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PathY5 > Blood Transfusion 2 > Flashcards

Blood Transfusion 2 Flashcards

1
Q

What defines an acute transfusion reaction?

A

<24 hours (Acute)

>24 hours (Delayed)

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2
Q

Which are the acute transfusion reactions?

A

Acute haemolytic (ABO incompatible)

Allergic/anaphylaxis

Infection (bacterial)

Febrile non-haemolytic

Respiratory
Transfusion associated circulatory overload (TACO)
Acute lung injury (TRALI)

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3
Q

Which are the delayed transfusion reactions?

A

Delayed haemolytic transfusion reaction (antibodies)

Infection
viral, malaria, vCJD

TA-GvHD

Post transfusion purpura

Iron overload

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4
Q

What are the two worst problems associated with transfusion?

A

Acute transfusion reaction

Wrong blood transfused

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5
Q

What are the symptoms of a transfusion reaction?

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

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6
Q

How do you monitor someone post transfusion?

A

Monitoring may be the ONLY way to detect reaction, if patient is unconscious:
Baseline temp, pulse, respiratory rate, BP before transfusion starts
Repeat after 15 mins (as most, but not all, reactions will start within 15 mins)
Ideally repeat hourly and at end of transfusion (as occasionally reactions start after transfusion finished)

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7
Q

What is a febrile non haemolytic transfusion reaction?

A

During / soon after transfusion (blood or platelets), rise in temperature of 1C, chills, rigors

Common before blood was leucodepleted, now rarer
Have to stop or slow transfusion; may need to treat with paracetamol

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8
Q

What is the cause of febrile non haemolytic transfusion reaction?

A

White cells can release cytokines during storage

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9
Q

How does an allergic transfusion reaction present?

A

Common especially with plasma
Mild urticarial or itchy rash sometimes with a
wheeze.

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10
Q

How do you treat an allergic transfusion reaction?

A

During or after transfusion.

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

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11
Q

What is the cause of an allergic transfusion reaction?

A

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

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12
Q

What are the symptoms and signs of acute intravascular haemolysis?

A

Restless, chest/ loin pain, fever, vomiting, flushing, collapse, haemoglobinuria (later);
↓BP & ↑HR (shock), ↑Temp

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13
Q

How is wrong blood given?

A

failure of bedside check giving blood;
wrongly labelled blood sample;
laboratory error

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14
Q

How do you test for wrong blood?

A 
Take samples for FBC, biochemistry,
coagulation, repeat x-match and Direct
Antiglobulin Test (DAT).
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15
Q

How do you manage wrong blood given?

A

Discuss with haematology doctor ASAP

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16
Q

Which antibody is involved with wrong blood?

A

IgM

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17
Q

What are the symptoms of bacterial contamination?

A

Restless, fever, vomiting, flushing, collapse.

↓BP & ↑HR (shock), ↑Temp

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18
Q

What is the pathogenensis of bacterial contamination?

A

Bacterial growth can cause endotoxin production which causes immediate collapse
From the donor (low grade GI, dental, skin infection)
Introduced during processing (environmental or skin)
Platelets >red cells > frozen components (storage temp)

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19
Q

How are red cells stored?

A

At 4 degrees (PLT at RTP)

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20
Q

How do you prevent bacterial contamination from donor?

A

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

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21
Q

How do you prevent bacterial contamination from storage/ inspection?

A

Red cells: Store always in controlled fridge 4C; 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 22C; 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

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22
Q

What is anaphylaxis?

A

“Severe, life-threatening reaction soon after start of transfusion”
↓BP & ↑HR (shock),
very breathless with wheeze,
often laryngeal &/or facial oedema

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23
Q

What is the mechanism of anaphylaxis/ IgA deficiency?

A

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

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.

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24
Q

What is TACO?

A

TRANSFUSION ASSOCIATED CIRCULATORY OVERLOAD (TACO)

= pulmonary oedema / fluid overload

25
Q

Why does TACO happen?

A

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

26
Q

What are the clinical features of TACO?

A

Clinical features: SOB, ↓O2 sats, ↑HR, ↑BP; CXR: fluid overload / cardiac failure.

27
Q

What is a TRALI?

A

ARDS tbh but after transfusions

28
Q

What are the clinical features of TRALI?

A

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

29
Q

What is the mechanism of TRALI?

A

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)

30
Q

What are the two classes of delayed haemolytic transfusion reaction?

A

Alloimunisation

Extravascular Haemolysis (as IgG) so takes 5-10 days

31
Q

What is alloimmunisation?

A

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

32
Q

What is Extravascular Haemolysis?

A

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

33
Q

What are the lab findings in delayed haemolytic reaction?

A

Haemolysis tests: increased bilirubin, decreased Hb, increased retics haemoglobinuria over few days
Test U&Es – as can cause renal failure
repeat G&S for ? new antibody

34
Q

What are transfusion associated infections?

A

Malaria
Viral infection
Variant CJD

35
Q

What is SHOT?

A

SHOT is a national reporting scheme for serious hazards of transfusion
There are divided into
pathological reactions that may not be preventable
Reactions that are possible or probably preventable by improving practice
Adverse events caused by error

36
Q

When do symptoms of blood infections show?

A

Symptoms months or years after

37
Q

How bad is the problem of infections in transfusions?

A

Rely on questioning donors about wellbeing
Never zero risk – so don’t transfuse unnecessarily!
Current estimates of getting viral infection from a donation:
hepatitis B – 1 in 1.3 million
HIV – 1 in 6.5 million
hepatitis C – 1: 28 million

38
Q

Why is CMV bad?

A

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

39
Q

Why is parvovirus bad?

A

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

40
Q

Why us V CJD bad?

A

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

What is TaGVHD?

A

Rare, but always fatal
Donor’s blood contains some lymphocytes (able to divide)
Normally, patient’s immune system recognises donor’s lymphocytes as ‘foreign’ and destroys them

42
Q

What is the pathogenesis of TaGVHD?

A

In ‘susceptible’ patients (eg.. very IS) - lymphocytes not destroyed
Lymphocytes recognise patient’s tissue HLA antigens as ‘foreign’ – so attack patient’s gut, liver, skin and bone marrow -
Causes severe diarrhoea, liver failure, skin desquamation, bone marrow failure -> death weeks to months post transfusion
Prevent: irradiate blood components for very immunosuppressed; or patients having HLA matched components.

43
Q

What is post transfusion purpura?

A

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

44
Q

What is the mechanism of PTP?

A

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

45
Q

How do you treat PTP?

A

IVIG (infusion)

46
Q

What is immune modulation?

A

Possible increased rate of infections post-op and increased recurrence of cancers in patients who have blood transfusion - conflicting studies - uncertain

47
Q

How does iron overload occur?

A

If lots of transfusion (eg:>50) over time accumulate iron (not excreted); 200-250mg of iron per unit of blood
Can cause organ damage - liver, heart, endocrine etc
Prevent by iron chelation (exjade) with transfusions once ferritin >1000 eg: used in Thalassaemics - monthly transfusions

48
Q

What is haemolytic disease of the foetus and newborn (HDFN)?

A

People lacking a red cell antigen can form corresponding
antibody if exposed to antigen eg: Rh D negative patient
forms anti-D

49
Q

When can anti D formation in HDFN occur?

A

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.

50
Q

What are the clinical features of HDFN?

A

Only IgG antibodies can cross the placenta.
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)

51
Q

What is the treatment of HDFN?

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

52
Q

How is intra uterine transfusion given?

A

If necessary, intra-uterine transfusion can be given to fetus
Specialised centres, highly skilled - needle in umbilical vein
At delivery - monitor baby’s Hb and bilirubin for several days as HDN can get worse for few days
Can give exchange transfusion to baby if needed to Lower bilirubin and Increase Hb; plus phototherapy to Lower bilirubin

SUBSEQUENT PREG ARE WORSE

53
Q

How do we prevent HDFN?

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

54
Q

What is the MOA of prophylactic anti D Ig?

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

55
Q

What are sensitising events?

A
  1. Give anti-D at delivery if baby is RhD positive
  2. Give anti-D Ig for ‘sensitising events’ during pregnancy, where FMH 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

**Do not know if fetus is RhD positive or RhD negative

56
Q

How do you dose Anti D?

A

At least 250 iu - for events before 20 weeks of pregnancy
At least 500 iu - for events any time after 20 weeks of pregnancy (including delivery)
Sometimes a larger dose is needed for larger bleeds, so an FMH test (Kleihauer test) is always done if > 20 weeks pregnant and at delivery, to determine if more anti-D is needed than the standard dose, if the fetal bleed is large

125 iu can prevent sensitisation from a 1mL FMH

So : 500 iu covers up to 4mL fetal red cells
1250 iu covers up to 10mL
1500 iu covers up to12mL

57
Q

What is Routine antenatal anti-D prophylaxis (RAADP)?

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

58
Q

What are other important antibodies?

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
IgG Anti-A and anti-B antibodies from Group O mothers
can cause mild HDN
usually not severe (phototherapy)

59
Q

Simplify TRALI and TACO

A 
TRALI = ARDS in transfusion 
TACO = heart failure in transfusion

PathY5 (98 decks)

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