Page 502 - Medicine and Surgery

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498 Chapter 12: Haematology and clinical immunology

Delayed haemolytic reactions occur in patients pre- in blood products. If the ECG shows a prolonged QT

viously sensitised to minor blood group antigens (eg interval i.v. calcium gluconate is required.
Duffy, Kell, Kidd) by previous transfusion or preg- Hyperkalaemia from degeneration of red cells within
nancy. Patient may develop anaemia and jaundice stored blood particularly if there is associated renal
about a week after the transfusion. failure.
Urticarial transfusion reactions are of unknown ae- Hypothermia from infusion of cold blood may pre-

tiology but possibly result from antibodies reacting cipitate a cardiac arrest.
with plasma proteins in the transfusion. The trans- Acute respiratory distress syndrome may occur due
fusion should be slowed or stopped and an antihis- to hypovolaemia, poor tissue perfusion or if patients
tamine given (e.g. chlorpheniramine). are over-transfused.
Non-haemolytic or febrile transfusion reactions are

due to the presence of antibodies to leucocytes in
the transfusion. Patients typically develop flushing, Clinical immunology
tachycardia, fever and rigors towards the end of trans-
fusion.
Anaphylactic transfusion reactions can occur in IgA
Allergy
deficient individuals (1 in 600 individuals) medi-
ated by histamine and other vasoactive mediators Hypersensitivity reactions
(see below). Patients develop vasodilation, hypoten- There are five basic types of hypersensitivity reactions
sion, bronchoconstriction and laryngeal constric- (see Table 12.11)
tion. It is treated as for anaphylaxis (see page 499).
Anyfuture transfusions should be with washed red
Type I hypersensitivity (allergy)
cells, autologous blood or blood from IgA deficient
On the first encounter with an antigen IgE antibodies
donors.
are formed. These bind to a receptor on the surface of
If atransfusion reaction is suspected any ongoing trans-
mastcells.Onsubsequentcontactswiththeantigenthere
fusion should be stopped. The remaining blood unit and
is cross-linking of IgE on the mast cells which triggers
a sample of the patient’s blood should be sent to the lab-
them to degranulate releasing histamine and other pre-
oratory for repeat cross match. Other supportive treat-
formedmediators(seeFig.12.15).Thereactionalsotrig-
ments may be required.
gersarachadonicacidmetabolismleadingtotheproduc-
tion of leukotrienes, prostaglandins, prostacyclins and
Problems of massive transfusion thromboxane. The clinical reaction is characterised by
vasodilation, bronchoconstriction, and localised tissue
Transfusionequivalenttoreplacingtheentirecirculating
oedema (see also anaphylaxis page 499).
volume within a 24 hour period is defined as a massive
transfusion.Thismayberequiredfollowingtrauma,gas-
Type II hypersensitivity (antibody dependent
trointestinal or obstetric haemorrhage.
cytotoxic hypersensitivity)
Thrombocytopenia may result from the underlying

Type II hypersensitivity is mediated by antibodies, these
bleeding and because there are no platelets in packed
may be directed at:
redcells. In severe cases platelet transfusion may also
be required.
Coagulation factor deficiency results from the dilu- Table 12.11 Hypersensitivity reactions

tion effect of massive fluid transfusion as there is a
Type I IgE and mast cells-mediator release and
lack of factors in packed red cells. There may also be secondary inflammation.
aconsumptive coagulopathy due to ongoing bleed- Type II IgG directed against self-antigens.
ing. Patients may require fresh frozen plasma and/or Type III Immune complex mediated damage.
cryoprecipitate. Type IV Damage caused by activated T cells.
Type V Stimulatory antibody mimics the action of a
Hypocalcaemia results from the sodium citrate

hormone.
(which chelates calcium) used as an anti-coagulant