Adverse Effects of Transfusion Flashcards
Give some examples of how adverse effects of transfusion have been mediated
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
Over time how has transfusion related infection changed over the years?
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
How has blood safety and cost of a pack changed over the years?
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
Comment on the risk of harm from a transfusion in 2022 in the UK
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
What is haemovigilance?
Definition
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
What is the role of haemovigilance in transfusion transmitted infection
haemovigilance is how we know about these infections
When was the National Haemovigilance Office set up and where?
What is its role?
Set up in 1999 located in the IBTS
To collect anonymised reports of transfusion associated adverse reactions and events from healthcare professionals
What are the ten roles of the national haemovigilance office?
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
What does HPRA stand for?
Health Product Regulatory Authority
What is a serious reaction?
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
What is a serious event?
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
Give a brief on the EU Directive
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
Comment on the approximate risks of transfusion complications
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
What is the estimated residual risk of HBV< HIV and HCV
HBV = 1 in 2 million
HIV = 1 in 15 million
HCV = 1 in 15 million
i.e. 1 in every 90 years
What is the risk of a transfusion event in 2017
1 per 1431 units issued
What are the seven most common transfusion reactions reported to SHOT
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
What affects gvhd risk
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
What are the most common reactions in Irelang
Febrile non haemolytic transfusion reactions = 41
Anaphylais/hypersensitivity = 30
Hypotensive transfusion reactions = 4
Unclassified reaction = 7
What does NHO define as an acute transfusion reaction?
Reactions occurring within 24 hours of the administration of blood or blood components
There was an infection of HepC in 2022 explain this?
This was related back to a 1992 transfusion but was only confrimed in 2022
What were the NHO findings in 2021
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
When was the last transfusion related infection of hep B in Ireland?
2017 was the last breakthrough of HepB
What are the leading causes of transfusion related deaths in 2022?
Delays
TACO -> leading cause year on year
Pulmonary-non-Taco
IBCT-WCT
PCC
HTR
FAHR
UCT
Comment on trends in transfusion related deaths over he years
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
TACO accunts for what % of transfusion-associated fatalities?
34%
How many deaths and mismmatches do we get in ireland
No deaths
Only about 1 missmatch every few years in Ireland
About 6 missimatches in the UK
How are complications of transfusion categorised?
Non-infectious vs infectious
What are classed as acute reactions?
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
What are classed as delayed reactions
DHTRs
HLA immunity
GvHD
PTP
Immunomodulation
Iron overload
What is immunomodulation?
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
Who do we see iron overload in?
We see it in SCD patients
- often need large and frequent transfusions
What are the symptoms of an acute haemolytic transfusion reaction?
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
What are haemolytic transfusion reactions?
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
What does DIC stand for?
Disseminated Intravascular Coagulation
What is complement
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
What are the three main functions of complement
Cell activation and chemotaxis
Cell lysis
Opsonisation where foregin organisms are coated with complement and are subsequently phagocytosed
What are the side effects of complement activation?
Increased vascular permeability
Blood vessel dilation
Hypotension
Fever
Excessive activation of the blood coagulation cascade
What are the two end results of complement activation?
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
What are the steps of the classical complement pathway?
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
Talk about DIC, how does it occur?
Complement activation can lead to formation of red cell fragments that act as thromboplastin and thus coagulopathy occurs
Talk about complement in intravascular haemolysis
Seen in ABO mismatches
Some blood group antibodies can activate large amounts of complement, resulting in gross red cell haemolysis, particularly in vivo
Talk about complement in extravascular haemolysis
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
Talk about complement activation in blood group serology
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
What triggers complement activation?
Ag/Ab reactions
How does complement activation cause vasodilation and hypotension
Fragments of C3a and C5a cause histamine release from mast cells causing vasodilation and hypotension, bronchial and intestinal smooth muscle contraction
How can intravascular haemolysis lead to DIC
Red cell stroma can act as a ‘thromboplastin’ like agent to initiate the clotting cascade
If this is uncontrolled it can cause DIC
What antibodies are most commonly indicated in haemolytic transfusion reaction fatalities
ABO
Multiple antibodies
JK and Fy antibodies are associated with 13/37 fatalities
NB: both duffy and kidd are complement activaters
Talk about the ferquence of haemolytic transfusion reaction fatalities
They are trending downwards from less than 10 in 2012 to about 5 in 202
How is TRALI trending in the US
Trending downwards
From a peak of 35 in 2006 to as low as 4 in 2018
How is TACO trending in the US
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
What happens in a febrile reaction
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
What has been a massive decreaser in febrile reactions?
Leucodepletion
Talk about febrile reactions from platelets
Important to check for bacterial contamination as these can also cause release of pyrogens etc
What temperature rise is indicative of a febrile reaction
Rise of 1.5 degrees celsius
How are febrile reactions treated
Treated with paracetemol - transfusion can be continued if theres no evidence of haemolysis
How do allergic/anaphylactic reactions occur?
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
How are allergic/anaphylactic reactions treated?
If symptoms are mild, then administration of anti-histamines and continue transfusion
Talk about anaphylaxis
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
How is anti-IgA anaphlaxis treated?
IgA deficient products such as washed platelets
Can also reduce the amount of circulating IgA through apheresis
How common is IgA deficiency
IgA deficiency 1/500 but complete deficiency is rare
1/20,000 can have an anti-IgA reaction
What makes anaphylatic reactions considered serious
Ag/Ab complexes that form generate C3a/C5a which act as powerful vasodilators
severe reactions may require Ig antigen/antibody levels e.g. IgA
What are the most common reations to platelets?
FNHTR
TRALI
TACO
AA
HTR (ABO antibodies)
What antibodies are most causative of platelet reactions
HLA or HPA antibodis
NB: these are the most common causes of refractoriness
What does platelet refractoriness mean for the patient?
Platelet transsfusions become ineffective -> platelets carry the antigen
Specific matched donors ar required
This usually means platelet apheresis donors are needed
What are the most common antibodies in post transfusion purpura
Anti-HPA-1a
Anti-HPA-5b
What happens with the antibodies produced in post transfusion purpura
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
What is transfusion associated dyspnea
anything that cannot be defined as TACO or TRALI
a grey area in symptoms between these two
pul,onary dyspneoa
Talk about the trends in pulmonary reports to the NHO year on year
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
How does TACO differ from TRALI
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
What is the ISBT definition of TAD
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
How many cases of TAD were reported to NHO in 2022?
2 reports of TAD
Dont know the cause of why these two patients have respiratory distress
When did TRALI stop being an issue and why?
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
What will TRALI look like
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
Whatis the cause of 90% of TRALI?
90% is caused by anti-HLA antibodies
What is TRALI, how does it occur
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
What antibodies commonly cause TRALI
anti-HLA or anti-HNA
What are anti-HNA antibodies, how are they involved in TRALI
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
What products are and arent risks for TRALI
SD plasma or octaplas arent risk products
FFP is a risk product -> hence why female multiparous donors arent used
What is the mortality of TRALI
Approximately 5% -> 1 in 20 die
What are the symptoms of TRALI
Severe acute onset within 4 hours after transfusion
Respiratory distress
Hypoxia
Pulmonary infiltrates
What is the source of the antibodies in TRALI
Either pre-formed leukocyte antibodies in the donor
But sometimes also in the recipient
List the TRALI implicated products
Whole blood
Red cell concentrates
Granulocyte concentrates
Platelet concentrated (pooled or apheresis)
FFP
Cryoprecipitate
IvIg
S/D treate plasma -> rare case report
Talk about TRALI caused by donor antibodies which cross-react with patient white cells
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
90% of TRALI is caused by donor antibody, what is the remaining 10% caused by?
Patient antibody vs donor cells - the antigen has been transfused in the component
What product is the most common cause of TRALI associated death
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
What is the mechanism behind TRALI
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
What is the 2 hit theory of TRALI
First hit = attraction neutrophils
Second hit = HLA/HNA or lipids
need to look up more on 2 hit
What are the treatment options for TRALI
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
Why arent women allowed to donate plasma
The more pregnancies you have the more HLA antibodies you have
How do we prevent TRALI in platelets
Male only donors and platelet additive solution
Hence
talk about the clinical course of TRALI
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%
What are five preventative measures of TRALI
- permanent deferral of donors implicated in previous TRALI
- Testing multiparous women for HLA and granulocyte specific antibodies
- Not using multiparous women as apheresis donors - lots of plasma
- removal of plasma from cellular blood components
- changes in component processing - pooling plasma! PAS in platelets
Talk about the incidence of TRALI
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
What is TACO
Pulmonary oedema is the main threat due to volume overload
Headache, hypertension, dyspnoea and heart failure suggestive of TACO
Who is most at risk for TACO
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
What product puts one at high risk of TACO and why
Albumin solutions
Albumin can drag in double its volume of water
albumin shift large volumes of extravascular fluid into the intravascular space
How can you differentiate TACO from TRALI
TACO = hypertension -> blood underpressure -> fluid pushed into lungs
TRALI = hypotension -> permeated blood vessels - fluid leaking out
What are the symptoms of TACO
Dyspnoea
Hypertension
Raised Brain natiuretic peptide
Hypoxia
Pulmonary oedema
normal or decreased left ventricular function
increased pulmonary artery occlusion pressure
What are the symptoms of TRALI
Dyspnoea
Hypotension
Fever
No change in BNP
Hypoxia
Leukpenia
Thrombopenia
Pulmonary oedema
How does the fluid produced in TACO differ from TRALI
TACO = dilute liquid, watery, low protein concentration
TRALI = full content plasma, higher protein content
Talk about hypothermia as an adverse affect of transfusion
Occurs during the rapid infusion of ‘chilled’ blood straight from the fridge
Ventricular arrhythmias result
Haemostasis can be impaired
Who is most at risk of hypothermia
Neonates or those undergoing massive transfusion
How do we prevent hypothermia
Pre-warm blood
Blood warming devices -> must meet a standard
Pre-warmed blood is desirable even with smaller volumes of transfused blood
Define a delayed haemolytic transfusion reaction
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
What antibodies are usually implicated in DHTRs
Antibodies to many blood group antigens are implicated
Some of these activate complement
What are some tell-tale signs of a DHTR
There is no improvement with transfusion and no evident bleeding
It might be encountered in the lab e.g. a positive DAT
What happens to red cells in a DHTR and what are the symptoms
RBCs are coated and removed extra vascularly by splenic and liver macrophages
How common are DHTRs in Ireland
We get between 7 and 10 per year
Talk about the Delayed transfusion reaction reported to NHO in 2022
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
In Ireland what antibodies are most often seen to cause delayed heamolytic reactions, as reported to NHO
Anti-JKa caused 5 of the 8 reactions in 2022
Other antibodies involved include anti Fya, anti-C/c and anti E/e
What is transfusion associated graft versus host disease
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
How does transfusion associated graft versus host disease manifest?
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
How is TA-GVHD treated?
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
How does gamma irradiation work to prevent TA-GVHD
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
How does TA-GVHD occur
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
Where in the world is the most TAGVHD and why is this
Most common in Japan
This is because of the small HLA pool over there
Who should receive irradiated products
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
How has TAGVHD trended over the years
SHOT figures for 1996-1999 recorded that TAGVHD was the commonest cause of TA death @12 cases but its very rare today
When does TA_GVHD occur
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
What does TRIM stand for?
Transfusion Related Immune Modulation
What is TRIM
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
What is thought to cause TRIM
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
Talk about iron overload as a result of transfusion
Consequence of multiple red cell transfusions over a long period of time
Resembles haemochromatosis
Affects the skin, endocrine glands, liver and heart
Who is most at risk of iron overload
SCD patients
Thallassemia patients
How do we treat iron overload
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
Talk about using desferrioxamine to treat iron overload
Binds fe2+ but also binds magnesium and calcium thus causing lots of other side effects hence dificult to use
How is iron overload diagnosed
Diagnosed in histology using a perls pressian blue stain on bone marrow to look for haemosiderin deposits
Why is transfusion for SCD/Beta thalassemia so difficult
They have long term requirements - will need transfusions frequently
Often difficult serology
Difficulties in supplying compatible blood
Iron overload
Talk about SCD patients are their need for transfusion
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
Why is it difficult to get blood for SCD patients
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
What is thought to be one of the reasons why rate of crisis increases as SCD patients get older, particularly in teen years
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
Give an example of a typica SC case of transfusion history
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
Give an example of a typica SC case of transfusion history
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
What is standard dosage of desferrioxamine therapy
500mg-1g/night
How do we try to prevent antibody production in SCD patients
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
What are some other non-specific examples of adverse reactions to transfusion
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
