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Year 5 - Pathology > HAEM: Blood transfusion > Flashcards

HAEM: Blood transfusion Flashcards

1
Q

Which two ways help determine ABO blood groups?

A
  • Determined by
  • (1) antigens on RBC membrane,
  • (2) naturally occurring IgM in the plasma
    • IgG reacts against atypical RBC antigens
    • IgM reacts against normal RBC antigens
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2
Q

Apart from ABO, list some other blood group antigens.

A
  • Other blood group antigens – Kell (K), M, N, S, Duffy (Fy), Kidd (Jk)
    • Duffy and Kidd are known for causing delayed transfusion reactions
    • The level of anti-Duffy and anti-Kidd decline with age
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3
Q

What is the consequence of giving ABO incompatible blood vs other antigen incompatible(e.g. Duffy and Kidd)?

A

ABO - Massive intravascular haemolysis

Duffy and Kidd - delayed transfusion reaction, but the antibodies against these decline with age

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4
Q

What % of population are RhD -ve?

A

15% (85% are RhD positive)

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5
Q

What is the consequence of giving RhD +ve to an RhD-ve patient?

A

Will sometimes induce formation of Anti-D this does not cause any acute problem and will be picked up by the lab next time they need blood

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6
Q

What is the problem of making anti-RhD in pregnancy and having an RhD-ve fetus?

A

Anti-D made by an Rh -ve mother exposed to Rh +ve blood –> haemolytic disease of the newborn or severe fetal anaemia and heart-failure (hydrops fetalis) in RhD -ve females of child bearing potential

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7
Q

What is the difference between crossmatch and group and save?

A

GROUP and SCREEN – check ABO group and plasma antibodies in patient (done each time it is requested for that patient)

Full crossmatch – checks patient’s blood against donor blood specifically

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8
Q

How is blood GROUP testing carried out?

A
  • (1) Use known anti-A, anti-B and anti-D reagents against the patient’s RBCs
  • (2) Reverse group: known A and B groups red blood cells are mixed with the patient’s plasma (IgM antibodies)
    • This group acts as an internal control – if it does not match, this is an anomalous result
    • New-borns often have a weak reverse group as their ABs have not developed fully yet
  • A positive result causes agglutination at the top
  • A negative result will mean that the red cells stay suspended at the bottom of the vial
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9
Q

How is blood SCREEN carried out?

A
  • Antibody screen on patient’s plasma – avoid a delayed transfusion reaction with _IgG_ antibodies…
    • (1) use 2 or 3 reagent RBCs containing all important RBC antigens between them
    • (2) incubate patient’s plasma and screening cells using the Indirect Antiglobulin Technique (IAT)
      • (a) Patient serum containing specific antibody added to reagent RBCs
      • (b) Add Anti-Human Globulin (AHG) to promote agglutination
      • (c) If +ve, reaction creates bridges between RBCs coated in IgG antibodies à visible clumps
      • https://youtu.be/PozNhjmxvG0?t=44 = good distinction of the types of Coomb’s test!
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10
Q

Why do you do a group and save every time?

A

SCREEN: Antibody screen:

It is impossible to test for all RBC antigens

1-3% of patients have developed antibodies to >1 RBC antigens (i.e. due to previous transfusion or pregnancy)

Immune antibodies are IgG - these can cause a DELAYED transfusion reaction; extravascular haemolysis (As opposed to naturally occurring IgM antibodies that cause an IMMEDIATE intravascular haemolysis)

A 10-cell panel is used to identify RBC antibodies

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11
Q

What kind of panel and how many components are used in antibody screening in blood?

A

10-cell panel is used

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12
Q

How is SEROLOGICAL crossmatching done? Which method is only done in emergency?

A
  • Serological crossmatching:
    • Full Crossmatch (uses IAT):
      • Patient’s plasma is incubated with donor red cells at 37 degrees for 30-40 mins
      • Detects antibody-antigen reaction that destroys the RBCs leading to extravascular haemolysis
      • Add antiglobulin reagent to cause cross-linking
      • IgG antibodies bind to RBCs but do not crosslinking (why the AHG added in an IAT test)
    • Immediate Spin [EMERGENCY Scenario Only]:
      • Incubate patient’s plasma and donor red cells for 5 minutes only and spin
      • Will only detect ABO incompatibility
      • IgM anti-A and/or anti-B bind to RBCs, fix complement and lyse the cell
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13
Q

When is Kell antigen negative blood specifically given?

A

Women of child-bearing age

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14
Q

What is the traceability tag on blood?

A

Allows for 100% traceability from donor to recipient

Kept for 30 years

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15
Q

What is the use of ELECTRONIC crossmatch?

A

Compatibility of blood determined by IT system without physical testing of donor cells against plas,a

This is quick and less staff involved and better stock management

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16
Q

What are the pillars of blood transfusion?

A
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17
Q

How quickly is each blood component given and how is each stored?

A
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18
Q

What are the indications for a blood transfusion in a patient?

A
  • Is the patient bleeding?
  • What are the blood results?
  • Is the patient symptomatic?
  • Will a transfusion solve the problem?
  • What are the risks of transfusion?
  • Are there alternative treatments?
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19
Q

If the patient is male, what blood is given in an emergency?

A

O positive

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20
Q

Why is plasma tranfusion given quicker?

A
  • The reason platelets need to be given more quickly is because they are stored at room temperature and so bacteria can contaminate it quite quickly –> if patient develops a temperature stop the platelets and take blood cultures
    • The platelets should then be sent back to the lab for microbiological testing
  • A reaction with plasma is more likely to be allergic as plasma is frozen and so is unlikely to be contaminated by microbes
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21
Q

Which component should be compatible when giving RBC/ platelets/ plasma? How long can thawed FFP be used vs cryoprecipitate?

A

FFP - kept for 24hrs once thawed, kept at 4oC

Cryo - used over 24, kept at RT

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22
Q

Describe the MSBOS.

A

MSBOS = maximum surgical blood ordering schedule

  • Based on negotiation between surgeons and transfusion lab about predictable loss for planned surgery
  • Some operations rarely need blood whereas others will always need blood (e.g. AAA repair)
  • For elective surgery, the patient should be group and screened before the operation
  • If antibodies are not present, a crossmatch is NOT needed but the sample should be saved in the fridge
  • If unexpected need for blood –> provided <10 mins (by electronic issue as no antibodies are present)
  • If antibodies are present, ALWAYS CROSSMATCH
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23
Q

What are the indications and triggers for RBC transfusions?

A
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24
Q

What are the indications and triggers for platelet transfusion? When is this transfusion best given?

A

During the procedure

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25
Q

What are the contraindications to platelet transfusion?

A
  • Contraindications:
    • Heparin-induced thrombocytopaenia and thrombosis
    • Thrombotic thrombocytopenic purpura (TTP)
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26
Q

What rise in plt does 1 unit of platelets cause?

A
  • 1 unit of platelets –> increase platelet count by 30-40 x 109/L

Platelet dysfunction can be caused by drugs (e.g. aspirin, clopidogrel)

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27
Q

What are the indications and triggers for FFP transfusion?

A

NB: no longer just collected from non-UK donors

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28
Q

What is best used for transfusion when trying to reverse warfarin?

A

Not FFP - this contains all clotting factors

Prothrombin complex concentrate (PCC) - contains factors 2, 7, 9, 10

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29
Q

Which blood components are GROUP matched but not crossmatched?

A

Platelets and FFP

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30
Q

How are blood bottles labelled?

A

At the bedside

Hand-written labels

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31
Q

What instances can patients get their own blood during a surgery?

A
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32
Q

When is CMV negative/irradiated/washed blood used?

A
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33
Q

When can O positive blood be given in an emergency?

A

Females over 50 and males

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34
Q

What can be given instead of blood in a major transfusion lasting <3 hours? When is this contraindicated? What is done is these steps do not work?

A

TXA 1g bolus followed by 1g over 8 hours

Contraindicated in GI bleeding

If bleeding continues give 1:1 RBC:FFP usually 4 units of each. Fibrinogen concentrate 50mg/kg if more than 4 units of blood transfused.

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35
Q

List some types of acute reactions (<24 hours) with blood transfusion.

A
  1. Acute haemolytic (ABO incompatible)
  2. Allergic/anaphylaxis
  3. Infection (bacterial)
  4. Febrile non-haemolytic
  5. Respiratory
    1. Transfusion associated circulatory overload (TACO)
      • MOST COMMON ACUTE REACTION
      • 1 in 100,000 mortality risk (very preventable)
      • Often pre-existing cardiac/respiratory problems
    2. Acute lung injury (TRALI)
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36
Q

List some examples of delayed transfusion reactions (>24 hours).

A
  • Delayed haemolytic transfusion reaction (antibodies) – Duffy and Kidd
  • Infection (viral, malaria, vCJD)
  • TA-GvHD (week or 2 after transfusion)
  • Post transfusion purpura
  • Iron overload
37
Q

What is SHOT and how does it divide transfusion reaction?

A

SHOT - serious hazard of trasfusion

  1. Non-preventable pathological reactions
  2. Preventable reactions (through improved practice)
  3. Adverse events caused by error
38
Q

What are the FIRST signs of an acute reaction?

A
  • Rise in temperature or pulse
  • Drop in BP
39
Q

What are 5 other general symptoms of acute reaction to transfusion?

A
  • Fever
  • Rigors
  • Flushing
  • Vomiting
  • Dyspnoea
  • Pain at transfusion site
  • Loin pain/chest pain
  • Urticaria
  • Itching
  • Headache
  • Collapse
40
Q

If the patient is unconscious how do you detect the transfusion reaction?

A
  • MONITORING
    • Baseline temperature, pulse, RR, BP before transfusion
    • Repeat after 15 mins (most reactions start within 15 mins)
    • 0min–> 15m–> 1hr –> 1hr… –> end
    • Repeat hourly and at the end of the transfusion
41
Q

What is FNHTR and when does it occur? Why is it less common now? How is it treated?

A

Febrile Non-Haemolytic Transfusion Reaction = MILD/MODERATE

  • Occurs during/soon after transfusion (blood or platelets)
  • May cause a rise in temperature by around 1 degree, chills and rigors
    • Common before blood was leucodepleted (now rarer)
    • Caused by the release of cytokines from white cells during storage

Tx: transfusion stopped or slowed and may need to be treated with paracetamol

42
Q

Describe the cause of allergic transfusion reactions. When does it occur? Which patients? How is it treated?

A
  • Common, especially with plasma (proteins in plasma)
  • Causes a mild urticarial or itchy rash sometimes with a wheeze – caused by allergy to donor plasma proteins
  • Can occur during or after (even after patient has left) transfusion à transfusion usually stopped or slowed
  • Recipients have a history of atopy

Tx: IV antihistamines

43
Q

Describe the signs and symptoms associated with ABO incompatibility reactions. How severe is this reaction?

A

Symptoms and signs of acute intravascular haemolysis (IgM-mediated) - this is SEVERE/FATAL.

  • General:
    • restless,
    • chest/loin pain,
    • fever,
    • vomiting,
    • flushing,
    • collapse,
    • haemoglobinuria (later)
  • Monitoring:
    • Low BP,
    • High HR,
    • High Temperature
44
Q

What are 3 causes of ABO incompatibility reactions?

A
  • Failure of bedside check
  • Wrongly labelled blood sample
  • Laboratory error
45
Q

What is the management (incl investigations) for acute haemolytic reactions due to ABO incompatibility?

A
  • FBC
  • Biochemistry
  • Coagulation
  • Repeat X-match
  • Direct antiglobulin test (DAT)
46
Q

What are the signs and symptoms of bacterial contamination reactions in transfusion? How severe is this reaction?

A

Presents similarly to ABO mismatch - SEVERE/FATAL

General:

  • restless,
  • fever,
  • vomiting,
  • flushing,
  • collapse

Monitoring:

  • Low BP,
  • High HR,
  • High Temperature
47
Q

What is the source of bacterial contamination in blood and what causes this reaction? Which blood components are most likely to be contaminated?

A
  • Bacterial growth can cause endotoxin production which causes immediate collapse
  • 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)

Order of likelihood of contamination:

  • Platelets (stored at room temperature) > RBCs > FFP
48
Q

List 3 ways in which bacterial contamination of blood can be prevented.

A
  1. Donor questioning + arm cleaning + diversion of first 20 mL into a pouch (used for testing)
  2. Management of RBCs:
    • 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
  3. Platelet management:
    • Stored at 22 degrees
    • Shelf-life: 7 days
    • Screened for bacteria before release
49
Q

Describe the presentation of an anaphylaxis reaction to blood transfusion.

A

SEVERE/FATAL

Occurs soon after the start of transfusion:

  • Shock = Drop in BP + Rise in HR
  • Very breathless with wheeze
  • Often laryngeal and/or facial oedema
50
Q

What is the mechanism of anaphylaxis reaction in blood transfusion? When are these reactions likely to be more severe?

A

IgE mediated - IgE antibodies in the patient cause mast cell degranulation

Usually not severe, except in the case of IgA deficiency (common 1 in 600, in 25% anti-IgA antibodies form when exposed from donor, only a minority have a severe reaction)

51
Q

What is the pathophysiology of TACO? How severe is it? What are 5 clinical features?

A

Trasnfusion associated cirulatory overload (TACO); moderate/severe/fatal and is common (1 in 100,000)

Cause: lack of attention to fluid balance, RF such as cardiac impairment, renal impairemnt, hypoalbuminaemia, very young/old.

Clinical features:

  • CXR (fluid overload)
  • SoB
  • Low O2 saturations
  • Fluid overload
  • High HR
  • High BP
  • Cardiac failure
52
Q

What is TRALI in blood transfusion reaction? When is it more common(what component)? What are 5 clinical features? What is seen on CXR?

A

TRALI = transfusion related acute lung injury; looks like ARDS (more common in FFP or platelet transfusion); no clinical fluid overload; SEVERE/FATAL.

  • Clinical features:
    • SoB
    • Low O2 saturations
    • Fever
    • High HR
    • High BP
  • CXR = bilateral pulmonary infiltrates during/within 6 hours of transfusion due to circulatory overload and other causes
53
Q

What is the mechanism of TRALI?

A

Mechanism:

  • Anti-WBC antibodies in donor blood
  • These interact with WBCs in the patient
  • Aggregates WBCs stick to pulmonary capillaries –> release neutrophil proteolytic enzymes and toxic O2 metabolites –> lung damage (however, this mechanism is incompletely understood)
54
Q

What is the managemnt of TACO?

A

Diuretics (immediately responds to these if TACO is the cause, raised JVP initially)

TRALI does NOT resoond to diuretics (no JVP)

55
Q
A
56
Q

Which DONORS should you use for plasma/platelets? Why?

A

MALE donors

no pregnancy or previous transfusions, so no HLA/HNA ABs

57
Q

Which delayed reaction is most common? What is the mechanism? When does the reaction to occur?

A

Delayed haemolytic transfusion reaction - caused by Duffy and Kidd antigens and others

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

Further transfusions with RBCs expressing same antigens –> antibodies will lyse RBCs (extravascular haemolysis)

This is IgG-mediated so takes 5-10 days

58
Q

What investigations are done for delayed haemolytic transfusion reaction? What is a complication of this? What is the management?

A
  1. Haemolysis Tests:
    • High bilirubin
    • Low Hb
    • High reticulocytes
    • Haemoglobinuria over a few days
    • Test U&E because it can cause renal failure
  2. Repeat the group and screen and look for new antibodies that may have been made against the transfused red cells

NB: Patients on admission after transfusion will have haematuria/dark urine and Hb will be lower than it was before the transfusion.

59
Q

What type of antibody are anti-A and anti-B vs anti-Rh, anti-Duffy and anti-Kidd?

A

Anti-A/B - IgM

Others are IgG

60
Q

What are 3 examples of dealyed infections due to blood transfusion?

A

Malaria

Viral infections

Variant CJD (Mad Cow Disease)

61
Q

When does CMV occur following blood transfusion in patients? Which patients get CMV negative blood? How do you prevent CMV in blood?

A
  • Very immunosuppressed patients (e.g. stem cell transplant) can get fatal CMV disease
  • CMV -ve products are only given to pregnant women and neonates
  • Leucodepletion/irradiation removes CMV in WBCs (‘washing’ done for IgA deficient patients)
62
Q

When does parvovirus occur following blood transfusion in patients? What are the complications of this infection?

A
  • Affects foetuses and patients with haemolytic anaemias (e.g. sickle cell, hereditary spherocytosis)
  • Causes temporary red cell aplasia – so affects those with RBCs of a shortened life span
63
Q

How do we prevent CJD in blood?

A
  • NO TEST
  • Blood services exclude transfused patients as donors as a precaution
64
Q

How soon after transfusion does transfusion associated GvHD occur? How severe is it?

A
  • Rare but ALWAYS FATAL (can take weeks to months to come on after transfusion)
65
Q

What is the pathophysiology of transfusion associated 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 patient’s tissue HLA antigens as foreign and attack (gut, liver, skin and bone marrow)
66
Q

What are the features/complications of transfusion associated GvHD?

A
  • Diarrhoea
  • Liver failure
  • Skin desquamation
  • Bone marrow failure
  • DEATH
67
Q

How do you prevent transfusion assciated GvHD in patients?

A

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

68
Q
A
69
Q

When does post-transfusion purpura occur? Which patients are most affected by post-transfusion purpura?

A
  • Appears 7-10 days after transfusion of blood or platelets and usually resolves in 1-4 weeks but can cause life-threatening bleeding
  • Affects Human Platelet Antigen (HPA) 1a -ve patients previously immunised via pregnancy or transfusion (HPA-1a AB)
70
Q

What is the management of post-transfusion of blood or platelets?

A

IVIG

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

Exact mechanism is unkown

71
Q

What are the consequences of immune modulation (delayed reaction post transfusion)?

A

Possible increased rate of infections post-operatively and increased recurrence of cancer in patients who have blood transfusions however, the evidence is conflicting

72
Q

How much iron is in each unit of blood? What are the consequences? How is it treated?

A

200-250mg of iron per unit of blood

Damage to liver, heart and endocrine organs.

Requires chelation

73
Q

How do anti-RhD antibodies form in -ve patients?

A
  • By receiving blood transfusions
  • In pregnancy (foetal red cells enter the mother’s circulation during pregnancy or at delivery)
74
Q

What kind of consequences are there in pregnancy of RhD antibodies?

A
  1. 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
  2. In a subsequent pregnancy, if the mother has another RhD-positive foetus, the antibodies will destroy foetal red cells leading to severe anaemia ± HDN

Consequences:

  • Foetal anaemia (haemolytic)
  • Haemolytic disease of the newborn (anaemia, high BR à builds up after birth as not removed by placenta)
75
Q

Which antibodies can cross the placenta?

A

Only IgG

76
Q

How much should Hb rise per litre of blood?

A

10g/L increase in Hb

77
Q

How do we prevent haemolytic disease of the newborn? Will there be a problem if the foetus is RhD-ve?

A
  1. MOTHER: All women have a group and screen at around 12 weeks (booking) and again at 28 weeks; if there is an antibody against red cell antigens present then levels should be checked (high/rising suggests it is more likely to affect the foetus)
  2. FATHER: Check if the father has the antigen (and hence whether the baby could inherit it)
  3. FOETUS: Check ffDNA sample (allows identification of the baby’s RhD group) – if baby is RhD -ve, there’s no problem; monitor foetus for anaemia (MCA Doppler ultrasound); the baby may need to be delivered early because HDN gets a lot worse in the last few weeks of pregnancy
78
Q

How can the foetus be monitored for anaemia in the presence of anti-RhD antibodies in the mother?

A

MCA Doppler Ultrasound (NB: because IgG is crossing the placenta)

79
Q

How are intrauterine transfusions done and when?

A
  • The transfusion is done via the umbilical vein

NB: monitor baby’s Hb and BR for several days after delivery as HDN can get worst; may need exchange transfusion if BR too high or Hb too low (phototherapy can help reduce BR)

80
Q

If the foetus gets HDN, what is the prognosis for subsequent pregnancies?

A

Subsequent pregnancies usually fare WORSE

81
Q

What is the best prevention strategy for HDN? When do these not work?

A
  • If an RhD -ve woman of childbearing age needs a blood transfusion, ALWAYS give RhD -ve blood
  • IM injection of anti-D immunoglobulin can be given at times when the mother is at risk of sensitisation
    • ​For this to be effective, the anti-D injection must be given within 72 hours of the sensitising event
    • It does NOT work if the mother has already been sensitised and developed anti-D in the past
82
Q

What is the mechanism of anti-D immunoglobulin action?

A
  • The RhD +ve 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
  • For this to be effective, the anti-D injection must be given within 72 hours of the sensitising event
  • It does NOT work if the mother has already been sensitised and developed anti-D in the past
83
Q

List 4 different sensitising events for anti-RhD development.

A
  • At delivery if the baby is RhD positive
  • Foeto-maternal haemorrhage is likely to occur (and you do NOT know the Rh status of the baby)
    • Spontaneous miscarriages if surgical evacuation needed and therapeutic terminations
    • Amniocentesis and chorionic villous sampling (CVS)
    • Abdominal trauma (falls and car accidents)
    • External cephalic version (turning foetus)
    • Stillbirth or intrauterine death
84
Q

What doses of anti-D are given in different events?

A
  • Doses of Anti-D:
    • At least 250IU (for events <20w gestation)
    • At least 500IU (for events >20w gestation)
      • Sometimes a larger does is needed for larger bleeds

A foeto-maternal haemorrhage test (Kleihauer test) done if >20w gestation and at delivery, to determine if more anti-D is needed than the standard dose if the foetal bleed is large

85
Q

How do you calculate the anti-D necessary to prevent sensitisation from FMH event?

A
86
Q

Why has RAADP (rotine antenatal anti-D prophylaxis) been introduced?

A

1% will become anti-D sensitised with no obvious event so anti-D prophylaxis is given to prevent this:

  • 1 large dose (1,500IU) at 28w
  • 2 smaller doses (500, 500 IU) at 28w and 34w
87
Q

Which other antibodies can cause severe HDN?

A

Anti-C and anti-kell but usually less severe than anti-D - Kell causes reticulocytopenia in the foetus as well as haemolysis

IgG anti-A/B from group O mothers - usually treated with phototherapy

88
Q
A
89
Q

What is cffDNA testing? When is the earliest it can be done?

A

Rapid, non-invasive service for prediction of fetal D, C, c, E and K status, using cell-free foetal DNA in maternal blood for women who have allo-antibodies - can be done from 11+2 weeks gestation + results available in 10 days

Upon identification, mothers can be informed and prepared for further careful monitoring

Also identifies pregnant women who have antigen -ve foetuses and who therefore are not at danger from HDFN- then no anti-D needed

Year 5 - Pathology (89 decks)

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