Blood transfusion Flashcards
What are the 2 main blood group systems?
- RhD: based on presence or absence of Rhesus D surface antigen. In men it doesn’t matter as much they can have O+ if nothing else available cos won’t lead to HDN obv but matching is better to reduce transfusion reactions
- ABO: presence of A/B antigens on surface, antibodies produced to antigens that are not on your own RBC surface so type AB has no antibodies as they cant make antibodies against their own antigens, and type O has no antigens so has anti-A and anti-B antibodies
What is the significance of Rhesus grouping in pregnancy?
RhD- women will make RhD antibody if they are exposed to RhD+ blood - for the patient if they are given + blood is fine as they can’t attack their own RBCs that are negative for the antigen, however in pregnancy the anti-D antibodies can cause HDN
may be caused by sensitising events, or for the next child if the current one happens to be RhD=
Why is O negative the universal donor?
Although O blood as anti-A and anti-B antibodies in plasma, it has no antigens on the RBC, so even if recipient has antibodies they will not attack the RBC (probably)
What is the universal recipient?
AB positive
There are no antibodies in the plasma so they can’t mount an immune response to donor blood
Packed red cells
- Ind: Hb<70 (may be higher threshold), symptomatic anaemia, acute blood loss, severe sepsis Hb <90
- Given over 2-4h
- Specific risks are iron load if repeated, autoantibodies (so do a new G+S for extra transfusions after 3)
Fresh frozen plasma
Contains clotting factors
- Universal FFP donor is AB as lacks the antibodies in the plasma
- Ind: DIC, all major haemorrhage (usually after 2nd PRC), haemorrhage due to liver disease, prophylactically in some surgeries
- Given over 30 mins
Cryoprecipitate
Made from plasma, contains fibrinogen, vWF, factor VIII, fibronectin, small volume per unit
- Ind: DIC with low fibrinogen, vWD, massive haemorrhage esp in haemophilia
- Given stat
Platelets
*Ind: haemorrhagic shock from trauma, thrombocytopenia <20, or <30 with active bleeding, or <100 if severe bleeding/at a critical site like CNS. Not for ITP, TTP, heparin-induced!
General complications of PRC transfusions?
- Clotting abnormalities from dilution effect - reduce by giving FFP+plts after 4 PRC units
- Hypocalcaemia - citrate in preservative chelates calcium
- Hyperkalaemia - partial haemolysis
- Hypothermia - esp in major haemorrhage rapid transfusion can drop core temp
- Arrhythmias from hypothermia + hyperkalaemia
Acute haemolytic reaction
Usually cos of ABO incompatibility - activation of complement + cytokines - donor cells destroyed by recipient’s antibodies - haemolysis
CF: fever, urticaria, anxiety, haemoglobinuria, hypotension, generalised bleeding from DIC
Ix: low Hb, low haptoglobin, high LDH, high bili, positive DAT
M: stop transfusion, tell blood blank, supportive (O2, fluids, specialist)
Transfusion-associated circulatory overload (TACO)
CF: sudden sob, fluid overload, severe hypoxaemia
Ix: urgent CXR
M: oxygen + diuretics, prophylaxis if at risk (e.g. HF) with furosemide
Transfusion-related acute lung injury (TRALI)
A type of ARDS causing non-cardiogenic pulmonary oedema
CF: sob, hypotension, fever within 6h post-transfusion
high mortality, start high flow O2 + ITU input
Fluid overload
Each unit of PRC is 450ml so need to monitor esp in elderly + CHF
Mild allergic reactions
Pruritis - give an anti histamine like chlorphenamine than can continue transfusion
Non-haemolytic febrile reactions
Usually non-life threatening, antibodies against donor leucocytes (rather than in TRALI which is against recipients) - stop transfusion, give antipyretic + antihistamine
Anaphylaxis
Because recipient is allergic to protein components in the donor blood
Onset min-hour, need regular obs to identify
What are the potential delayed transfusion reactions?
- Infection e.g. vCJD, hep C (shouldn’t know but who knows)
- Delayed haemolytic reaction: antibodies to minor antigens like Kidd, 3-14d later due to secondary response. Causes drop in Hb, fever, jaundice, haemoglobinuria
- Graft vs host disease: HLA-mismatch esp when transfuse non-irradiated blood to immunocompromised pt. CF fever, skin involvement (may be TEN), D+V, mortality 100%
- Iron overload: esp in repeated transfusions, can cause cirrhosis, bronze diabetes, cardiomegaly, conduction disturbance, arthralgia, hyper pigmented skin
Who needs CMV negative blood products?
- Neonates, pregnant women, intra-uterine transfusion
- because CMV can cause sensori-neural deafness + cerebral palsy
*Pt who are likely to need BM/SC transplant in future, or who are on specific clinical trials
Who needs irradiated blood products?
- Hodgkin lymphoma, after SCT, receiving blood from 1st/2nd degree family members, after anti-thymocyte globulin therapy, on certain chemos, intra-uterine transfusion, in first 6m of age, congenital immune deficiency
- Is to reduce risk of graft vs host disease
What bloods are done before giving a transfusion?
Label at pt bedside
G+S - before XM, and if blood loss not anticipated but is a possibility, looks for blood groups + atypical antibodies, takes ~40m, doesn’t issue blood
XM - physically mixes pt plasma + donor red cells to look for immune reaction. If no reaction is released for use - takes ~40m. do if anticipate blood loss
Consenting for transfusions
- Informed written consent where possible, if regular only need at beginning, for surgical do when consent for procedure, for emergencies get written if time allows otherwise document verbal consent, emergency obv can do in unconscious
- Pros: depend on the condition
- Potential risks: extremely small risk of viral illness, very small risk of bacterial infection, risk of transfusion reaction (allergic or haemolytic), unknown but prob extremely small risk of vCJD, v small risk of receiving unsuitable product, alternative options
How many units should you prescribe for non-active bleeding?
.Usually 1 unit RBC, and re-assess after each transfusion
What do you give blood products through?
A green (18G) or grey (16G) cannula (otherwise haemolyse) through a blood giving set which has a filter in the chamber
What is the initial management of a suspected transfusion reaction?
- Stop transfusion, maintain venous access
- O2
- Crystalloid fluids in haemolytic
- Diuretics in TACO
- Adrenaline 0.5ml (500mcg) or 1:1000 IM + hydrocortisone infusion
How would you investigate symptomatic anaemia?
FBC - retics, MCV
Increased retics is appropriate - look for haemorrhage + haemolysis
Haematinics - for folate, B12, iron studies for ferritin
Haemolysis screen: blood film, DAT (positive in immune haemolysis, negative in non-immune haemolysis or non haemolysis), bilirubin + LDH (rises as released), haptoglobin (falls as it mops up free Hb), retics (increase)
Pathophysiology of haemolytic anaemia
- Hereditary: membrane disorders like HS, enzymopathies like G6PD deficiency, abnormal Hb like SCD/thalassaemia
- Acquired:
- Alloimmune like HDN or incompatible transfusion
- Autoimmune: warm caused by IgG (CLL, SLE, drugs), cold caused by IgM (mycoplasma, EBV), lymphoma
- Non-immune: microangiopathic haemolytic anaemia, TTP, HUS, hypersplenism, sepsis, malaria
Alloantibodies vs autoantibodies
Alloantibodies: produced against red cell antigens that aren’t on an individual’s own RBCs, transfusion + pregnancy can sensitise na individual
Autoantibodies: against red cell antigens on the individual’s own red cells
Why is it difficult to find compatible blood in AIHA?
The autoantibody can react with any of the red cell antigens causing agglutination reactions - all the tests may become positive
Can get around this by removing the autoantibody from the serum to see if there are alloantibodie,s however this obviously takes time to get the compatible blood
Outline the management of haemolytic anaemia
- Initial: steroids, folic acid, discontinue causative meds
- Supportive: iron chelation, red cell transfusions with IV Ig beforehand to reduce haemolysis
- Long-term: rituximab (stops B cells which are making the antibodies, but leaves T cells so preferred option), chemo for CLL, splenectomy if failing, alamtuzumab (also affects T cells so last line(
What is major haemorrhage and what are the CF?
Classified based on how much blood is lost
Causes tachypnoea, tachycardia, hypotension (tho may be normal), clamminess, cool peripheries, dizziness, confusion, evidence of external bleeding/swelling/bruising/peritoneal irritation
How would you manage a major haemorrhage?
- ABCDE with warmed IV crystalloid bolus, O neg emergency blood if indicated, direct pressure to control, reverse warfarin anticoagulation, anti-fibrinolytic (e.g. IV tranexamic acid but only in obstetrics), cell salvage machines may be used
- Activation of major haemorrhage protocol: nominate a blood bank coordinator, dial 2222, send all the bloods, fluid-warming devices + air warming blanket
- Depends on how much already given but generally 4 units of PRC given, then more red cells + FFP, then add more with platelets
- If trauma go straight to PRC + FFP + plts
- For stage 4 also give cryoprecipitate
- If XM blood not available PRC giveen as O neg for women + children and O pos for men
- NB FFP + cryo both need defrosting so can take about 20min
How much should 1 unit of PRC increase Hb by?
10g/L
Prothrombin complex concentrate
For emergency reversal of anticoagulation in patients with either severe bleeding or a head injury with suspected intracerebral haemorrhage, or prophylactically in emergency surgery
Cell saver devices
Collect pt blood lost during surgery then re-infuse it.
- Can reduce risk of blood borne infection, if type that washes blood before re-infusing
- Can be acceptable to Jehovah’s witnesses
- CI in cancer as risk of dissemination
Reversal of warfarin
- Stop warfarin
- Vitamin K reversal: oral takes 24h, IV 4-6h
- Fresh frozen plasma: less common now for 1st line, not appropriate in fluid overload, only use if HPC not available
- Human Prothrombin Complex (reversal within 1 hour)
- Bereplex 50 u/kg
- Rapid action but factor 6 short half life, therefore give with vitamin K
