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4.2 Blood Transfusion Science > Adverse Effects of Transfusion > Flashcards

Adverse Effects of Transfusion Flashcards

1
Q

Give some examples of how adverse effects of transfusion have been mediated

A

For any known infections: you have an infction, you get a test, the rate of infection drops off

There will always be emerging pathogens, we will always have new tests to develop

e.g. NAT for HepE -> done in Ireland but not in other countries -> policies differ from country to country etc

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2
Q

Over time how has transfusion related infection changed over the years?

A

HIV peaked in 80s but since screening has reduced to less than 1in 1,000,000 chance

HBV peaked in 1980s but has also reduced to 1 in 1,000,000

etc etct

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3
Q

How has blood safety and cost of a pack changed over the years?

A

To reducce the risks weve increased the cost

blood was about 100 dollars a unit but screening and LD has increased costs to about 250 dollars

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4
Q

Comment on the risk of harm from a transfusion in 2022 in the UK

A

Transfusions remain very sae with low risk of harm in relation to the number of blood componnts issued

The risk of TT infection is much lower than other complications

the risk of serious harm is in 15,449 components issued

The risk of death related to transfusion is 1 in 63,563 components issued

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5
Q

What is haemovigilance?
Definition

A

A set of surveilance procedures, from the collection of blood and its components to the follow up of recipients, to collect and assess information on unexpected or undesirable effects resultin from the therapeutic use of labile blood products and to prevent their occurrence or recurrence

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6
Q

What is the role of haemovigilance in transfusion transmitted infection

A

haemovigilance is how we know about these infections

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7
Q

When was the National Haemovigilance Office set up and where?
What is its role?

A

Set up in 1999 located in the IBTS

To collect anonymised reports of transfusion associated adverse reactions and events from healthcare professionals

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8
Q

What are the ten roles of the national haemovigilance office?

A

To receive, collate and follow up reports from hospitals and GPs of adverse reactions/events connected with transfusion of blood/blood products and provide feedback to those making the report

Advise on follow-up action deemed necessary

Report adverse reactions to the Health Product Regualtory Authority

Provide on-going support to hospital based TSO and to medical nursing and technical staff as appropriate

Produce National figures and report them

Advise on improvements to safe transfusion practice

Support development of clinical guidelines for hospitals in relation to the use of blood

Support audit functions of hospitals in relation to transfusion practice

Promote the development of full traceability regarding transfusion records

Report to the National Blood Users Group to develop national best practice in transfusion

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9
Q

What does HPRA stand for?

A

Health Product Regulatory Authority

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10
Q

What is a serious reaction?

A

An unintended response in the patient associated with the collection or transfusion of blood/blood components that is:
- fatal
- life threatening, disabling, incapacitating
- or which results in, or prolongs hospitalisation or morbidity

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11
Q

What is a serious event?

A

Any untoward occurrence associated with the collecting, testing, processing, storage and distribution that might lead to:
- death
- life-threatening, disabling or incapacitating conditions for patients
- or which results in, or prolongs, hospitalisation or morbidity

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12
Q

Give a brief on the EU Directive

A

Transponsed into Irish Law on 8th Novemember 2005

Mandates the reporting of serious reactions and events

Quality and safety have thus become prime concerns for blood establishments and hospital blood banks

ISO15189, INAB and accreditation now being enacted to implement the EU Directive

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13
Q

Comment on the approximate risks of transfusion complications

A

Death is very rare
Risk of infection is very low, less than 1 in 1million
Risk of febrile reactions most common at 1 in 1,000

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14
Q

What is the estimated residual risk of HBV< HIV and HCV

A

HBV = 1 in 2 million
HIV = 1 in 15 million
HCV = 1 in 15 million

i.e. 1 in every 90 years

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15
Q

What is the risk of a transfusion event in 2017

A

1 per 1431 units issued

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16
Q

What are the seven most common transfusion reactions reported to SHOT

A

Febrile,allergic or hypotensive reactions: 1 in 7,700
TACO: 1 in 25,300
Haemolytic transfusion reactions: 1 in 57,000
Transfusion-associated dyspnoea: 1 in 153,000
TRALI: 1 in 417,000
Post transfusion pupura: 1 in 2,543, 940
Transfusion associaed GVHD: 1 in 25,439,401

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17
Q

What affects gvhd risk

A

Depends on HLA donor pool
If very similar HLA donor and recipient then risk is higher

GVHD can be seen in non LD units even in immunocompetent individuals in these pools

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18
Q

What are the most common reactions in Irelang

A

Febrile non haemolytic transfusion reactions = 41
Anaphylais/hypersensitivity = 30
Hypotensive transfusion reactions = 4
Unclassified reaction = 7

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19
Q

What does NHO define as an acute transfusion reaction?

A

Reactions occurring within 24 hours of the administration of blood or blood components

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20
Q

There was an infection of HepC in 2022 explain this?

A

This was related back to a 1992 transfusion but was only confrimed in 2022

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21
Q

What were the NHO findings in 2021

A

133 serious adverse reaction reports -> 124 of these fell into the SAR category

78 SAR reports were mandaory (62%)

9 SAR reports did not progress -> were not followed up

1 report related to a TTI - but this wasnt accepted by the NHO

No reports of death

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22
Q

When was the last transfusion related infection of hep B in Ireland?

A

2017 was the last breakthrough of HepB

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23
Q

What are the leading causes of transfusion related deaths in 2022?

A

Delays
TACO -> leading cause year on year
Pulmonary-non-Taco
IBCT-WCT
PCC
HTR
FAHR
UCT

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24
Q

Comment on trends in transfusion related deaths over he years

A

Deaths are increasing from about 10 in 2010 to nearly 40 in 2020

Delays and TACO predominate as causes
- 12 delays in 2020
- 18 TACO in 2020

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25
Q

TACO accunts for what % of transfusion-associated fatalities?

A

34%

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26
Q

How many deaths and mismmatches do we get in ireland

A

No deaths

Only about 1 missmatch every few years in Ireland
About 6 missimatches in the UK

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27
Q

How are complications of transfusion categorised?

A

Non-infectious vs infectious

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28
Q

What are classed as acute reactions?

A

Haemolytic Transfusion Reactions
Febrile Non-Haemolytic Transfusion Reactions
Allergic/anaphylactic/urticarial reactions
TRALI
TACO
Non-immune haemolysis/embolus
Hypothermia
Hypocalcaemia - citrate overload-binding of ionised calcium

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29
Q

What are classed as delayed reactions

A

DHTRs
HLA immunity
GvHD
PTP
Immunomodulation
Iron overload

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30
Q

What is immunomodulation?

A

An unproven,proposed interaction of donor WBC or plasma factors with the recipients immune system

Increased graft survival, infection and tumour recurrenc rate is seen

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31
Q

Who do we see iron overload in?

A

We see it in SCD patients
- often need large and frequent transfusions

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32
Q

What are the symptoms of an acute haemolytic transfusion reaction?

A

Fever or chilld or both
Pain at infusion site -> usually first complaint but often missed if patient is unconscious
Flushing
Hypotension
Nausea/vomiting
Dyspnoea
Dark urine/haemoglobinuria
Oozing/bleeding under anaethetic

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33
Q

What are haemolytic transfusion reactions?

A

In vivo destruction of donor cells caused by antibodies in recipients circulation

Most serious involve ABO errors but many other antibodies can be implicated

DIC and organ failure are the most profound events

Strict adherence to specimen collection, reception, record keeping, testing and labelling of blood can minimise such reactions

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34
Q

What does DIC stand for?

A

Disseminated Intravascular Coagulation

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35
Q

What is complement

A

30 soluble proteins and 10 cell surfac receptors that in response to a stimulus interact to opsonise and clear or kill invading microorganisms or altered cells

Main components are numbered C1 through to C9

Theyre functionally inert until acivated when some components develop proteolytic activity

Three pathways exist: classic, alternate and lectin

Classical is initiated by an antigen/antibody complex

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36
Q

What are the three main functions of complement

A

Cell activation and chemotaxis

Cell lysis

Opsonisation where foregin organisms are coated with complement and are subsequently phagocytosed

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37
Q

What are the side effects of complement activation?

A

Increased vascular permeability
Blood vessel dilation
Hypotension
Fever
Excessive activation of the blood coagulation cascade

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38
Q

What are the two end results of complement activation?

A

C3b or C3d

C3b is active and results in complement pathway continueing to the MAC formation

C3d remains on cells -> no MAC -> no intravascular haemolysis -> can be detected by Kupfer cells though

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39
Q

What are the steps of the classical complement pathway?

A

C4 into C4a and C4b, b is deposited on the cell and acts as a C3 convertase

C2 into C2b and C2a, a is deposited on the cell

C3 into C3a and C3b -> C3b is deposited on the cell

C4b:C2a:C3b acts as a C5 convertase

C5 into C5a and b, b initiates formation of MAC

6, 7, and 8 join C5b to form MAC

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40
Q

Talk about DIC, how does it occur?

A

Complement activation can lead to formation of red cell fragments that act as thromboplastin and thus coagulopathy occurs

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41
Q

Talk about complement in intravascular haemolysis

A

Seen in ABO mismatches

Some blood group antibodies can activate large amounts of complement, resulting in gross red cell haemolysis, particularly in vivo

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42
Q

Talk about complement in extravascular haemolysis

A

Some blood groups activate complement at a slow rate

This results in accumulation of C3 molecules and subsequent phagocytosis and clearance by the liver and thus extravascular haemolysis occurs

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43
Q

Talk about complement activation in blood group serology

A

complement can cause lysis of blood samples - if pathway has gone to completion haemoglobinaemia will be evident i.e. free haemoglobin in plasma

complement can cause sensitisation of red cells -> this will cause a positive DAT as many anti-human globulin reagents contain anti-C3b/d as well as anti-IgG

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44
Q

What triggers complement activation?

A

Ag/Ab reactions

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45
Q

How does complement activation cause vasodilation and hypotension

A

Fragments of C3a and C5a cause histamine release from mast cells causing vasodilation and hypotension, bronchial and intestinal smooth muscle contraction

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46
Q

How can intravascular haemolysis lead to DIC

A

Red cell stroma can act as a ‘thromboplastin’ like agent to initiate the clotting cascade

If this is uncontrolled it can cause DIC

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47
Q

What antibodies are most commonly indicated in haemolytic transfusion reaction fatalities

A

ABO
Multiple antibodies
JK and Fy antibodies are associated with 13/37 fatalities

NB: both duffy and kidd are complement activaters

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48
Q

Talk about the ferquence of haemolytic transfusion reaction fatalities

A

They are trending downwards from less than 10 in 2012 to about 5 in 202

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49
Q

How is TRALI trending in the US

A

Trending downwards

From a peak of 35 in 2006 to as low as 4 in 2018

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50
Q

How is TACO trending in the US

A

Numbers remaining constant

In and around 10 cases every year

Mostly because this is up to clinicians and not lab work, and clinicians always over estimate how much blood has been lost - its a natural thing to do

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51
Q

What happens in a febrile reaction

A

Patient has pre-formed antibodies to white cell antigens - Human Lecucocyte Antigens encoded on Chr 6

Transfusion of white cells bearing these antigens causes phagocytosis by host monocytes, release of pyrogens/cytokines

Fever, flushing, tachycardia, rigors etc

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52
Q

What has been a massive decreaser in febrile reactions?

A

Leucodepletion

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53
Q

Talk about febrile reactions from platelets

A

Important to check for bacterial contamination as these can also cause release of pyrogens etc

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54
Q

What temperature rise is indicative of a febrile reaction

A

Rise of 1.5 degrees celsius

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55
Q

How are febrile reactions treated

A

Treated with paracetemol - transfusion can be continued if theres no evidence of haemolysis

56
Q

How do allergic/anaphylactic reactions occur?

A

Due to pre-formed anti-IgE antibodies on mast cells

Stimulated by soluble substances in donor plasma which bind to these antibodies

Can be triggered by anything, such as something the donor ate etc

This causes a histamine release resulting in urticaria (most common), rash, wheezing etc

Extreme allergies can be caused by IgA such as in Iga deficiency

57
Q

How are allergic/anaphylactic reactions treated?

A

If symptoms are mild, then administration of anti-histamines and continue transfusion

58
Q

Talk about anaphylaxis

A

Caused by antibodies to donor plasma proteins -> IgA, C4

IgA deficiency most common but Other allergens are possible e.g peanut

Rare occurrence but can be life hreatening

Clinical symptoms include respiratory distress, nausea, flushing, hypotension and shock

59
Q

How is anti-IgA anaphlaxis treated?

A

IgA deficient products such as washed platelets

Can also reduce the amount of circulating IgA through apheresis

60
Q

How common is IgA deficiency

A

IgA deficiency 1/500 but complete deficiency is rare

1/20,000 can have an anti-IgA reaction

61
Q

What makes anaphylatic reactions considered serious

A

Ag/Ab complexes that form generate C3a/C5a which act as powerful vasodilators

severe reactions may require Ig antigen/antibody levels e.g. IgA

62
Q

What are the most common reations to platelets?

A

FNHTR
TRALI
TACO
AA
HTR (ABO antibodies)

63
Q

What antibodies are most causative of platelet reactions

A

HLA or HPA antibodis

NB: these are the most common causes of refractoriness

64
Q

What does platelet refractoriness mean for the patient?

A

Platelet transsfusions become ineffective -> platelets carry the antigen

Specific matched donors ar required

This usually means platelet apheresis donors are needed

65
Q

What are the most common antibodies in post transfusion purpura

A

Anti-HPA-1a
Anti-HPA-5b

66
Q

What happens with the antibodies produced in post transfusion purpura

A

Anti-HPA-1a and anti-HPA-5b are produced which are cross-reactice with patients own platelets

PTP tends to cause delayed reactions - can take up to 7 days

This causes a massive drop in platelets down to below 10

67
Q

What is transfusion associated dyspnea

A

anything that cannot be defined as TACO or TRALI
a grey area in symptoms between these two
pul,onary dyspneoa

68
Q

Talk about the trends in pulmonary reports to the NHO year on year

A

TACO is by far most common over TRALI and TAD
cases of TACO is increasing year on year
20 in 2013 but over 35 in 2022 of TACO

69
Q

How does TACO differ from TRALI

A

TACO = cardiogenic, heart under too much pressure results in pulmonary oedema, liwuid starts to leak into the lungs

TRALI = heart works perfectly fine, pulmonary oedema, an immune process

TAD = symptoms of TACO but cannot prove overtransfused

70
Q

What is the ISBT definition of TAD

A

TAD is characterised by respiratory distress within 24 hours of transfusion that do not meet the criteria for TRALI, TACO or allergic raction

Respiratory distress should not be explained by the patients underlying condition or any other cause

71
Q

How many cases of TAD were reported to NHO in 2022?

A

2 reports of TAD

Dont know the cause of why these two patients have respiratory distress

72
Q

When did TRALI stop being an issue and why?

A

TRALI was an issue from late 1990s to about 10 years ago when we started SD treatment of plasma in 2000s

It hasnt been a poblem since then

NB: TRALI was the number 1 cause of fatalities in 2014

73
Q

What will TRALI look like

A

White fluid spilling out of lungs
TACO will also look like this
Uncommon to see fluid coming out of intubation though so up until it was discovered to be caused by antibodies we had no idea this was a symptom of transfusion

74
Q

Whatis the cause of 90% of TRALI?

A

90% is caused by anti-HLA antibodies

75
Q

What is TRALI, how does it occur

A

Severe, acute, reaction characterised by respiratory distress and pulmonary infiltratetes (oedema)

Leukocyte antigen/antibody complexes most likely cause - antibodies in donor plasma

These Abs react with patients leucocytes causing their activation and release of enzymes which damage pulmonary tissue and capillaries resulting in oedema of the lung

76
Q

What antibodies commonly cause TRALI

A

anti-HLA or anti-HNA

77
Q

What are anti-HNA antibodies, how are they involved in TRALI

A

anti-human nuetrophil antigens

Neutrophils line the lungs, theyre increased during inflammation

antibodies cause the release of vesicles from these

These granules have lots of super oxygen -> reactive oxygen species which leads to oedema of the lungs

78
Q

What products are and arent risks for TRALI

A

SD plasma or octaplas arent risk products

FFP is a risk product -> hence why female multiparous donors arent used

79
Q

What is the mortality of TRALI

A

Approximately 5% -> 1 in 20 die

80
Q

What are the symptoms of TRALI

A

Severe acute onset within 4 hours after transfusion

Respiratory distress
Hypoxia
Pulmonary infiltrates

81
Q

What is the source of the antibodies in TRALI

A

Either pre-formed leukocyte antibodies in the donor

But sometimes also in the recipient

82
Q

List the TRALI implicated products

A

Whole blood
Red cell concentrates
Granulocyte concentrates
Platelet concentrated (pooled or apheresis)
FFP
Cryoprecipitate
IvIg
S/D treate plasma -> rare case report

83
Q

Talk about TRALI caused by donor antibodies which cross-react with patient white cells

A

HLA class 1 or 2 antibodies

Granulocyte specific antibodies

Associated with al blood products that contains plasma

NB: 90% are this type of donor AB

84
Q

90% of TRALI is caused by donor antibody, what is the remaining 10% caused by?

A

Patient antibody vs donor cells - the antigen has been transfused in the component

85
Q

What product is the most common cause of TRALI associated death

A

FFP

Antibodies react with patients leucocytes -> antibody in donor plasma in 89% of cases

In 5-15% cases no antibody was found and in approx 5% antibodies were found in recipient plasma

86
Q

What is the mechanism behind TRALI

A

Antigen:antibody complexes form in the pulmonary capillaries

Cell activation and release of proteolytic enzymes and toxicoxygen metabolites from granulocytes/neutrophils

pulmonary distress, hypotension, fever

87
Q

What is the 2 hit theory of TRALI

A

First hit = attraction neutrophils

Second hit = HLA/HNA or lipids

88
Q

need to look up more on 2 hit

A
89
Q

What are the treatment options for TRALI

A

Oxygen support (approximatelyy 70% require mechanical ventilation) -> oxygen support but patient is still drowning

Fluid replacement (0.9% NaCl)

Pressor agents - increase BP -> reduces blood volume -> means not as much liquid coming into the lungs

Corticosteroids - if prolonged, slower acting

90
Q

Why arent women allowed to donate plasma

A

The more pregnancies you have the more HLA antibodies you have

91
Q

How do we prevent TRALI in platelets

A

Male only donors and platelet additive solution

Hence

92
Q

talk about the clinical course of TRALI

A

80 percent of cases resolve within 96 hours

however some cases may persist for at least 7 days
- these cases are associated with a greater difficulty in weaning off ventilator

No long term sequelae associated i.e. once lungs recover the patient is completely fine but mortality remains at 5%

93
Q

What are five preventative measures of TRALI

A
  1. permanent deferral of donors implicated in previous TRALI
  2. Testing multiparous women for HLA and granulocyte specific antibodies
  3. Not using multiparous women as apheresis donors - lots of plasma
  4. removal of plasma from cellular blood components
  5. changes in component processing - pooling plasma! PAS in platelets
94
Q

Talk about the incidence of TRALI

A

2010-15 SHOT - 9 cases reported giving an incidence in their reporting system of 1/250,000

However symptoms are not always obvious in patients so incidence might be greatly under reported

Cases possibly as high as 1:5000 but mild cases

Not much TRALI in Ireland

95
Q

What is TACO

A

Pulmonary oedema is the main threat due to volume overload

Headache, hypertension, dyspnoea and heart failure suggestive of TACO

96
Q

Who is most at risk for TACO

A

Young children and the elderly

Patients with compromised cardiac, renal or pulmonary status:
- cardiac blood is going to sit longer in lungs and fluid ill leak in

Most common in older small women transfused with large

NB: clinicians will always overestimate blood loss

97
Q

What product puts one at high risk of TACO and why

A

Albumin solutions
Albumin can drag in double its volume of water
albumin shift large volumes of extravascular fluid into the intravascular space

98
Q

How can you differentiate TACO from TRALI

A

TACO = hypertension -> blood underpressure -> fluid pushed into lungs
TRALI = hypotension -> permeated blood vessels - fluid leaking out

99
Q

What are the symptoms of TACO

A

Dyspnoea
Hypertension
Raised Brain natiuretic peptide
Hypoxia
Pulmonary oedema
normal or decreased left ventricular function
increased pulmonary artery occlusion pressure

100
Q

What are the symptoms of TRALI

A

Dyspnoea
Hypotension
Fever
No change in BNP
Hypoxia
Leukpenia
Thrombopenia
Pulmonary oedema

101
Q

How does the fluid produced in TACO differ from TRALI

A

TACO = dilute liquid, watery, low protein concentration

TRALI = full content plasma, higher protein content

102
Q

Talk about hypothermia as an adverse affect of transfusion

A

Occurs during the rapid infusion of ‘chilled’ blood straight from the fridge

Ventricular arrhythmias result

Haemostasis can be impaired

103
Q

Who is most at risk of hypothermia

A

Neonates or those undergoing massive transfusion

104
Q

How do we prevent hypothermia

A

Pre-warm blood

Blood warming devices -> must meet a standard

Pre-warmed blood is desirable even with smaller volumes of transfused blood

105
Q

Define a delayed haemolytic transfusion reaction

A

A reaction >24 hours but can be 5 days or more post transfusion

Usually due to ‘secondary immunisation e.g. a prior transfusion

Thought to be under reported, under-rated and under-diagnosed

Problems associated as at this point patient isnt being monitored every 30 minutes as on first day of transfusion

106
Q

What antibodies are usually implicated in DHTRs

A

Antibodies to many blood group antigens are implicated

Some of these activate complement

107
Q

What are some tell-tale signs of a DHTR

A

There is no improvement with transfusion and no evident bleeding

It might be encountered in the lab e.g. a positive DAT

108
Q

What happens to red cells in a DHTR and what are the symptoms

A

RBCs are coated and removed extra vascularly by splenic and liver macrophages

109
Q

How common are DHTRs in Ireland

A

We get between 7 and 10 per year

110
Q

Talk about the Delayed transfusion reaction reported to NHO in 2022

A

Immunological haemolysis due to other allo-antibody = 8 delayed reactions

11 reports received, 8 accepted by NHO

All reaction were in 51-70 years olds with one in a 70+

7 out of 8 patients made a full recovery

There was 1 report of death which was unreated to transfusion - patient was very unwell at time of transfusion

111
Q

In Ireland what antibodies are most often seen to cause delayed heamolytic reactions, as reported to NHO

A

Anti-JKa caused 5 of the 8 reactions in 2022
Other antibodies involved include anti Fya, anti-C/c and anti E/e

112
Q

What is transfusion associated graft versus host disease

A

Caused by wbcs in the donor pack
Its a cellular or antibody response against bone marrow
There is no treatment and it cannot be stopped
however it is very very rare today due to LD

NB: not the same as post BMT GVHD

113
Q

How does transfusion associated graft versus host disease manifest?

A

The whole body is attacked
Fever
Diarrhoea
Hepatitis
Pancytopenia
General infection
Subsequent death
90% fatal within 3 weeks -> no way of stopping the condition
Ranges from 3 to 30 week survival
An awful way to die

114
Q

How is TA-GVHD treated?

A

No effective treatment available, can only prevent

Gamma irradiation of blood products is the accepted preventative measure

LD alone may prevent TA-GVHD in immunocompetent recipients but this isnt enough for immunosuppressed individuals hence the need for irradiated blood

115
Q

How does gamma irradiation work to prevent TA-GVHD

A

1500cGY - 2500cGY or 25GY of gamma irradiation

Gamma irradiation renders donor T lymphocytes incapable of replication without major impact on the other elements of blood

116
Q

How does TA-GVHD occur

A

Two different cell types attack specific cells of bone marrow:
CD8+ clones directly cytotoxic to HLA class 1 epitopes
CD4+ clones directly cytotoxic to HLA class 11 epitopes

Increased levels of inflammatory cytokines such as IL-1, IL-2, TBF and interferon-y

These cytokines are associated with tissue injury, upregulating HLA expression, recruitment of further donor-derived T cells

117
Q

Where in the world is the most TAGVHD and why is this

A

Most common in Japan
This is because of the small HLA pool over there

118
Q

Who should receive irradiated products

A

IUT and exchange transfusions but not ‘top-ups’ (only if previous iut)
PBSC recipients
Alla and auto BMT recipients
Transfusions from family members (close HLA pool)
Hodgkins disease
Leukaemia
Immunodeficiency states such as SCID/HIV/AIDs etc

119
Q

How has TAGVHD trended over the years

A

SHOT figures for 1996-1999 recorded that TAGVHD was the commonest cause of TA death @12 cases but its very rare today

120
Q

When does TA_GVHD occur

A

Caused by envgraftment and clonal expansion of donor lymphs in a susceptible (immunosuppressed host)

The disease can also occur in transfusions of HLA similar donors and immunocompetent recipients

121
Q

What does TRIM stand for?

A

Transfusion Related Immune Modulation

122
Q

What is TRIM

A

Adverse chance in immune function in response to rbc transfusion

When a restrictive RBC transfusion strategy is associated with a reduced risk of health-care associated infection compared with a liberal transfusion strategy
-> implementation of a restrictive strategy may have the potential to lower the incidence of HCAI

123
Q

What is thought to cause TRIM

A

Thought to be due to white cells stored in packs

These wbcs release chemokines which work on recipient cells and results in immune supression

Patients transfused have an increased risk of recurrence of cancer but organ rejection is reduced

However this has been difficult to prove as transfused patients are often sicker and at a higher risk of transfusion

LD also hasnt prevented this affect - still an increased risk of infection with LD blood

124
Q

Talk about iron overload as a result of transfusion

A

Consequence of multiple red cell transfusions over a long period of time

Resembles haemochromatosis

Affects the skin, endocrine glands, liver and heart

125
Q

Who is most at risk of iron overload

A

SCD patients
Thallassemia patients

126
Q

How do we treat iron overload

A

The body has no way of processing excess iron -> haemocitrate builds up

Iron chelation is the treatment of choice

Desferrioxamine is used but this can cause side effects and the dosage is difficult to control

127
Q

Talk about using desferrioxamine to treat iron overload

A

Binds fe2+ but also binds magnesium and calcium thus causing lots of other side effects hence dificult to use

128
Q

How is iron overload diagnosed

A

Diagnosed in histology using a perls pressian blue stain on bone marrow to look for haemosiderin deposits

129
Q

Why is transfusion for SCD/Beta thalassemia so difficult

A

They have long term requirements - will need transfusions frequently
Often difficult serology
Difficulties in supplying compatible blood
Iron overload

130
Q

Talk about SCD patients are their need for transfusion

A

Over 33% of transfusions in James are SCD patients - theres been a huge increase in recent years

Crises are caused by infections and managing health hence peak of crisis in teenage years
Crises can be fatal and are usually extremely ainful

Eschange transfusions are used to treat crisis -> about 10 units transfused -> same treatment for iron overload - done over 2 hours

131
Q

Why is it difficult to get blood for SCD patients

A

Patients are mostly Ro but e -> we dont have these donors in ireland so we end up using dce blood -> out valuable O-s when we could be using O+ blood etc

We try to phenotypically match blood as best we can but lack the suitable donors

132
Q

What is thought to be one of the reasons why rate of crisis increases as SCD patients get older, particularly in teen years

A

Sickle cell patients have prolonged HbF
HbF often compensated for lack of health HbA and remains until teenage years
After HbF drops off the patient will start producing their own Hb and this is where the HbS crises begin

133
Q

Give an example of a typica SC case of transfusion history

A

Diagnosis as a child
Muti-transfused and multiple antibodies
Anti-E+Cw+S produced
Difficult to genotype -> DNA gnotype done in UK
Difficult to order compatible units
Post 40 RCC -> anti Kpa produced
Post 45 RCC -> anti-Jka produced

Frozen red cells required

134
Q

Give an example of a typica SC case of transfusion history

A

Diagnosis as a child
Muti-transfused and multiple antibodies
Anti-E+Cw+S produced
Difficult to genotype -> DNA gnotype done in UK
Difficult to order compatible units
Post 40 RCC -> anti Kpa produced
Post 45 RCC -> anti-Jka produced

Frozen red cells required

135
Q

What is standard dosage of desferrioxamine therapy

A

500mg-1g/night

136
Q

How do we try to prevent antibody production in SCD patients

A

Extensively phenotype on first sample
Phenotyped in the IBTS before transfusions begin
Try and give back their group as close as possible to prevent alloimmunisation

137
Q

What are some other non-specific examples of adverse reactions to transfusion

A

Mishandling of packs such as freezing or overheating

Immunisation in general

Simply giving an inappropriate product such as anti-D to an RhD positive woman or ailing to give CMMV neg or irradiated blood to the appropriate recipient

4.2 Blood Transfusion Science (18 decks)

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