be administered?

Answer 24

This is a TRICK QUESTION: Low fibrinogen means administer cryoprecipitate. However, notice that BOTH PT and APTT are low. If just fibrinogen was low, PT would be normal. Therefore, we instead administer FFP and only administer cryoprecipitate on top of this if fibrinogen is exceptionally low.

Question 25

Why is it important to know blood group of patient before administration of platelets? (x3)

Answer 25

Platelets have low levels of ABO antigens on them. But, wrongful administration is NOT deadly. The problems are:

• If a patient was blood group B, and given group A platelets, the patient’s anti-A antibodies will destroy the platelets, and the platelets will not last long in a patient.
• Platelets must be bathed in some plasma once donated, or they don’t really survive. This means that platelet donations will also contain some of the donor’s antibodies e.g. if Group O platelets are given to a Group A patient, the platelets would not be destroyed, but anti-A antibodies in the plasma of the donor will destroy some of the recipient’s blood.
• Need to know RhD group as well: This is because there is always some blood contamination in collected plasma – you can’t help it. If the donor is RhD pos, platelets should not be given to RhD neg recipients, as it would lead to RhD sensitisation and anti-D production.

Question 26

When are platelets used clinically? (x4)

Answer 26

• Bone marrow failure – as bone marrow produces platelets.
• Massive bleeding – because patients will lose some platelets.
• Acute DIC.
• If patient has low platelet count and about to go for surgery e.g. they were previously on anti-platelet drugs.

Question 27

What is prothrombin complex concentrate?

Answer 27

Made of clotting factors II (prothrombin), IX and X

Question 28

What are the indications for prothrombin complex concentrate?

Answer 28

• Prevent bleeding in Haemophilia B (Factor IX)
• Reverses the effects of warfarin and other Vitamin K antagonist