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HAEM - Abbie > 8. Blood transfusion II > Flashcards

8. Blood transfusion II Flashcards

1
Q

What are five acute adverse reactions (<24 hours) to blood transfusion?

A
  1. Acute haemolytic (ABO incompatible); allergic/anaphylaxis; infection (bacterial); febrile non-haemolytic; and respiratory: tranfusion associated circulatory overload (TACO) and acute lung injury (TRALI)
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2
Q

What are five delayed adverse reactions (>24 hours) to blood transfusion?

A
  1. Delayed haemolytic transfusion reaction (antibodies).
  2. Infection: viral, malaria, vCJD.
  3. TA-GvHD.
  4. Post transfusion purpura.
  5. Iron overload
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3
Q

What is the most common adverse reaction in transfusions?

A

Transfusion-associated circulatory overload (TACO) is the most common. Remember that transfusion reactions are not necessarily due to antibody-antigen incompatibility.

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4
Q

What are the earliest signs of an acute reaction after transfusion?

A

Rise in temperature or pulse, fall in BP, this can occur before the patient experiences any symptoms

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5
Q

In early detection of an acute reaction to transfusion, what symptoms may be noted?

A

Fevers, rigors, flushing, vomiting, dyspnoea, pain at transfusion site, loin pain/chest pain, urticaria, itching, headache, collapse

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6
Q

How do you detect a reaction if the patient is unconscious?

A

Monitoring may be the only way. Baseline temperature, pulse, RR , BP before transfusion; repeat after 15 mins (most reactions will start within 15 mins); repeat hourly and at the end of the transfusion

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7
Q

When does febrile non-haemolytic transfusion reaction occur?

A

It occurs during/soon after transfusion (blood or platelets).

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8
Q

What does febrile non-haemolytic transfusion reaction cause?

A

May cause a rise in temperature by around 1 degree, chills and rigors.

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9
Q

How common is febrile non-haemolytic transfusion reaction?

A

Common before blood was leucodepleted

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10
Q

What should be done in a febrile non-haemolytic transfusion reaction?

A

Transfusion should be stopped or slowed and may need to be treated with paracetamol

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11
Q

What is FNHTR caused by?

A

Caused by the release of cytokines from white cells during storage.

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12
Q

How common are allergic transfusion reactions?

A

COMMON especially with plasma

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13
Q

What symptoms does allergic transfusion reaction result in?

A

Causes a mild urticarial or itchy rash, sometimes with wheeze

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14
Q

When do allergic transfusion reactions tend to occur and in who?

A

Can occur during or after transfusion. More common in recipients with other allergies and atopic conditions.

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15
Q

What should be done in allergic transfusion reactions?

A

Transfusion is usually stopped or slowed. IV antihistamines are used to treat (and for prevention in the future).

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16
Q

What causes allergic transfusion reactions?

A

Caused by allergy to a plasma protein in the donor

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17
Q

Do allergic transfusion reactions recur?

A

It may not recur again but this is dependent on how common the plasma protein is.

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18
Q

Who are allergic transfusion reactions more common in?

A

More common in recipients with other allergies and atopic conditions

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19
Q

What are symptoms and signs of acute intravascular haemolysis (IgM-mediated) due to the wrong blood being given?

A

Restless, chest/loin pain. fever, vomiting, flushing, collapse, haemoglobinuria (later), low BP, high HR, high temperature.

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20
Q

What are the causes of wrong blood being given to a patient?

A

Failure of bedside check, wrongly labelled blood sample, laboratory error

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21
Q

What should you take samples for in cases where an acute haemolytic reaction may be taking place?

A

FBC, biochemistry, coagulation, repeat X-match, direct antiglobulin test (DAT).

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22
Q

What is the severity of wrong blood?

A

Severe or fatal

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23
Q

What is the severity of bacterial contamination of blood?

A

Severe or fatal

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24
Q

How does bacterial contamination present?

A

Similar to ABO mismatch (Restless, chest/loin pain. fever, vomiting, flushing, collapse, haemoglobinuria (later), low BP, high HR, high temperature, etc.)

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25
Q

Why does bacterial growth cause immediate collapse?

A

Bacterial growth can cause endotoxin production which causes immediate collapse

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26
Q

What is the source of bacterial contamination?

A

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)

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27
Q

What is the order of likelihood of bacterial contamination?

A

From most to least likely: platelets (stored at room temperature), red cells, FFP

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28
Q

How can we prevent bacterial contamination from donor?

A

Donor questioning + arm cleaning + diversion of first 20 mL into a pouch (used for testing)

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29
Q

How can we prevent bacterial contamination via red cells?

A

Store in a controlled fridge at 4 degrees, shelf-life: 35 days, if it is kept out for > 30 mins it needs to go back in the fridge for 6 hours. Complete transfusion should take place within 4.5 hours of leaving the fridge. With ALL components, look for abnormalities such as clumps of discoloured debris, brown plasma etc.

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30
Q

How can we prevent bacterial contamination via platelets?

A

Stored at 22 degrees and shelf-life: 7 days. Screened for bacteria before release. With ALL components, look for abnormalities such as clumps of discoloured debris, brown plasma etc.

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31
Q

What is the severity of anaphylaxis due to transfusion?

A

Severe, life-threatening reaction soon after the start of transfusion

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32
Q

What are the signs and symptoms in anaphylaxis?

A

Drop in BP, rise in HR, very breathless with wheeze, often laryngeal and/or facial oedema

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33
Q

What is the mechanism of anaphylaxis?

A

IgE antibodies in the patient cause mast cell degranulation

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34
Q

Most allergic reactions are NOT severe. But what can allergic reactions be severe in?

A

Reactions can be severe in IgA deficiency. In 25%, anti-IgA antibodies develop in response to exposure to IgA in the donor blood

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35
Q

What does transfusion-associated circulatory overload lead to?

A

Leads to pulmonary oedema/fluid overload.

36
Q

What is TACO often caused by?

A

Often caused by a lack of attention to fluid balance (especially in cardiac failure, renal impairment, hypoalbuminaemia, very young/old)

37
Q

What are the clinical features of TACO

A

Shortness of breath; low oxygen saturations; high heart rate; high blood pressure

38
Q

What can be seen on the CXR for TACO?

A

Fluid overload and cardiac failure

39
Q

How common is TACO and what is its severity?

A

TACO is very common. This can be moderate, severe or fatal

40
Q

What is transfusion-associated acute lung injury similar to?

A

Looks a bit like ARDS

41
Q

What are the clinical features of TRALI?

A

SOB, drop in oxygen saturation, rise in HR, rise in BP

42
Q

What does TRALI look like on CXR?

A

Bilateral pulmonary infiltrates during/within 6 hours of transfusion due to circulatory and other causes

43
Q

What is the mechanism of TRALI?

A

Anti-WBC antibodies in donor blood. These interact with WBCs in the patient. Aggregates of WBCs get stuck to pulmonary capillaries –> release of neutrophil proteolytic enzymes and toxic O2 metabolites –> lung damage. This mechanism is incompletely understood.

44
Q

Why is TRALI different to TACO?

A

This differs from TACO because the JVP will NOT be raised and the patient will NOT respond to furosemide

45
Q

How can we prevent TRALI?

A

This can be prevented by using male donors (who haven’t been pregnant (obviously) and have not had any previous blood transplantations) because they will not have antibodies against HLA

46
Q

What percentage of patients will develop an antibody against an RBC antigen they lack?

A

1-3% of all patients who are transfused will develop an antibody against and RBC antigen that they lack = alloimmunisation

47
Q

What leads to extravascular haemolysis in transfusion and how long does it take?

A

If the patient has another transfusion with RBCs expressing the same antigens, the antibodies will cause RBC destruction = extravascular haemolysis. This is IgG mediated so takes 5-10 days.

48
Q

What are tests for haemolysis?

A

High bilirubin; low Hb; high reticulocytes; haemoglobinuria over a few days (as they stop haemolysing the urine will clear); test U&E because it can cause renal failure; repeat the blood group and screen and look for new antibodies that may have been made against the transfused red cells.

49
Q

What are examples of transfusion-transmitted infections?

A

Malaria, viral infections, variant CJD (variant Creutzfeldt-Jakob disease), CMV, parvovirus

50
Q

When might symptoms of infection occur after the transfusion?

A

Symptoms may occur months or years after the transfusion. Rely on questions being answered by the donors. The risk is never zero.

51
Q

In which patients can CMV be fatal?

A

Very immunosuppressed patients (e.g. stem cell transplant) can get fatal CMV disease.

52
Q

What process removes CMVs?

A

Leucodepletion removes CMV in WBCs

53
Q

Who are CMV negative products given to?

A

CMV negative products are only given to pregnant women and neonates

54
Q

What test is there for vCJD to prevent infection?

A

NO test. Blood services exclude transfused patients as donors as a precaution.

55
Q

What is the severity of TA-GvHD?

A

Rare but ALWAYS FATAL

56
Q

What is the mechanism of TA-GvHD?

A
  • Donor’s blood will contain some lymphocytes that are able to divide.
  • Normally, the patient’s immune system will recognises these donor lymphocytes as foreign and destroy them.
  • In susceptible patients (very immunosuppressed), these lymphocytes are NOT destroyed.
  • Lymphocytes recognise the patient’s tissue HLA antigens as foreign, so attack the patient’s gut, liver, skin and bone marrow.
57
Q

What are the consequences of TA-GvHD?

A

Diarrhoea, liver failure, skin desquamation, bone marrow failure, DEATH - weeks to months after transfusion

58
Q

How can we prevent TA-GvHD?

A

Prevention: irradiate blood components for very immunocompromised patients or have HLA-matched components

59
Q

How long after transfusion does post-transfusion purpura occur?

A

Appears 7-10 days after transfusion of blood or platelets

60
Q

How long does it take for post-transfusion purpura to resolve and what is its severity?

A

Usually resolves in 1-4 weeks but can cause life-threatening bleeding

61
Q

Who does post-transfusion purpura affect?

A

Affects HPA-1a negative patients who have previously been immunised via pregnancy or transfusion. (Exact mechanism is unknown)

62
Q

What is the treatment for post-transfusion purpura?

A

IVIG

63
Q

Possible increased rate of infections post-operatively and increased recurrence of cancer in patients who have blood transfusions - true or false?

A

Not certain - The evidence is conflicting. (This is an example of immune-modulation?)

64
Q

What can accumulate if someone has lots of transfusions? And why is this bad?

A

Iron will accumulate in their body. This can damage the liver, heart and endocrine organs.

65
Q

How much iron is there per unit of blood?

A

There is about 200-250 mg of iron per unit of blood

66
Q

How can we prevent iron overload?

A

Attempt to prevent using iron chelators (e.g. exjade) with transfusions once ferritin > 1000.

67
Q

People lacking a red cell antigen can form corresponding antibodies if exposed to the antigen (e.g. RhD negative person may develop anti-D antibodies). What are two ways this can happen? (NOTE: Some antigens are more likely to stimulate antibodies than others)

A

By receiving blood transfusions. In pregnancy (foetal red cells enter the mother’s circulation during pregnancy or at delivery).

68
Q

Why might a RhD negative mother have issues with her second pregnancy, even though she did not experience issues in the first pregnancy?

A
  • 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.
  • Then, in a subsequent pregnancy, if the mother has another RhD-positive foetus, the antibodies will destroy foetal red cells leading to SEVERE ANAEMIA.
  • Only IgG antibodies can cross the placenta.
69
Q

What are consequences of haemolytic disease of the newborn?

A

Foetal anaemia (haemolytic). Haemolytic disease of the newborn (anaemia plus high bilirubin - which builds up after birth because it is no longer removed by the placenta)

70
Q

Which Ig can cross the placenta?

A

Only IgG

71
Q

Which is the most important antibody for causing haemolytic disease of the newborn?

A

Anti-D is the MOST IMPORTANT antibody for causing haemolytic disease of the newborn

72
Q

How can we investigate RhD incompatibility and haemolytic disease?

A
  • All women have a group and screen at around 12 weeks and again at 28 weeks.
  • If there is an antibody against red cell antigens present: check if the father has the antigen (and hence whether the baby could inherit it); monitor level of AB (high/rising suggests it is more likely to affect the foetus), check ffDNA sample (allows identification of the baby’s RhD group); monitor foetus for anaemia (MCA Doppler ultrasound).
73
Q

How can we manage RhD incompatibility and haemolytic disease?

A
  • Carry out Ix
  • The baby may need to be delivered early because haemolytic disease of the newborn gets a lot worse in the last few weeks of pregnancy.
  • Sometimes, intrauterine transfusion may be needed if the baby is very anaemic.
  • The transfusion is done via the umbilical vein.
  • Subsequent pregnancies usually fare WORSE.
74
Q

How can we prevent haemolytic disease due to anti-D?

A

If an RhD negative woman of childbearing age needs a blood transfusion, ALWAYS give RhD negative blood. An IM injection of anti-D immunoglobulin can be given at times when the mother is at risk of fetomaternal bleeding (e.g. at delivery).

75
Q

How does the anti-D immunoglobulin work?

A

The RhD positive 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.

76
Q

When must anti-D immunoglobulin be given to be effective?

A

For this to be effective, the anti-D injection must be given within 72 hours of the sensitising event.

77
Q

When will anti-D immunoglobulin not work?

A

It does NOT work if the mother has already been sensitised and developed anti-D in the past.

78
Q

When should anti-D immunoglobulin be given?

A

At delivery if baby is RhD positive. For sensitising events during pregnancy where fetomaternal haemorrhage is likely to occur (and you do NOT know the Rh status of the baby). E.g. spontaneous miscarriages if surgical evacuation needed and therapeutic terminations; amniocentesis and chorionic villous sampling; abdominal trauma (falls and car accidents); external cephalic version (turning foetus); stillbirth or intrauterine death.

79
Q

How much anti-D immunoglobulin is needed to prevent sensitisation from a 1mL FMH?

A

125 iu can prevent sensitisation from a 1mL FMH

80
Q

How much anti-D immunoglobulin is needed for events < 20 weeks gestation?

A

At least 250 iu for events < 20 weeks gestation

81
Q

How much anti-D immunoglobulin is needed for events > 20 weeks gestation?

A

At least 500 iu - for events > 20 weeks gestation. Sometimes a larger does is needed for larger bleeds. FMH test can be done.

82
Q

Why is a fetomaternal haemorrhage test (Kleihauer test) done if > 20 weeks gestation and at delivery?

A

To determine if more anti-D is needed than the standard dose if the foetal bleed is large.

83
Q

What percentage of pregnancies have no obvious sensitising events yet RhD negative mothers become sensitised?

A

About 1%

84
Q

How can we prevent sensitising events in RhD negative mothers (even if they have no obvious sensitising events)?

A

To prevent this, routine anti-D prophylaxis can be given in the 3rd trimester. Usually a dose of 1500 iu anti-D Ig at 28-30 weeks.

85
Q

What are other important antibodies to consider?

A

Anti-c and anti-Kell can cause severe HDN. This is usually less severe than anti-D

86
Q

What does Kell lead to?

A

Kell causes reticulocytopaenia in a foetus as well as haemolysis.

87
Q

What causes mild HDN in group O mothers and how is it treated?

A

IgG anti-A and anti-B antibodies from group O mothers can cause mild HDN. This can usually be treated with phototherapy.

HAEM - Abbie (16 decks)

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