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Haematology - Path > Blood transfusion 1 & 2 > Flashcards

Blood transfusion 1 & 2 Flashcards

1
Q

What are the different blood groups, antibodies present and antigens present?

A

ABO groups are determined by

a) by the antigens (sugars) on the red cell membrane.
b) the naturally-occurring antibodies (IgM) in the plasma.

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2
Q

What will happen if you give someone the wrong blood?

A

If you give an ABO incompatible blood transfusion it will cause massive INTRAVASCULR haemolysis and this is potentially fatal

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3
Q

What are the differences between Rh negative and positive?

A

Red cells which carry the RhD antigen are ‘RhD positive’

•These patients can receive RhD negative (just a waste!) or RhD positive red cells

RhD negative patients lack the RhD antigen

  • These patients can make immune anti-D if exposed to RhD positive red cells
  • Immune anti-D antibodies are IgG, which do not cause direct agglutination of RBCs
  • so not immediate haemolysis & death,
  • but delayed haemolytic transfusion reaction;
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4
Q
  1. How is Anti-D formed?
  2. How can Anti-D be a problem for a fetus?
A
  1. Although giving RhD-positive blood to an RhD-negative patient 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. RhD-negative blood would then be issued.
  2. Immune Anti-D made by a Rh negative mother exposed to Rh positive blood, can cause haemolytic disease of the newborn or severe fetal anaemia and heart-failure (hydrops fetalis) in RhD-negative females of child bearing potential.
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5
Q

Despite Rh D, what are the other Rh antigens?

A

There are some other Rh antigens e.g. C, c, E and e

+ many other blood groups antigens e.g. Kell (K), M, N, S, Duffy (Fy), Kidd (Jk).

Duffy and Kidd are notorius for causing delayed haemolytic transfusion reactions. The antibody weans with time, so can be harder to pick up in older individuals

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6
Q

What proportion of the population is Rh negative and Rh positive?

A

85% of the population are RhD-positive and 15% RhD-negative

RhD-negative cells can safely be given to anyone

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7
Q
  1. before transfusion, always check ABO and RhD group, how is it done?
  2. What is a positive and negative result?
A
  • use known anti-A and anti-B and anti-D reagents against patient’s RBCs
  • And “reverse group”: known A and B group RBCs against patient’s plasma (IgM antibodies)
  1. Positive result: agglutination (clumping)

Negative result:Red cells stay suspended

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8
Q
  1. Why might someone have a immune RBC antibodies?
  2. Why must an antibody screen be done before transfusion?
A
  1. As a result of transfusion and/or pregnancy. Unlike the naturally-occurring antibodies associated with the ABO system, immune antibodies form on exposure to red cell antigens that are different to those expressed on the patient’s own RBCs.
  2. Must identify clinically significant RBC antibodies and transfuse RBCs that are negative for that antigen. The immune antibodies are important because they can form an antibody:antigen complex with the transfused red cells and this results in EXTRAVASCULAR HAEMOLYSIS in the spleen – a delayed haemolytic transfusion reaction
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9
Q
  1. How is an antibody screen done on a patient’s plasma?
  2. what is negative and what is a positive result?
A
  1. We screen the patient’s plasma for IgG antibodies by mixing with 2 or 3 reagent cells that, between them, express all the important red cell antigens. These reagent red cells are blood group O.

¨Screen by incubating the patient’s plasma and screening cells using IAT** technique

**INDIRECT ANTIGLOBULIN TECHNIQUE (bridges red cells coated by IgG, which can’t themselves bridge 2 red cells – to form a visible clump. Takes 30 mins’ incubation at 37°C)

2.

  • If there is an immune antibody the red cells will clump – POSITIVE SCREEN
  • If there is no antibody the red cells stay in suspension – NEGATIVE SCREEN
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10
Q

What blood is given to women of child-bearing age and why?

A

We give K-negative blood to women of childbearing potential because anti-K can cause HDFN. 85-90% of the population is K-negative.

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11
Q

How does serological crossmatch work?

A

Traditionally the donor cells were mixed with the patient’s plasma and incubated at 37°C and then an antiglobulin reagent added to see if there was any antigen:antibody interaction that made the blood INCOMPATIBLE. This is known as a SEROLOGICAL CROSSMATCH. It takes at least 40 minutes and is not suitable in an emergency.

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12
Q
  1. What is a electronic ‘crossmatch’?
  2. Why do this instead of serological crossmatch?
A
  1. Electronic issue (EI) is the selection and issue of red cell units where compatibility is determined by IT system, without physical testing of donor cells against patient plasma.

2.

  • Quicker
  • Fewer staff needed
  • No need to have blood standing by ‘just in case’
  • Remote issue
  • Better stock management
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13
Q

When and why do we give blood/components?

A

The decision to transfuse is based on the whole clinical picture

  1. Is the patient bleeding?
  2. What are the blood results?
  3. Is the patient symptomatic?
  4. Will a transfusion solve the problem?
  5. What are the risks of transfusion?
  6. Are there alternative treatments?
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14
Q

Describe checks needed, storage and transfusion for red cells, plasma and platelets

A
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15
Q

What are some transfusion indicators and triggers for transfusing red cells to a patient?

A

Transfusion indication:

  • Major blood loss - trigger = if 30% blood volume lost
  • Peri-op, critical care - trigger = Hb <70/L vs 80g/L
  • Post-chemo - trigger = Hb <80g/L - higher threshold as chemo patients don’t have the same reserves
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16
Q

What is maximum surgical blood ordering schedule?

A

Red cells often allocated to a patient but, if not used, are taken

back into stock…repeatedly.

So, MSBOS is based on negotiation between surgeons and

transfusion lab about predictable blood loss for ‘routine’ planned

Surgery.

Some operations rarely need blood – e.g: gall bladder op

Some operations always need blood – e.g: aortic aneurysm repair

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17
Q

Describe these special requirements and when they are required:

  1. CMV negative blood
  2. Irradiated blood
  3. Washed
A
  1. CMV negative blood - only required for intra-uterine and neonatal transfusions (new guidance 2012). Also for elective transfusion in pregnant women (baby in-utero is exposed to maternal transfusion)
  2. Irradiated blood - required for highly immunosupressed patients, who cannot destroy incoming donor lymphocytes: which can cause (fatal) transfusion associated graft versus host disease (TA-GvHD)
  3. Washed - red cells and platelets are only given to patients who have severe allergic reactions to some donors’ plasma proteins
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18
Q

What are some transfusion indicators and triggers for transfusing platelets to a patient?

A
  • Massive transfusion - trigger = aim plts >75x109/L
  • Prevent bleeding (post chemo) - trigger = if <10x109/L (<20 if sepsis)
  • Prevent bleeding (surgery) - trigger <50 x109/L (<100 if in critical site e.g. eye, CNS)
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19
Q

In what condition is platelet transfusion contraindicated?

A

Heparin-induced Thrombocytopenia Thrombosis (HiTT)

Thrombotic Thrombocytopenic Purpura (TTP)

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20
Q

What are some transfusion indicators and triggers for transfusing FFP to a patient?

A
  • Massive transfusion - trigger = blood loss >150ml/min
  • Disseminated intravascular coagulopathy - trigger = WITH bleeding
  • Liver disease and risk - trigger - PT ratio >1.5xnormal
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21
Q
  1. What clotting factors are in FFP?
  2. What is FFP not used for?
  3. What is the adult dose?
A

all clotting factors

However, FFP is not the treatment of choice to reverse warfarin: PCC (prothrombin complex concentrate) is (IX, II, X & bit of VII)

Adult dose is 15ml/kg

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22
Q

Are platelets and FFP crossmatched?

A

No, but the right group should be selected. Only red cells are crossmatched

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23
Q

What are some of the following adverse reactions to transfusions that can occur:

  1. Acutely <24 hours?
A

Acute

  1. Acute haemolytic (ABO incompatible)
  2. Allergic/anaphylaxis
  3. Infection (bacterial)
  4. Febrile non-haemolytic
  5. Respiratory
  • Transfusion associated circulatory overload (TACO)
  • Acute lung injury (TRALI)
24
Q

What are some of the adverse reactions that can happen after 24 hours? so delayed?

A
  1. Delayed haemolytic transfusion reaction (antibodies) -
  2. Infection -

viral, malaria, vCJD

  1. TA-GvHD - day 7 onwards
  2. Post transfusion purpura
  3. Iron overload
25
Q

What are the signs and symptoms of an acute reaction to a transfusion?

A
  • Many acute reactions start as: rise in temp or pulse, or fall in BP, even before patient feels symptoms
  • Symptoms: depends on cause, but can include:
  • Fever, rigors, flushing, vomiting, dyspnoea, pain at transfusion site, loin pain/ chest pain, urticaria, itching, headache, collapse etc

If unconscious, monitoring may be the only way to detect a reaction

26
Q

What is Febrile Non-haemolytic transfusion reaction?

What is the cause?

A
  • During / soon after transfusion (blood or platelets), rise in temperature of 1°C, chills, rigors
  • Common before blood was leucodepleted, now rarer
  • Have to stop or slow transfusion; may need to treat with paracetamol
  • Cause: White cells can release cytokines during storage
  • Mild/moderate reaction
27
Q
  1. What is allergic transfusion reactions?
  2. How is it treated?
  3. What is the underlying cause?
A
  1. Mild urticarial or itchy rash sometimes with a wheeze. During or after transfusion.

2.

  • Usually have to stop or slow transfusion
  • IV antihistamines to treat (and prevent in future, if recurrent)

Cause:

  • Common especially with plasma
  • Allergy to a plasma protein in donor so may not recur again, depending on how common the allergen is
  • Commoner in recipients with other allergies and atopy
28
Q
  1. What happens when someone is given the wrong blood? signs and symptoms?
  2. What should be done?
  3. Why does it occur?
A
  1. Symptoms and signs of acute intravascular haemolysis- IgM
  • Restless, chest/ loin pain, fever, vomiting, flushing, collapse, haemoglobinuria (later);
  • Can be severe/fatal
  • ↓BP & ↑HR (shock), ↑Temp

2.

  • Take samples for FBC, biochemistry,
  • coagulation, repeat x-match and Direct
  • Antiglobulin Test (DAT).
  • Discuss with haematology doctor ASAP

3.

  • Failure of bedside check giving blood
  • Wrongly labelled blood
  • Lab error
29
Q
  1. What happens when someone is given blood that has bacterial contamination?
  2. Why does it occur?
A
  1. Restless, fever, vomiting, flushing, collapse.

↓BP & ↑HR (shock), ↑Temp

2.

  • Bacterial growth can cause endotoxin production which causes immediate collapse

Where do bacteria come from?

  • From the donor (low grade GI, dental, skin infection)
  • Introduced during processing (environmental or skin)
  • Platelets >red cells > frozen components (storage temp)
30
Q

How can bacterial contamination of blood products be prevented?

A
  • Donor questioning + arm cleaning + diversion of first 20mL into a pouch (used for testing)
  • Red cells: Store always in controlled fridge 40C; shelf-life 35 days. If out for >½ hour, need to go back in fridge for 6 hours. Complete transfusion of blood within 4.5h of leaving fridge i.e. transfuse over 4hrs max
  • Platelets: stored at 220C; shelf-life 7 days (as now screened for bacteria before release)
  • All components: look for abnormalities e.g. clumps of discoloured debris; brown plasma etc
31
Q
  1. Describe what happens in anaphylaxis
  2. What is the mechanism of anaphylaxis?
  3. what happens in IgA deficiency?
A
  1. Anaphylaxis can happen in response to blood reactions:
  • “Severe, life-threatening reaction soon after start of transfusion”
  • •↓BP & ↑HR (shock),
  • •very breathless with wheeze,
  • •often laryngeal &/or facial oedema
  1. Mechanism:
    * IgE antibodies in patient cause mast cell release of granules & vasoactive substances. Most allergic reactions are not severe, but some can be e.g. in:
  2. IgA deficiency:
  • 1:300 - 1:700 (common); where in 25%, anti-IgA antibodies develop in response to exposure to IgA (transfusion – especially with plasma);
  • But only minority ever have transfusion reactions- frequency is 1:20,000 - 1:47,000.
32
Q
  1. What is transfusion associated circulatory overload?
  2. What are the signs and symptoms?
A
  1. TACO is a respiratory complication of transfusiom

2.

  • Transfusion associated circulatory overload = pulmonary oedema / fluid overload
  • Often lack of attention to fluid balance, especially in cardiac failure, renal impairment, hypoalbuminaemia; very young and very old.
    • 1 unit of blood may be enough to raise Hb in smaller patients
    • Clinical features: SOB, ↓O2 sats, ↑HR, ↑BP;
    • CXR: fluid overload / cardiac failure.
33
Q
  1. What is transfusion related acute lung injury (TRALI)? And signs and symptoms
  2. What is the mechanism?
  3. How can it be prevented?
A
  1. TRALI = acute lung injury/ARDS
  • SOB, ↓O2 sats, ↑HR, ↑BP; (similar to TACO)
  • CXR: bilateral pulmonary infiltrates during/within 6 hr of transfusion, not due to circulatory overload or other likely causes
  • Will not have a raised JVP and will not respond to furesomide unlike other resp conditions as a reaction to transfusion
  1. Mechanism
  • Anti-wbc antibodies (HLA or neutrophil Abs) in donor
  • Interact with corresponding ag on patient’s wbc’s
  • Aggregates of wbc’s get stuck in pulmonary capillaries → release neutrophil proteolytic enzymes & toxic O2 metabolites → lung damage
  • Mechanism not fully understood, antibodies don’t always cause problems

Prevention - male donors for plasma & platelets (no pregnancy or transfusion, so no HLA/HNA antibodies)

34
Q

Which blood product is at the highest risk of being contaminated by bacteria and why?

A

Platelets, then red blood cells and then FFP - based on the temperature they are stored at

35
Q

Define alloimmunisation

A

1-3% of all patients transfused develop an ‘immune’ antibody to a RBC antigen they lack

36
Q

What is extravascular hemolysis?

A

If the patient has another transfusion with RBCs expressing the same antigen, antibodies cause RBC destruction.

Can take 5-10 days to emerge as IgG reaction

37
Q

What will haemolysis tests show in delayed haemolytic transfusion reactions?

A
  • Haemolysis tests: increased bilirubin, decreased Hb, increased reticulocytes
  • haemoglobinuria over few days
  • Can become jaundiced
  • Test U&Es – as can cause renal failure

Check for new antibodies that may have formed causing this delayed reaction

38
Q

What are 3 transfusion transmitted infections? ( no donors with these infections currently can donate blood)

A
  • Malaria
  • Viral infection
  • Variant CJD
39
Q

What is the risk of getting the following infections from a transfusion (2017)

  • hepatitis B
  • HIV
  • hepatitis C
A
  • hepatitis B – 1 in 1.3 million
  • HIV – 1 in 6.5 million
  • hepatitis C – 1: 28 million
40
Q

Explain why the following infections need to be avoided in blood products:

CMV

Parvovirus

V-CJD

A

CMV – Very immunosuppressed (stem cell transplant) patients can get fatal CMV disease, but leucodepletion removes CMV (in wbc’s). Only give CMV negative now for pregnant women (fetus) & neonates.

Parvovirus – causes temporary red cell aplasia - affects fetuses and patients with haemolytic anaemias eg: sickle cell; hereditary spherocytosis

V-CJD – no test. Only 4 cases. but blood services exclude transfused patients as donors, as precaution. Also obtain plasma for those born after 01.01.1996, from outside the UK

41
Q
  1. What happens in transfusion associated graft-versus host disease (TaGVHD)
  2. what are the symptoms?
  3. How can it be prevented?
A

Rare, but always fatal

1.

  • Donor’s blood contains some lymphocytes (able to divide)
  • Normally, patient’s immune system recognises donor’s lymphocytes as ‘foreign’ and destroys them
  • In ‘susceptible’ patients (eg.. very Immunosuppressed) - lymphocytes not destroyed
  • Lymphocytes recognise patient’s tissue HLA antigens as ‘foreign’ – so attack patient’s gut, liver, skin and bone marrow -
  1. Causes severe diarrhoea, liver failure, skin desquamation, bone marrow failure è death weeks to months post transfusion
  2. Prevent: irradiate blood components for very immunosuppressed; or patients having HLA matched components.
42
Q
  1. What is post transfusion purpura?
  2. Who does it affect?
  3. What is the treatment?
A
  1. Purpura appears 7-10 days after transfusion of blood or platelets and usually resolves in 1 to 4 weeks but can cause life threatening bleeding

Due to very low platelets <20x109/l

  1. Affects HPA -1a negative patients - previously immunised by pregnancy or transfusion (anti-HPA-1a antibody)

exact mechanism of own platelet destruction, as HPA-1a negative! ?innocent bystander mechanism

  1. Treatment – infusion of IVIG
43
Q
  1. What is iron-overload?
  2. What can it cause?
  3. How can it be prevented?
A
  1. If lots of transfusion (eg:>50) over time accumulate iron (not excreted); 200-250mg of iron per unit of blood
  2. Can cause organ damage - liver, heart, endocrine etc
  3. Prevent by iron chelation (exjade) with transfusions once ferritin >1000 eg: used in Thalassaemics - monthly transfusions
44
Q

Why do people form Anti-D and how does it occur?

A

People lacking a red cell antigen can form corresponding

antibody if exposed to antigen eg: Rh D negative patient

forms anti-D:

  • by receiving blood transfusion
  • in pregnancy - by fetal red cells entering mother’s circulation at delivery or during pregnancy

Some antigens are more likely to stimulate antibodies than

others.

45
Q

What is haemolytic disease of the Newborn?

A

HDN occurs when the mother has antibodies against the fetus’ red cells caused fetal red cell destruction e.g. Anti-D

46
Q

Describe how Anti-D is formed through pregnancy and when it becomes a problem.

A

First pregnancy, if the mother is Rh negative and the fetus is Rh positive, fetal RhD positive red cells will cross the placenta during delivery

6 months late, anti-D forms in the mother due to exposure of these RhD positive cells

In the second pregnancy if the fetus is RhD positive, and the mother is still RhD negative but with Anti-D antibodies, the maternal anti-D will cross the placenta, coat fetal RhD positive cells causing red cell destruction in the fetal liver and spleen

47
Q
  1. What are anti-D?
  2. What are the clinical features of HDFN?
A
  1. Anti-D is IgG antibodies, as only IgG can cross the placenta
  2. If mother has high levels of IgG antibody - it can destroy fetal red cells, if they are positive for the corresponding antigen
  • Fetal anaemia (haemolytic)
  • Haemolytic disease of newborn (anaemia plus high bilirubin - which builds up after birth as no longer removed by placenta)
48
Q

What is the treatment for pregnancy when the mother already has red cell antibody?

A

All pregnant women have G&S at around 12 weeks

(booking) and again at 28 weeks to check for RBC

Antibodies. If antibody present:

  • check if father has the antigen (so baby could inherit it)
  • monitor level of antibody (high or rising - more likely to affect fetus)
  • Check ffDNA sample

Monitor fetus for anaemia – MCA Doppler ultrasound.

If necessary, intra-uterine transfusion can be given to fetus

Deliver baby early, as HDN gets a lot worse in last few weeks of pregnancy

49
Q

Anti-D s the most important antibody for causing HDFN. How can it be prevented?

A

Prevention of sensitisation in first place:

always transfuse RhD negative females of child bearing

potential with RhD negative blood. Can give intra-muscular

injection of anti-D immunoglobulin, at times when mother

is at risk of a fetomaternal bleed e.g. at delivery

50
Q

What is the action of prophylactic anti-D immunoglobulin?

A

RhD positive (fetal) red cells get coated with anti-D Ig and then they get removed by the mother’s reticuloendothelial system (spleen) before they can sensitise the mother to produce anti-D antibodies

to be effective - must give anti-D injection within 72 hours of the ‘sensitising event’

it does not work if the mother has already been sensitised (developed anti-D) in the past

51
Q

During what sensitising events (potential production of Anti-D) is anti-D Ig given?

A
  1. Give anti-D at delivery if baby is RhD positive
  2. Give anti-D Ig for ‘sensitising events’ during pregnancy, where FMH (feto-maternal haemorrhage) is likely to occur**
  • spontaneous miscarriages if surgical evacuation needed and therapeutic terminations
  • amniocentesis and chorionic villous sampling
  • abdominal trauma (falls and car accidents)
  • external cephalic version (turning the fetus)
  • stillbirth or intrauterine death
52
Q

What are the doses for Anti-D?

  1. Before 20 weeks of pregnancy?
  2. After 20 weeks of pregnancy?
A
  1. At least 250 iu - for events before 20 weeks of pregnancy
  2. At least 500 iu - for events any time after 20 weeks of pregnancy (including delivery)

Usually now dose of 1500iu anti-D Ig at 28-30 weeks

53
Q

What is routine antenatal anti-D prophylaxis?

A
  • About 1% of pregnancies have no obvious ‘sensitising events’, yet RhD negative mothers become sensitised
  • To prevent this, routine anti-D prophylaxis can be given in 3rd trimester
  • Usually, dose of 1500 iu anti-D Ig at 28-30 weeks
54
Q

Apart from Anti-D what other antibdodies can cause HDN?

A

Anti-c and anti-Kell can cause severe HDN

  • usually less severe than anti-D
  • Kell causes reticulocytopenia in fetus as well as haemolysis - As suppresses bone marrow

IgG Anti-A and anti-B antibodies from Group O mothers can cause mild HDN

  • usually not severe (phototherapy)
55
Q
A

Haematology - Path (11 decks)

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