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YEAR 5: Haematology PM > Haem: Blood Tranfusions 2 > Flashcards

Haem: Blood Tranfusions 2 Flashcards

1
Q

How are acute and delayed transfusion reactions defined?

A

Acute < 24 hours

Delayed > 24 hours

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2
Q

List some causes of acute transfusion reactions.

A
  • Acute haemolytic (ABO incompatibility)
  • Allergic/anaphylaxis
  • Infection (bacterial)
  • Febrile non-haemolytic
  • Respiratory (TACO, TRALI)

TACO - Transfusion associated cardiovascular overload
TRALI - Transfusion related acute lung injury

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3
Q

List some causes of delayed transfusion reactions.

A
  • Delayed haemolytic transfusion reaction
  • Infection (viral, malaria, vCJD)
  • TA-GvHD
  • Post-transfusion purpura
  • Iron overload
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4
Q

What are some early clinical signs that might be suggestive of acute transfusion reaction?

A
  • Rise in temperature
  • Tachycardia
  • Fall in BP

NOTE: these can occur before the patient experiences any symptoms

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5
Q

List some symptoms of an acute transfusion reaction.

A
  • Fever
  • Rigors
  • Flushing
  • Vomiting
  • Dyspnoea
  • Pain at transfusion site
  • Chest pain
  • Urticaria and itching
  • Collapse
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6
Q

If the patient is unconscious, how might you detect an early transfusion reaction?

A
  • Baseline temperature, pulse, RR and BP before transfusion
  • Repeat every 15 mins (most reactions start within 15 mins)
  • Repeat hourly and at the end of the transfusion
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7
Q

What are the clinical features of a febrile non-haemolytic transfusion reaction?

A
  • Occurs during/soon after transfusion (of blood or platelets)
  • Rise in temperature, chills and rigors

Unpleasant, but not life-threatening

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8
Q

What causes febrile non-haemolytic transfusion reactions?

A

Release of cytokines from white cell during storage

NOTE: this used to be common before blood was leucodepleted

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9
Q

How is febrile non-haemolytic transfusion reaction treated?

A

Slow/stop the transfusion and treated with paracetamol

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10
Q

Describe the clinical features of an allergic transfusion reaction.

A
  • Mild urticarial or itchy rash
  • Sometimes causes a wheeze

Common especially with plasma transfusions

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11
Q

How is an allergic transfusion reaction managed?

A
  • Stop or slow the transfusion
  • IV antihistamines
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12
Q

What usually causes allergic transfusion reactions?

A

Allergy to donor plasma proteins

NOTE: it is more common in patients with a history of atopic disease and it may not recur

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13
Q

List some symptoms of an acute haemolytic transfusion reaction.

A

Symptoms

  • Chest/loin pain
  • Fever
  • Vomiting
  • Flushing
  • Collapse
  • Haemoglobinuria (later)

Obs

  • Low BP
  • High HR
  • High Temp
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14
Q

In an acute haemolytic transfusion reaction, why is it important to take a blood sample?

A

Send for FBC, biochemistry, coagulation, repeat X-match and DAT

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15
Q

What is the cause of acute haemolytic transfusion reaction?

A

Tranfusion of wrong ABO blood group leading to IgM-mediated intravascular haemolysis

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16
Q

How does bacterial contamination from donated blood products present?

A

Similarly to sepsis/ABO mismatch

  • Fever
  • Vomiting
  • Flushing
  • Collapse

Obs (shock)

  • Low BP
  • Increased HR
  • Increased temperature
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17
Q

What happens when bacteria infect donated blood products?

A
  • Bacteria can produce an endotoxin that causes immediate collapse
  • The bacteria could have come from the donor or from the processing of blood products
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18
Q

List blood products in order of likelihood of getting contaminated?

A
  • Platelets (most likely)
  • RBCs
  • Plasma (least likely)
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19
Q

What measures can be taken to reduce the likelihood of bacterial contamination?

A
  • Donor questioning
  • Arm cleaning
  • Diversion of first 20 mL into a pouch
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20
Q

Describe the storage and shelf-life of RBCs.

A
  • Stored in 4 degree fridge for 35 days
  • If kept out for >30 mins -> cannot be re-stored
  • Complete transfusion must take place within 4.5 hours of leaving the fridge
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21
Q

Describe the storage and shelf-life of platelets.

A

Stored at 22 degrees for 7 days

NOTE: they are screened for bacteria before release

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22
Q

What are clincial features of anaphylactic reaction to blood products.

A

Severe and life-threatening reaction that starts soon after start of transfusion

  • Occurs within seconds/minutes
  • Drop in BP
  • Rise in HR
  • Very breathless with a wheeze
  • Laryngeal or facial oedema

NOTE: most allergic reactions to blood products are not this severe

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23
Q

What is the mechanism of anaphylactic reaction to blood products?

A

Caused by IgE-mediated mast cell degranulation

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24
Q

Which patient group is more likely to have severe allergic reactions to blood products?

A

IgA deficient patients - anti-IgA antibodies may develop in response to exposure to IgA in donor’s blood

Most likely to occur with plasma transfusion

25
Q

What are the signs of transfusion associated circulatory overload (TACO)? When does it present?

A

Signs are due to pulmonary oedema/fluid overload

  • SoB
  • Low oxygen saturations
  • High HR
  • High BP
  • Raised JVP

Usually caused by a lack of attention to fluid balance (especially in cardiac failure, hypoalbuminaemia, extremes of age)

Presents within 6 hours of transfusion

NOTE: this is the most common pulmonary complication to transfuson

26
Q

What are the CXR features of TACO?

A

Fluid overload

Cardiac failure

27
Q

What are the main clinical features of TRALI?

A

Looks like ARDS

  • SoB
  • Drop in oxygen saturation
  • Rise in HR
  • Rise in BP
28
Q

What CXR features would you expect to see in TRALI?

A

Bilateral pulmonary infiltrates within 6 hours of transfusion, NOT due to circulatory overload and other causes.

29
Q

Outline the mechanism of TRALI.

A
  • Anti-WBC antibodies (HLA or neutrophil) in donor blood interact with WBC in the patient
  • Results in release of neutrophil proteolytic enzymes and toxic oxygen metabolites in the pulmonary vasculature
  • This leads to lung damage

Mechanism actually not fully understood

30
Q

What are the main differences between TACO and TRALI?

A

JVP - raised in TACO, not in TRALI
Furosemide - response in TACO, not in TRALI

31
Q

How can TRALI be avoided?

A

Using male donors (haven’t been pregnant) who haven’t had a transplant or transfusion so they will not have produced antibodies against HLA

32
Q

What is alloimmunisation?

A
  • The process of developing antibodies against an antigen
  • 1-3% of people receiving transfusions will develop antibodies against an RBC antigen that they lack
33
Q

What are the consequences of alloimmunisation with regards to blood transfusions?

A

Delayed haemolytic transfusion reaction
- Repeat transfusion with blood containing the antigen will lead to extravascular haemolysis

  • This is IgG mediated so will take 5-10 days
34
Q

What are the typical blood test results you expect to see during a haemolytic episode?

A
  • High bilirubin
  • Low haemoglobin
  • High reticulocytes
  • High LDH
  • Positive DAT
  • Haemoglobinuria (for a few days until haemolysis stops)

NOTE: U&E should be tested to check for renal failure. Also group and screen should be repeated to check for the development of new antibodies

35
Q

In which patient groups is CMV dangerous?

A
  • Very immunosuppressed (e.g. SCT)
  • Pregnant women
  • Neonates

Usually removed by routine leukodepletion

36
Q

What is the dangerous effect of parvovirus infection?

A

Causes temporary red cell aplasia

37
Q

Which patients are most affected by parvovirus infection?

A
  • Foetuses
  • Patients with haemolytic anaemia (e.g. sickle cell disease)
38
Q

What precaution can be made by blood donation services to prevent transmission of vCJD?

A

Blood services exclude people who have had transfusions in the past as donors.

39
Q

Describe the mechanism of transfusion-associated GvHD

A
  • Donor blood will contain some lymphocytes that are capable of dividing
  • Normally, the patient’s immune system will recognise and destroy these foreign lymphocytes
  • In the very immunosuppressed patients, the donor lymphocytes are not destroyed
  • They begin to recognise patient HLA as foreign and begins attacking it
  • This damages the gut, liver, skin and bone marrow

NOTE: this is always fatal

40
Q

What are the clinical manifestations of transfusion-associated Graft-versus-Host disease?

A
  • Severe diarrhoea
  • Liver failure
  • Skin desquamation
  • Bone marrow failure

Death then occurs within weeks to months

41
Q

How can transfusion-associated graft-versus-host disease be prevented?

A

Irradiate blood components for very immunocompromised patients
(or HLA matched blood components)

42
Q

At what point after transfusion does post-transfusion purpura happen?

A

7-10 days after transfusion of platelets or red blood cells

NOTE: it usually resolves in 1-4 weeks but can cause life-threatening bleeding

43
Q

Which patient group tends to be affected by post-transfusion purpura (PTP)?

A
  • HPA-1a negative patients who have previously been immunised by pregnancy or transfusion
  • These patients produce anti-HPA-1a antibodies
  • These then attack donor AND patient platelets
44
Q

How is post-transfusion purpura treated?

A

IVIG

45
Q

How much iron is there in a unit of blood?

A

200-250 mg

46
Q

How can iron overload be prevented?

A

Iron chelators (e.g. desferrioxamine)

Used when once ferritin >1000

47
Q

What are the consequences of iron overload?

A

End organ damage affectin heart, liver, endocrine organs

48
Q

What is haemolytic disease of the foetus and newborn?

A

Anaemia and high bilirubin in the newborn caused by delayed haemolytic reaction from maternal antibodies

NOTE: anti-D is the most important antibody for causing haemolytic disease of the newborn

49
Q

What are some complication haemolytic diease of foetus and newborn?

A
  • Severe foetal anaemia
  • Hydrops fetalis
  • Kernicterus
50
Q

When should all women have a group and screen during pregnancy?

A
  • 12 weeks (booking)
  • 28 weeks
51
Q

If anti-D antibodies are detected in a pregnant women, what further steps should be taken?

A
  • Check if the father has the antigen
  • Monitor the level of antibody
  • Check cffDNA
  • Monitor foetus for signs of anaemia (MCA doppler ultrasound)
  • Deliver the baby early because it gets a lot worse around term
52
Q

What intervention may be performed if the foetus is found to be very anaemic?

A

Intrauterine transfusion into the umbilical vein

53
Q

How can haemolytic disease of the newborn be prevented?

A
  • If an RhD-negative woman of childbearing age needs a blood transfusion, always use RhD-negative blood
  • Prophylactic anti-D given 28 and 34 weeks gestation
  • IM anti-D can be given at times of possible sensitising events

NOTE: for anti-D immunoglobulin to be effective, it needs to be given within 72 hours of a sensitising event and it does not work if the mother has already developing anti-D antibodies

54
Q

Outline the mechanism of action of anti-D immunoglobulin.

A
  • RhD-positive cells of the foetus get coated by exogenous anti-D
  • These will then be removed by the mother’s reticuloendothelial system (spleen) before they can sensitise the mother’s immune system
55
Q

List some occasions in which anti-D immunoglobulin should be given.

A
  • At delivery if the baby is found to be RhD-positive
  • Spontaneous miscarriages if surgical evacuation was needed
  • Surgical termination of pregnancy
  • Amniocentesis and chorionic villous sampling
  • Abdominal trauma
  • External cephalic version
  • Stillbirth or intrauterine death
56
Q

What doses of anti-D tend to be given?

A

Less than 20 weeks = 250 iU

More than 20 weeks = 500 iU

57
Q

Which test is done if a sensitising event occurs >20 weeks to determine if more anti-D is needed?

A

Kleihauer test

58
Q

When should anti-D be routinely given to RhD-negative women?

A

500 iU at 28 weeks and 34 weeks
OR
1500 iU at 28-30 weeks

59
Q

List some other antibodies (aside from RhD) that can cause haemolytic disease of the newborn.

A
  • Anti-c and anti-Kell can cause severe HDN (less severe than RhD)
  • Anti-Kell causes haemolysis and reticulocytopaenia in the foetus
  • IgG anti-A and anti-B can cause mild HDN in group O mothers (usually treated with phototherapy)

YEAR 5: Haematology PM (18 decks)

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