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4.2 Blood Transfusion Science > Haemolytic Transfusion Reactions > Flashcards

Haemolytic Transfusion Reactions Flashcards

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1
Q

What are the two types of haemolytic transfusion reactions?

A

Acute
Delayed

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2
Q

What are acute haemolytic transfusion reactions?

A

IgM-mediated reactions
Reactions occur within 24hours
Never events - should never happen
Recipient already has antibodies present
Often associated with ABO mismatch
Severe reactions with significant mortality
Only occur due to malpractice - antibodies missed

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3
Q

What are delayed haemolytic transfusion reactions?

A

IgG mediated
Often Rh associated
Duffy and kidd also seen
Mild-severe reactions
Low mortality

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4
Q

What are the signs and symptoms of acute versus delayed haemmolytic transfusion reactions?

A

Acute: dramatic and severe, rapid onset
- fever, chills, flushing
- pain at site of infusion
- tachycardia, tachypnea, hypotension
- lower back pain - indicative of kidney damage
- haemoglobinemia, haemoglobinuria

Delayed: >24 hours post transfusion
- fever or temperature increase of >1 degrees
- with/without chills
- unexplainable decrease in Hb and Hct
- occassional mild jaundice

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5
Q

what are the major compplications of acute versus delayed haemmolytic transfusion reactions

A

Acute:
- DIC
- renal failure -> kidneys blocked
- irreversible shock
- death

Delayed:
- None -> less severe reaction

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6
Q

What are the causes of acute versus delayed haemmolytic transfusion reactions

A

Acute:
- complement activation
- ABO incompatibility

Delayed:
- anamnestic response to red cell antigen
- alloantibody missed or not demonstrated e.g. Kidd

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7
Q

Lab results of acute versus delayed haemmolytic transfusion reactions

A

Acute:
- DAT+
- increased plasma free haemoglobin
- increased serum bilirubin
- decreased haptoglobin and haemoglobinuria

Delayed:
-DAT positive
-Post transfusion antibody screen positive
- decreased Hb/Hct

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8
Q

Management of acute versus delayed haemmolytic transfusion reactions

A

Acute:
- treat hypotension and DIC
- maintain renal blood flow
- diuretics

Delayed:
- provide antigen-negative donor units
- no additional treatment needed

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9
Q

Prevention of acute versus delayed haemmolytic transfusion reactions

A

Acute:
- avoid errors of mislabellled samples and patient ID design system to decrease chaces of technical error

Dealyed:
- check patient records for old antibodies

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10
Q

Comment on the mortality of ABO incommpatiblity

A

Causes a couple of deats every year due to ABO mismatch across the world

Ireland has about 6/7 mismatches a year but never any deaths

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11
Q

List the three main non-haemolytic transfusion reactions

A

Non-haemolytic adverse events such as TRALI

Febrile non-haemolytic reactions

Allergic reactions

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12
Q

Why can haemolytic transfusion reactions be hard to diagnose?

A

Due to the broad clinical spectrum of symptoms
- some patients only become immunised with allo-antibodies
- sometimes there will be no symptoms but DAT+ etc
- Only symptom might be a faliure of Hb to rise following transfusion
- they can also be severe and life-threatening

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13
Q

Haemolytic transfusion reactions can be acute, delayed or mild give examples of causative antibodies in each

A

Acute = ABO
Mild = Rh
Delayed = complement binding Duffy and Kidd

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14
Q

What % of errors are detected in the lab?

A

80% of all clinical errors are detected in the lab

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15
Q

What are some of the main causes of HTRs

A

Nearly always human error e.g. misidentification of patient, wrong blood product or wrong blood sample

Some reactions are unavoidable e.g. delayed haemolytic reactions caused by a very weak antibody that could not be detected at cross-match/effurvescent antibodies e.g. anti-Jka

Laboratory errors seem to be less frequent but possible e.g. misinterpretation of an antibody panel leading to wrong unit being transfused - ruled out wrong antibody

Often several minor mistakes e.g. missing incorrectly labelled tue can lead to majojr damage

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16
Q

What does SHOT report on in terms of the causes of HTRs

A

Errors or human factors played a part in 77.6% of reports

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17
Q

What is an IBCT

A

Incorrect blood component transfused

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18
Q

What are some errors known to cause of HTRs

A

Collection of blood from the incorrect patient
Incorrect labelling of blood samples
Misidentification of sample at blood bank
Issuance of wrong unit from blood bank
Transfusion of blood to incorrect patient
Alloquoting a patient sample to improperly labelled test tube
- e.g. taking wrong section from wrong unit at crossmatch

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19
Q

What are some contributing factors that can cause HTRs
i.e. what might cause HTR but doesnt definitely

A

Insufficient segregation of units
Preprinted sample labels
Patients with similar or identical names
Sequential patient identifieers
Verbal and STAT orders
Manual issuance of blood
Simultaneous processing of specimens from multiple patients
Tested the correct sample but recorded results on the wrong patient record
Overriding computer error messages

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20
Q

Who are the main bodies on haemovigilance

A

SHOT
- annual SHOT report

National Haemovigillance Office

FDA

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21
Q

How many wbits were reported to NHO in the past few years

A

71 in 2020
56 in 2021
56 in 2022
78 in 2023

*

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22
Q

What are the main causes of wbits according to NHO 2022?

A

Detail not correctly ID at phlebotomy
Sample remotely labelled
Sample not labelled by person taking sample
Patient not correctly ID at admission
Deatil on sample not transcribed from ID band

NB: most errors are bedside errors

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23
Q

WBITS are a common cause of near miss events, what percentage do the make up?

A

60-70% of near miss events are wbits

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24
Q

80% of most errors reported to SHOT are caused by what?

A

Patient identification and sample labelling errors

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25
Q

When are errors detected

A

Nearly all errors are detected during testing or at authorisation of results i.e. in the lab

Responsiblity fals on the lab to detect these

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26
Q

Why are wbits not reported to haemovigilance

A

Haemovigilance arent concered with wbits
Theyre only concerned with components
hence not mandatory to report wbits to haemovigilance

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27
Q

Why would you get away with a wbit 50% of the time?

A

50% of population is group O

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28
Q

Comment on the trends in ABO incompatible transfusions over the year

A

Number of ABO incompatible transfusions has decreased over the past 20 years
- up to 30 a year in 1990s but now only a few a year

The number of ABOi related deaths are decreasing as well

ABOi red cell transfusions are trending upwards

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29
Q

What does SHOT claim are the reasons for increase in ABOi red cell transfusions

A

Understaffed labs - people working too hard - under too much pressure

The harder staff work the more wbits that are missed etc

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30
Q

Give some specific examples of errors that cause HTRs

A

Where a BMT patient was given blood of new blood type by a MS instead of O- while still changing blood type

In A&E where a sample was taken from an incorrect patient WBIT

Unable to detect hidden antibodies due to antibodies against frequent antigens such as anti-c

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31
Q

Talk in detail about the HTR caused by the anti-c

A

Anti-c antibody caused positivity in all but 2 cells, hidden anti-Jka reactivity
Woman transfused two units
Developed haematuria and sever back pain within 5 hours of transfusion of the 2nd unit
Post transfusion an anti-c and anti-JK were found
When pre-transfusion sample was reviewed the anti-Jka was identified
The 2nd unit transfused was positive for Jka

The Jka had been excluded in error - Jka negative units should have been issues
The MS was on duty and working alone out of hours, no second person available to check
The MS was fully trained and experienced ->human error, just a mistake

Patient made a full recovery, the reaction was noted due to error

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32
Q

Give some examples of incorrect ABO transfused for plasma products

A

Group B solvent detergent plasma was selected instead of AB Octaplas for a patient whose blood group was AB
- one unit eas initially issued and transfused
- error was discovered when further SD plasma was issued during the same transfusion event
- The MS involved in the error was assisting his colleague during a massive haemorrhage

Group A SD plasma was issued for a patient who was blood group AB
- occurred during a massive haemorrhage
- The MS had changed blood groups when issuring red cells, issuing group A to the patient as there were no further AB red cells in stock
- Group A SD plasma instead of uniplas was issued
- sinple lapse of concenentration where the MS was extremely aware of changing blood group
- occurred at 6-7am on a bank holiday morning when scientist as working alone

  • there was no evidence of haemolysis in these patients and neither suffered any harm
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33
Q

To who do we report Serious adverse events?

A

National Haemovigilance Office (NHO)

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34
Q

In 2021 how many incorrect ABO transfusions with no reaction did we have, what were these caused by?

A

5 were detected - all 5 errors occured in the lab

Three were from the same hospital -> would have been investigated
Four stated incorrect component was issued
One stated historical reports had not been checked
Human error was cited as the causative factor in al 5 reports

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35
Q

What are the leading causes of transfusion-associated fatalities in the USA (reported by the FDA)?

A

TACO
TRALI
Contamination
HTR (ABO) -> 7% of total cases
Anaphylaxis
TR- type not determined
HTR (non-abo)

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36
Q

What antibodies are most common in TR fatalities

A

ABO (14/39)
Multiple antibodies (4/36)
Fya(4/36)

Jk and Fy antibodies account for about 1/3 of fatalities - combined results from individual antibody cases but are often seen in combination with others

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37
Q

How are HTR fatalities trending in the US?

A

Trending downwards

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38
Q

Talk about the SHOT UK 2023 report on HTRs

A

53 reports
2 daeths
Major morbidity in 18 cases
Trending upwards

39
Q

Talk about the two deaths related to HTR in UK in 2023

A

Fatal HTR in a SCD patient following an unnecessary elective exchange transfusion:
- SCD patient had been scheduled for an exchange transfusion in advance of elective surgery
- patient was informed that surgery had been cancelled but this wasnt communicated to haematology team and the exchange transfusion went ahead
- five days later patient present to ED with severe pain consistent with a delayed HTR
- patient later collapsed and suffered a cardiac arrest

Death attributed to hyperhaemolysis with delays in treatment
- another SCDP with an existing heart condition presented to haematology outpatients with severe pain 5 days post transfusion
- patient referred to ED where admitted for suspected hyperhaemolysis and transferred to the ICU
- treatment with IVIG, methylprednisolone and eculizumab and was showing recovery but then suffered cardiac arrest and died

40
Q

Why do SCD patients tend to suffer from a large percentage of HTRs

A

They tend to be in a pro-inflammatory phase
They tend to produce more antibodies
They are not immunocompromised like the majority of our other patients who recieve transfusions

41
Q

According to the SHOT UK report 2023 what antibodies tend to cause DHTR versus Acute HTRs

A

Delayed:
- Duffy and Kidd mostly

Acute:
- Kidd
- anti-Wr8

42
Q

What factors determine the response of a patient in a HTR

A

Potency of recipients ABO antibodies -> immunocompromised or not

Immunogenicity of antigen e.g. 10% K vs 70% D

HLA of recipient - good responder or not

Their efficiency at activating complement

Volume transfused (very little needed for severe ABO)

Rate of infusion -> major haemorrhage

Anaesthetic -> can mask reaction - can be hard to interpret clinical symptoms

High titre ABO antibodies in transfused plasma can cause acute HTR

43
Q

Talk about the extravascular destruction of red cells

A

Physiological senescent red cells
Pathology -> cell - mediated -> seen in autoimmune conditions
Spleen and liver
Usually IgG

44
Q

Talk about intravascular immune destruction of red cells

A

Pathology - complement-mediated
Usually IgM
Never happens naturally - should never happen
Usually way worse outcome than extravascular

45
Q

What are the two types of haemolysis

A

Figure 1: complement-mediated intravascular destruction of RBCs
Figure 2: IgG antibody-mediated extravascular destruction of RBCs

46
Q

talk about the pathophysiology of complement-mediated intravascular destruction of rbcs

A

rbcs sensitised by IgG antibody
C1 complement recognition unit
C2aC3C4b complement activation unit
C5b6789 membrane attack complex
MAC formation (intravascular haemolysis)
RBC lysis

47
Q

Talk about IgG antibody-mediated extravascular destruction of RBCs

A

IgG antibodies coat rbcs
Reticuloendothelial cells have FC receptors that detect FC tails of antibodies on rbcs
RBCs are either ingested, form spherocytes or are lysed -> extravascular haemolysis

48
Q

What are the steps in the classical complement pathway

A

C4b -> C2a -> C3b

Spontaneous activation of C3 -> C3 trends to be trigger happy

C3b -> C5 convertase

C5b -> C5b, 6, 7, 8 -> tipping point reached and MAC is formed

49
Q

What happens if C3d is formed

A

This stops complement
No MAC is formed

50
Q

What does C3a do?

A

Pro-inflammatory - anaphylatoxin

(same as C5a)

51
Q

What does C3b do?

A

Opsonisation and phagocytosis

52
Q

How can we indirectly measure the degree of intravascular haemolysis from a blood sample?

A

Lactate dehydrogenase is released from rbcs when MACs are formed

Hence raised LDH indicated intravascular haemolysis

Haptoglobins such as Hb and bilirubin will also be raised

53
Q

What are the consequences of complement activation?

A

C3a and C5a are powerful anaphylatoxins

These cause degranulation of mast cells leading to histamine and serotonin release
- serotonin responsible for nausea and sick feeling

The outcomes are vasodilation and hypotension (brought on by histamine), bronchial and intestinal smotth muscle contraction

54
Q

Talk about the roles of cytokines in transfusion reactions

A

IL-1, IL-8 and TNF are released by monocytes with resultant fever and coagulation disorders

They are released in response to C3a and C5a from complement cascade

TNF activates the “intrinsic” coagulation cascade, contributing towards DIC

“In vitro” models of ABO incompatibilties have demonstrated this cytokine involvement

55
Q

What does IL-1, IL-8 and TNF do

A

IL-1 is a pyrogen
IL-8 is a chemotactic factor
TNF can activate coaglation on its own

56
Q

Other than through cytokines, how does a transfusion reaction induce its affects

A

Antigen/antibody complexes can activate Hageman factor (FXII) -> thus intrinsic coagulation pathway is activated -> FXII has the same reaction as if cells were exposed to tissue (factor)

FXIIa can then activate the Kinin system to product bradykinin which is a powerful vasodilator which is what results in a blood pressure fall

57
Q

Talk about the activation of the kinin system

A

Prekallikrein - an inactive coagulation factor is converted to Kallikrein by FXIIa

Kallikrein then acts on kininogens and converts them to kinins such as bradkinin

58
Q

What does the action of FXIIa have

A

Renal damage or failure
Haemoglobinaemia
Haemoglobinuria
DIC -> first platelets are consumed and all factors used
Pulmonary damage
Death

59
Q

What complement component is responsible for extravascular haemolysis

A

C3b marks rbcs for extravascular haemolysis through phagocytosis

60
Q

What are some symptoms of acute haemolytic transfusion reaction?

A

Fever or chills or both
Pain at infusion site
Flushing
Hypotension
Nausea/vomiting
Dyspnoea
Dark urine
Oozing/excessive bleeding-under anaesthetic

61
Q

What is the telltale symptom of a HTR, give an example of where this was absent?

A

Hypotension

there was a case in the Mater where there was a query HTR but the patient was hypertensive and not hypotensive
- this was due to the patient partner bringin in heroin and injecting it in with the transfusion hence the hypertension

62
Q

How is a HTR investigated by the lab?

A

Clerical checks
Inspection of the post tranfusion sample
DAT on both the pre and post transfusion samples as well as a group and screen and crossmatch
FBC
Coagulation tests such as PT, APTT, FDPs and D-dimers
Hapoglobins and LDH
Urinalysis for haemoglobinuria
Blood cultures to rule out a bacteraemia as symptoms are similar

63
Q

How do we treat a HTR

A

Prevention!!! -> best cure is prevention - should be able to avoid all but kidd and duffy
Steroids, fluids, mannitol and IVIG
fluids and diuretics
Dopamine
Treatment of any underlying coagulopathy
Resume red cell transfusion as necessary and when possible
Report to HVO and they will report to NHO

64
Q

How do we treat a HTR

A

Prevention!!! -> best cure is prevention - should be able to avoid all but kidd and duffy
Steroids, fluids, mannitol and IVIG
fluids and diuretics
Dopamine
Treatment of any underlying coagulopathy
Resume red cell transfusion as necessary and when possible
Report to HVO and they will report to NHO

65
Q

How is IVIG used?

A

IVIG will inhibit macrophages by forming complexes that look like Ag-Ab reactions
These complexes will bind to Fc receptors on macrophages and thus prevent a haemolytic anaemia

IVIG can thus be used in all inflammatory conditions

66
Q

How can mannitol be used in a HTR?

A

Mannitol can be used to increase urine output by drawing water into the renal tubules and thus helping to flush Hb from the kidneys

67
Q

How can dopamine be used in the treatment of a haemoytic transfusion reaction?

A

Dopamine increases cardiac output and thus enhances renal perfusion

68
Q

How can fluids be used to treat HTRs

A

They help prevent hypotension -> blood volume expander

69
Q

How can diuretics be used for HTRs?

A

Increase urine output -> prevents Hb build up in idneys and thus prevents AKI

70
Q

Give some examples of how underlying coagulopathy should be treated in a HTR

A

Frozen plasma, platelets, cryo/fibrinogen or FVIIa

71
Q

What are the five future potential treatment options for HTRs?

A

Etanercept (Enbrel): a soluble TNFa receptor

Infliximab (Remicade): anti-TNFa

Anakinra (Kineret): recombinant IL1ra

Activated protein C

Compliment inhibitors

72
Q

How can activated protein C be used in the treatment of HTRs?

A

APC is essentially the breaks on the coagulation cascade
APC has saved thousands of livee since its development
Mostly used in DIC and meningitis
-> has saved thousands of meningitis children

73
Q

List the characteristics of an acute-type HTR

A

IgM mediated
Carbohydrate antigens e.g. ABO, Lewis, P
T-cell independent
Naturally occurring - antibodies developed naturally
Direct agglutinin
C5b-C9 (MAC formation)
Intravascular haemolysis
Mild HDFN (if any at all)

74
Q

List the characteristics of Delayed-type HTRs

A

IgG mediated
Protein antigens e.g Rh, Kidd etc
T-cell dependent
Prior RBC exposure
Antiglobulin i.e. Coombs test
C3b, C3bi or none
Extravascular
Sever HDFN

75
Q

HTRS are most common in what patient cohort, give an example of where this is evident and why this occurs?

A

30% of HTRs in James are in SCD patients
- due to incompatible transfusions resulting in immunisation
- Black SCD patients and a white population
- SCD patients often Dce but this is rare in caucasians (most are dce) -> hence we tend to give our O-s to SCDs -> wasting O-s
-A lot of these patients often require exchange transfusions whereby they need up to ten units a month etc

76
Q

Talk about the relative potency of different red cell antigens

A

A comparison of the actual frequency with which particular alloantibodies are found with the calculared frequency of the opportunity for immunisation

e.g. 10% for anti-K, which is nine times more immunogenic than Fya

Phenotypic frequencies of the various blood group antigens does not correlate well with the predicted antibody specificities i.e. glycoproteins and protein antigens are best presented to the immune system than carbohydratae antigens - better immunogens

77
Q

List some of the reasons for different immunogenicity strengths

A

Nature of the antigen i.e. glycoproteins vs carbs
Wide or restricted expression i.e. just rbcs or tissues
Density on rbcs, thousands or millions of copies etc
Structural difference e.g. C/c vs D/d
Homogenous/heterogenous populations - high/low frequency of antigen on donor rbcs -> lower expression if heterogenous etc
Tolerance -> increase if trasnfused underr 1
Immunosuppression e.g. leukaemia patients
Immune status or inflammation - e.g. hyper reactive in SCD
HLA type

78
Q

Give an example of a widely expressed rbc antigen

A

Fya on brain, lung, kidney and rbcs compared to K mostly only on rbcs

79
Q

Talk about tolerance in under 1 year olds

A

Baby’s body has nont recognised self versus non-self yet
Babies transfused within the first year of life tend to produce less antibodies later in life
Anything baby was transfused with under 1 will just be seen as self later in life

80
Q

What are some contributors to HTR susceptibliity

A

Multiple transfusions - especially if discrepancies between recipient and donor population as with SCD

Genetic propensity - HLA type dependent

Recipient related - inflammation or infection increasing risk of immunisation

Component related - white blood cells or cytokines

81
Q

What are some populations likely to undergo multiple transfusions?

A

Sickle cell Disease
Thalassemia
- both of these are exposed to discrepancies due to donor population

Myelodysplastic syndrome
AIHA

82
Q

What percentage of the population has antibodies?

A

2% of the general population has antibodies and about 8% of the hospital population has antibodies
- most of these are women exposed during pregnancy in general population

83
Q

Talk about HLA and immunisation risk

A

If you have DRB1 01 you are way more likely to produce an anti-JKa while DRB1 04 makes you way more likely to produce an Fya

HLA DRB1 15 is a responder - will often produce new antibody after every transfusion
- can be really difficult to get blood for as even 2 antibodies makes it really difficult
HLA DRB1 0901 may confer some level of protection

84
Q

How can white blod cells and cytokines in blood components contribute to HTRs

A

Leukodepletion carried out pre-storage removes wbcs before they break down and release cytokines
However this is not done in America, leucodepletion only done where necessary at the bedside as it increases the cost of a rbc pack by 40%

85
Q

Talk about immunisation in thalassemia patients

A

When only ABO and D matched, 21% form clinically signifciant Abs after 6 years of transfusions

84% of the Abs producedwere anti-Rh or anti-K
- hence why we not Rh and K type

When ABO, Rh and K matched, only 3.7% form alloantibodies

Tolerance was noted with lower incidence of Ab development when Tx started in 1st year of life -< 5.2%

86
Q

Talk about immunisation in SCD

A

18.6% rate of immunisation in SCD -> Rh and K again

Rate increased with the number of transfusions

Typical specificities were anti-K, C, E and Jkb antigens are these are more common in white populations than blacks

Ror (Dce/dce) - making Anti-C and E case for Ror matching
-> need for ce blood but whites mostly dce while blacks mostly Dce -> we end up giving up our O-s to these patients as we dont have enough Dce blood for them

87
Q

Talk about immunisation in AIHA

A

Increased frequency of alloantibodies in AIHA cases
Difficulties in recognition of same
Agument for more fully phenotyped blood

88
Q

What are some factors which may influence the in vivo survival or transfused red cells

A

IgG subclass of antibody
-> IgG1 and IgG3 are more potenet causes of HTRs
-> With Ig2 and Ig4 there tends to be no complication with incompatible transfsuion

Ability of the antibody to active complement

No of antigen sites on the rbcs

Thermal range of the antibody

Volume of blood transused

Presence of inhibitory blood group substances in donor plasma

Activity of recipients mononuclear phagocytic system -> HLA presentation etc

89
Q

When might you see intravscular haemolysis vs extravascular haemolysis

A

Intravascular: ABO mismatches or some “cold AIHA” and PCH

Extravascular: liver/spleen involvement splenic destruction - more efficient as PCV of blood in spleen is higher
-> less competition between plasma IgG molecules and bound antibodies for receptor sites compare to the liver
-> plasma skimming effec of the spleen means less competition with free plasma IgG

90
Q

When might you see intravscular haemolysis vs extravascular haemolysis

A

Intravascular: ABO mismatches or some “cold AIHA” and PCH

Extravascular: liver/spleen involvement splenic destruction - more efficient as PCV of blood in spleen is higher
-> less competition between plasma IgG molecules and bound antibodies for receptor sites compare to the liver
-> plasma skimming effec of the spleen means less competition with free plasma IgG

91
Q

What is the skimming effect in the spleen

A

This is where there is a reduction in the distance between red blood cels and macrophages in the spleen
- this makes the spleen very effctive at detecting IgG coated red cells
- if spleen is removed x6 times more antibody is needed to have the same amount of haemolysis

-> red cells essentially pushed towards receptors on macrophages in spleen

92
Q

What can stop C3 froming C3b and thus intravascular haemolysis?

A

Inhibitors may degrade C3 to C3d molecules on red cells
C3d means no haemolysis
C3d means cells are subsequently released from the liver and re-enter circulation etc

93
Q

Compare intra vs extra-vascular haemolysis results in the lab in terms of peripheral smear, haptoglobins, urine and DAT

A

Intravascular:
- schistocytes on smear
- decrease or absent haptoglobins
- urine haemosiderin ++
- urine haemoglobin ++
- negative direct DAT

Extravascular:
- spherocytes
- mild decrease in haptoglobin
- negative urine haemosiderin
- negative urine haemoglobin
- positive direct DAT 4+

4.2 Blood Transfusion Science (3 decks)

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