RBC Transfusion in Sickle (bsh 2016(1) & 2016(2))
Intro
Goals of Tx in Sickle
Improving oxygen-carrying capacity by correcting anaemia
Preventing or reversing complications of SCD related to vaso-occlusion and haemolysis by decreasing the proportion of HbS in relation to HbA
Common steady state haemoglobin levels:
60-90 in HbSS
70-90 in S/B0 Thal
90-120 in S/B+ Thal
90-140 in HbSC
Also document baseline reticulocyte count for comparison in acute illness
Avoiding hyperviscosity
HbS %
Sickling complications are related to HbS %
No single target covers all indications but aiming for HbS <30% is general rule
Keeping HbS <30% reduces rates of stroke, ACS, priapism, avascular necrosis
Hb
Post-transfusion Hb should not exceed baseline Hb, esp if HbS% remains >30%
Post-transfusion Hb may be set higher in context of chronic transfusion programme as HbS % will be lower and so lower risk of hyperviscosity.
Transfusing in Acute Illness
General Principles
Contact pt’s primary hospital for their baseline Hb, retic count, transfusion history and red cell pheno/geno-type and history of alloantibodies.
Patients should carry a card stating their phenotype +/- alloantibodies
Aim to prevent need for transfusion with good SCD management – i.e. incentive spirometry, analgesia, hydration.
Long term complications of transfusion
Alloimmunisation - Hydroxycarbamide reduces transfusion requirements
Iron Overload
3 monthly ferritin
MRI liver 1-2 yearly if suspected or proven overload
Use of automated red cell exchange prevents or even corrects iron overload
Transfusion-Transmitted Infection
Immunise against Hep B
Annual Hep B/C and HIV testing if transfused
Top Up vs Exchange Transfusion
Indication
Top-up preferred for treatment of symptomatic severe anaemia
Exchange preferred for immediate or sustained reduction in complications of SCD
Hyperviscosity
Risk of hyperviscosity at a given Hb is dependent on Hb S% and Hct
Hyperviscosity reduces oxygen delivery and exacerbates sickling.
Viscosity effect of sickle cells is reduced by presence of normal red cells
However simple top-up will also raise Hct, negating the effect of reduced HbS%
Iron balance
Top-up causes increased in total iron
Manual exchange decreases rate of iron loading by 40% compared to top-up
Automated exchange can achieve neutral or negative iron balance
Alloimmunisation
Automated exchange consumes more units than top-up or manual exchange but does not appear to increase risk of alloantibody formation.
Venous Access
Limits exchange in many patients
Indwelling venous catheters an option but high complication rate – inf and thrombosis
Resources
Exchange has higher resource and financial requirements than top-up
Automated exchange
Reduces HbS% faster than manual as plasma, platelets and white cells are returned to patient.
Takes 2 hours if good IV access
More effective and so allows 6-weekly transfusion intervals
Limits or eliminates iron loading
SE: Dilutional thrombocytopenia, hypocalcaemia, line complications, fluid shifts
Manual Exchange
Aim to exchange 30% of blood volume and so achieve 30% HbA.
Typically remove 4 units, transfuse 3 units and replace remaining vol with saline
Usually increases Hb by 10-20g/l
Laboratory Aspects
Use ABO, extended Rh- and Kell matched blood as a minimum standard
Significant differences in RBC antigen frequencies between Caucasian and African donors contributes to alloimmunisation.
Sensitisation occurs against Rh variants identifiable on molecular genotyping but not by serological methods.
Compatibility testing
Fully automated systems for ABO typing should be used
Antibody screening should always be part of pre-transfusion testing
For those not on a regular transfusion programme, antibody screening should be repeated after every transfusion episode.
Serology should be performed within 72 hours prior to transfusion if recently transfused.
Extended phenotype/genotype
C, c, E, e, K, k, JKa, JKb, Fya, Fyb, S, s
Should be performed on all patients at baseline
If S-, s- then perform U typing
Offer RBC genotyping (Free with NHSBT in 2016/17 but no longer)
Blood product Selection
Matched for full Rh and K antigens as a minimum
R0 wherever possible for R0 patients. rr can be used if R0 unavailable in emergency
Match for historical antibodies as may not be identified on current serology.
As of 2023, it is no longer recommended to select ‘fresh blood’ for any patient >1 year old. This change has been circulated by NHSBT. Formal addendums to the BSH guidelines will follow. (This replaces the original recommendation: Red cells should be <10 days old for top-up, <7 days for exchange).
Haemolytic Transfusion reactions
Classical Delayed Haemolytic Transfusion Reaction (DHTR)
Anamnestic immune responses in alloimmunised patients
Occur in 5-10% of transfused patients
Fever + Jaundice + Anaemia 7-10 days after transfusion +/- sickling pain
There is clear lab evidence of haemolysis with a fall in HbA %
Alloantibody often identified
Hyperhaemolysis
Sub-type of DHTR - some debate over whether it is truly its own entity.
Severe sickle pain + fever + haemoglobinuria
Destruction of both donor and patient red cells
Post-transfusion Hb lower than pre-transfusion
HbS and HbA detectable in urine by HPLC
DAT often negative and alloantibody not identifiable
Further transfusion worsens haemolysis but should not be withheld in life-threatening anaemia. Transfuse with IVIg + IV Methylprednisolone.
Rituximab may have a role.
AIHA
Auto Anti-e is most common
5-10% of transfused SCD patients
More common in multiply alloimmunised patients and molecular Rh typing is starting to show that many supposed autoantibodies are actually Rh alloantibodies against Rh alleles not detectable by serology.
Intro to Indications for transfusion
2 main goals
Correction of anaemia
And/or reduction of HbS in proportion to HbA
The low steady state Hb in SCD is the result of the low oxygen affinity of HbS and therefore not a reason to transfuse on its own.
Emergency Transfusion with the primary aim of correcting acute anaemia
Acute anaemia in SCD = Fall in Hb >20g/l below steady state value.
Causes include:
Decreased production, sequestration and increased destruction.
Assessment: History of recent transfusion, haemodynamic status, liver and spleen size. FBC and reticulocytes.
Aplastic Crisis
Acute anaemia + reticulocytopenia. Hb often falls by >40g/l from baseline
Usually due to Parvovirus B19
Spontaneous recovery after 7-10 days of aplasia
Simple transfusion usually sufficient
Acute splenic sequestration
Acute anaemia + reticulocytosis + sudden splenic enlargement
Commonest <1 y.o. (later in HbSC)
Life-threatening in severe cases
Small volume simple transfusion up to steady state Hb
Risk of hyperviscosity when red cells return to circulation
High risk of recurrence —> splenectomy if 2 or more episodes
Acute hepatic sequestration
Acute anaemia + reticulocytosis + sudden liver enlargement
Small volume simple transfusion up to steady state Hb
Risk of hyperviscosity when red cells return to circulation
Increased haemolysis during painful crisis
Hb often drops during painful crisis
Usually recovers spontaneously
Simple transfusion not usually indicated unless drop of >20g/l or Hb <50g/l
Other causes of exacerbation of anaemia
HU therapy – severe anaemia is usually due to intercurrent illness, not myelosuppression from the drug. Stop drug temporarily and restart when Hb recovers.
Sickle cell nephropathy – slow Hb decline which may become symptomatic.
Emergency Transfusion with the primary aim of reducing HbS in relation to HbA
Acute Chest Syndrome (ACS)
Simple transfusion aiming for target Hb 100-110 g/l prevents progression to respiratory failure in mild ACS if given early.
Consider exchange if PaO2 <9.0 kPA on room air or other signs of deterioration.
Exchange recommended if
Severe ACS
Failure to respond to simple transfusion
Patients with Hb >90g/l (little leeway for simple Tx)
Acute Ischaemic Stroke
Aim for HbS <30%
Simple or exchange but must be performed urgently at time of stroke
Avoid hypovolaemia and aim Hb of 100g/l
Acute multi-organ failure
Complicates severe painful crises
More common in mild SCD where steady state Hb is higher
Exchange transfusion required
Mesenteric (‘Girdle’) Syndrome
Rare, severe sequestration in mesenteric vascular bed, liver and lungs
Mimics peritonitis and ileus. Often progresses to include ACS.
Exchange transfusion required
Severe Sepsis
Aggravates sickling. Simple or exchange transfusion may be beneficial
Acute intrahepatic cholestasis
Extreme conjugated hyperbilirubinaemia. Mechanism poorly understood
High mortality from liver failure and bleeding
No established treatment but exchange transfusion should be tried.
Acute priapism
Priority treatment is penile aspiration/irrigation followed by intracavernosal injection of sympathomimetic drugs.
Simple/exchange transfusion may aid peri-op optimization is surgery required.
Chronic Transfusion
Primary Stroke prevention in children (2-16 y.o.)
STOP and STOP2 trials - Transfusion to maintain HbS <30% in children with SS or S/B-thal with average Transcranial Doppler Ultrasonography (TCD) velocities >200cm/s in the internal carotid or middle cerebral artery reduces risk of first stroke by 92%
TWiTCH trial – Switching to HU after at least one year of transfusion is non-inferior to continuing with chronic transfusion provided no severe cerebral vasculopathy on MRA.
Secondary prevention of silent cerebral infarction in children
In children identified as having silent cerebral infarcts, discuss risks and benefits of chronic transfusion with parents. MRA may help risk stratify patients
Secondary prevention of overt stroke in children
Maintain HbS <30% long-term
SWiTCH trial – compared transfusion + chelation vs HU + phlebotomy. Trial stopped early due to clear superiority of transfusion + chelation.
Primary Stroke Prevention in Adults
No evidence to guide practice
What to do when turn 17 if had been on chronic transfusion? Discuss with patient
Secondary Stroke Prevention in Adults
Investigate as per any other patient – AF, carotid artery disease etc
Maintain Hb <30% long-term if stroke attributed to SCD
Recurrent ACS
HU is 1st line
Consider chronic transfusion if HU fails or contraindicated
Frequent painful crises
Hospital admission ≥3 x per year due to crises is ass. with increased risk of early death
HU therapy is 1st line
Chronic transfusion if HU fails or contraindicated.
Chronic transfusion reduces hospital admissions from 2 to 0.2 per patient per year
Other possible indications
Based on case-by-case discussion with patient
Priapism, avascular necrosis, sickle retinopathy lack evidence but may be appropriate
Could be considered in ESRF, pre and post kidney transplant
Preoperative Transfusion
(N.B. See also 2021 guideline from Association of Anaesthetists for peri-op management in SCD)
Anaesthesia and surgery increase sickle-related complications
Optimise oxygenation, warmth and hydration peri-operatively
Should be performed in centres with specialist haemoglobinopathy support.
Role of routine preoperative transfusion
TAPS 2013 study – small numbers, but ACS occurred post-op in 27% of untransfused compared to 3% of transfused patients undergoing low to medium risk surgery.
Optimal preoperative transfusion regimen
No good evidence to guide practice
Suggest simple transfusion if Hb <90g/l to achieve Hb of 100g/l prior to low to medium risk surgery.
Exchange considered if high-risk surgery, severe SCD or other significant co-morbidities.
Emergency Surgery
No good evidence
Do not delay emergency surgery for transfusion, rather perform intra-op or post-op
Transfusion in Pregnancy
Maternal complications in SCD
Sickle problems, pre-eclampsia, pre-term labour and increased rate of c-section.
Fetal complications in SCD
Intra-uterine growth restriction, prematurity and increased risk of fetal loss
Conflicting evidence on prophylactic transfusion
Recommend prophylactic transfusion if:
History of previous severe SCD complications
Repeated SCD complications during pregnancy
If other serious co-morbidities present