Blood transfusion 2 Flashcards

1
Q
  1. What is the difference between acute and delayed transfusion reactions?
A

Acute < 24 hours

Delayed > 24 hours

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2
Q
  1. List some causes of acute transfusion reactions.
A
Acute haemolytic (ABO incompatibility)
Allergic/anaphylaxis 
Infection (bacterial)
Febrile non-haemolytic 
Respiratory (TACO and TRALI)
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3
Q
  1. 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

Transplant-associated circulatory overload (TACO)

A
  1. What is the most common transfusion reaction?
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5
Q
  1. What are some early features that might be suggestive of acute transfusion reaction?
A

Rise in temperature or pulse
Fall in BP
NOTE: these can occur before the patient experiences any symptoms

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6
Q
  1. List some symptoms of an acute transfusion reaction.
A
Fever 
Rigors
Flushing 
Vomiting 
Dyspnoea 
Pain at transfusion site 
Collapse
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7
Q
  1. If the patient is unconscious, how might you detect an early transfusion reaction?
A

Baseline temperature, pulse, RR and BP before transfusion
Repeat ever 15 mins (most reactions start within 15 mins)
Repeat hourly and at the end of the transfusion

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8
Q
  1. 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
NOTE: this used to be common before blood was leucodepleted

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9
Q
  1. What causes febrile non-haemolytic transfusion reactions?
A

Release of cytokines from white cell during storage

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10
Q
  1. How is febrile non-haemolytic transfusion reaction treated?
A

Slow/stop the transfusion and treat with paracetamol

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11
Q
  1. Describe the clinical features of an allergic transfusion reaction.
A

Mild urticarial or itchy rash

Sometimes causes a wheeze

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12
Q
  1. How is an allergic transfusion reaction managed?
A

Stop or slow the transfusion

IV antihistamines

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13
Q
  1. What usually causes allergic transfusion reactions?
A

Allergy to plasma protein in the donor

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

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14
Q
  1. Which blood product is most likely to cause an allergic transfusion reaction?
A

Plasma

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15
Q
  1. List some symptoms of an acute haemolytic transfusion reaction.
A
Chest/loin pain 
Fever 
Vomiting 
Flushing 
Collapse 
Haemoglobinuria
Low BP 
High HR 
High Temp
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16
Q
  1. 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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17
Q
  1. How does bacterial contamination from donated blood products present?
A

Similarly to ABO mismatch

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18
Q
  1. What causes bacterial infection from 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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19
Q
  1. List blood products in order of likelihood of getting contaminated?
A

Platelets (MOST LIKELY)
RBCs
Plasma (least likely)

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20
Q
  1. 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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21
Q
  1. Describe the storage and shelf-life of RBCs.
A

Stored in a 4 degree fridge for 35 days
If it is kept out for > 30 mins it cannot go back in the fridge

Complete transfusion must take place within 4.5 hours of leaving the fridge

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22
Q
  1. Describe the storage and shelf-life of platelets.
A

Stored at 22 degrees for 7 days

NOTE: they are screened for bacterial before release

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23
Q
  1. Describe the clinical features you would expect to see in an anaphylactic reaction to blood products.
A

Occurs soon after starting transfusion
Drop in BP
Rise in HR
Very breathless with a wheeze
Laryngeal or facial oedema
NOTE: it is caused by IgE-mediated mast cell degranulation
NOTE: most allergic reactions are not this severe

24
Q
  1. 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)

25
Q
  1. What causes TACO and what are the main clinical features?
A
Usually caused by a lack of attention to fluid balance (especially in cardiac failure, hypoalbuminaemia, extremes of age) 
Leads to pulmonary oedema 
SOB 
Low oxygen saturations 
High HR 
High BP 
NOTE: this is very common
26
Q
  1. What are the CXR features of TACO?
A

Fluid overload

Cardiac failure

27
Q
  1. 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
  1. What CXR features would you expect to see in TRALI?
A

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

29
Q
  1. Outline the mechanism of TRALI.
A

Anti-WBC antibodies in donor blood interact with WBC in the patient
Aggregates of WBCs get stuck to pulmonary capillaries resulting in the release of neutrophil proteolytic enzymes and toxic oxygen metabolites
This leads to lung damage

30
Q
  1. What are the main differences between TACO and TRALI?
A

JVP is not raised and the patient will not respond to frusemide in TRALI

31
Q
  1. How can TRALI be avoided?
A

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

32
Q
  1. What is alloimmunisation?
A

The process of developing antibodies against an antigen

NOTE: 1-3% of people receiving transfusions will develop antibodies against an RBC antigen that they lack

33
Q
  1. What are the consequences of alloimmunisation with regards to blood transfusions?
A

Repeat transfusion with blood containing the antigen will lead to extravascular haemolysis
This is IgG mediated so will take 5-10 days

34
Q
  1. What are the typical blood test results you expect to see during a haemolytic episode?
A

High bilirubin
Low haemoglobin
High reticulocytes
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
  1. In which patient groups is CMV dangerous?
A

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

36
Q
  1. What is the dangerous effect of parvovirus infection?
A

Causes temporary red cell aplasia

37
Q
  1. Which patients are most affected by parvovirus infection?
A

Foetuses

Patients with haemolytic anaemias (e.g. sickle cell disease)

38
Q
  1. 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
  1. Describe the mechanism of transfusion-associated Graft-versus-Host Disease.
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 susceptible patients (very immunosuppressed), the lymphocytes are not destroys
They begin to recognise patient HLA as foreign and begins attacking it (damages the gut, liver, skin and bone marrow)
NOTE: this is always fatal

40
Q
  1. What are the clinical manifestations of transfusion-associated Graft-versus-Host Disease?
A
Diarrhoea 
Liver failure 
Skin desquamation 
Bone marrow failure 
Death (weeks to months)
41
Q
  1. How can transfusion-associated Graft-versus-Host Disease be prevented?
A

Irradiate blood components for very immunocompromised patients

42
Q
  1. Which patient group tends to be affected by post-transfusion purpura?
A

HPA-1a negative patients who have previously been immunised by pregnancy or transfusion

43
Q
  1. How is post-transfusion purpura treated?
A

IVIG

44
Q
  1. How can iron overload be prevented?
A

Iron chelators (e.g. exjade)

45
Q
  1. What is haemolytic disease of the newborn?
A

Anaemia and high bilirubin in the newborn

NOTE: the bilirubin builds up in the newborn after birth because they no longer have a placenta to remove it

46
Q
  1. When should all women have a group and screen during pregnancy?
A

12 weeks

28 weeks

47
Q
  1. 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

48
Q
  1. What intervention may be performed if the foetus is found to be very anaemic?
A

Intrauterine transfusion into the umbilical vein

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

49
Q
  1. 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
IM anti-D immunoglobulin 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

50
Q
  1. 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

51
Q
  1. 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

52
Q
  1. What doses of anti-D tend to be given?
A

Less than 20 weeks = 250 iU

More than 20 weeks = 500 iU

53
Q
  1. Which test is done if a sensitising event occurs > 20 weeks to determine if more anti-D is needed?
A

Kleihauer test

54
Q
  1. When should anti-D be routinely given to RhD-negative women?
A

Usually 500 iU at 28 weeks and 34 weeks

NOTE: can also be 1500 iU at 28-30 weeks

55
Q
  1. 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)