In this section
For information pertaining to EMR management of transfusion reactions, refer to the tip sheet for guidance.
Each blood product transfused carries a small risk of an acute
or late adverse effect.
The most common immediate adverse reactions to transfusion are
fever, chills and urticaria. The most potentially significant
reactions include acute and delayed haemolytic transfusion
reactions and bacterial contamination of blood products. During the
early stages of a reaction it may be difficult to ascertain the
Immediate patient management comprises stopping the transfusion,
reperforming the pretransfusion checklist, documenting
observations, providing immediate patient care and contacting the
treating medical officer.
In certain cases of mild urticarial reactions or the presence of
repeated chill-fever reactions in multiply transfused patients, the
medical officer may elect to restart the transfusion after
evaluation and treatment of the patient.
This flow chart describes the signs and symptoms of acute transfusion reactions and the immediate management required.
Consider possible transfusion reaction where there is a change or deterioration in the patient’s condition.
Transfusion reaction will be added to the EMR FYI flag. Further details can be added to this. It will carry over to future admissions.
A Medical practitioner is responsible for documenting details of the transfusion reaction and their review of patient in EMR via progress notes. Smart text for transfusion reactions is available to assist this.
Clinical Haematology staff will review transfusion reactions. This report is available in the laboratory results “transfusion reaction evaluation” and include details of reaction, action taken to manage and any pre-medications or specific product requirements for further transfusions.
Moderate to serious transfusion reactions are also reported internally via VHIMS by clincial haematology team.
Additional samples sometimes required (as directed by
Cause: Fever and chills during
transfusion are thought to be caused by recipient antibodies
reacting with white cell antigens or white cell fragments in the
blood product or due to cytokines which accumulate in the blood
product during storage. Fever occurs more commonly with platelet
transfusion (10-30%) than red cell transfusion (1-2%).
It is important to distinguish from fever due to the patient's
underlying disease or infection (check pretransfusion temperature).
Fever may be the initial symptom in a more serious reaction such as
bacterial contamination or haemolytic reaction.
Investigation: Fever can be the
initial sign in more severe transfusion reactions (haemolytic or
bacterial sepsis) and should be taken seriously.
Follow the steps 'immediate management of an acute transfusion
reaction'. For isolated fever or chills in some
patients, the medical officer may elect to restart the transfusion.
If the fever is accompanied by significant changes in blood
pressure or other signs and symptoms, the transfusion should be
ceased and investigated
Check for HLA antibodies in patients having repeated febrile
Prevention: A proportion of patients
who have febrile reactions will have similar reactions to
subsequent transfusions. Many are prevented by leucocyte filtration
(either bedside or pre-storage).
Cause: Seen in approximately 1% of
recipients and caused by foreign plasma proteins. On rare occasions
they may be associated with laryngeal oedema and bronchospasm.
Management: If urticaria occurs in
isolation (without fever and other signs), slow the rate or
temporarily stop transfusion. If symptoms are bothersome, consider
administering an antihistamine before restarting the transfusion.
If associated with other symptoms, cease the transfusion and
proceed with investigation.
Investigation: In the case of mild
urticarial reactions with no other signs or symptoms, it is not
necessary to submit blood specimens for investigation. It is also
usually possible to restart the transfusion. Such a decision should
be made after assessment by the treating doctor.
Anaphylactic and anaphylactoid reactions have signs of
cardiovascular instability including hypotension, tachycardia, loss
of consciousness, cardiac arrhythmia, shock and cardiac arrest.
Sometimes respiratory involvement with dyspnoea and stridor are
Cause: In some cases patients with IgA
deficiency who have anti-IgA antibodies can have these
Management: Immediately stop
transfusion, supportive care including airway management may be
required. Adrenaline may be indicated. Usually given as 1:1000
solution, 0.01mg/kg s.c./i.m. or slow i.v. Anaphylaxis
Investigation: IgA levels and anti-IgA
Prevention: Patients with anti-IgA
antibodies require special blood products such as washed red blood
cells and plasma products prepared from IgA deficient donors.
Manage further transfusion in consultation with the
Cause: The majority of haemolytic
reactions are caused by transfusion of ABO incompatible blood, eg
group A, B or AB red cells to a group O patient. Most haemolytic
reactions are the result of human error such as the transfusion of
properly labelled blood to the wrong patient, or improper
identification of pretransfusion blood samples.
Non-immune haemolysis of RBCs in the blood container or during
administration can occur due to physical disruption (temperature
changes, mechanical forces, non-isotonic fluid)
Symptoms: Chills, fever, pain (along
IV line, back, chest), hypotension, dark urine, uncontrolled
bleeding due to DIC.
Management: Immediately stop
transfusion. Notify hospital blood bank urgently (another patient
may also have been given the wrong blood!). These patients usually
require ICU support and therapy includes vigorous treatment of
hypotension and maintenance of renal blood flow.
Prevention: Proper identification of
the patient from sample collection through to blood administration,
proper labelling of samples and products is essential. Prevention
of non-immune haemolysis requires adherence to proper handling,
storage and administration of blood products.
NOTE: ABO Haemolytic reactions are reported to DOH
as a sentinal
Cause: Bacteria may be introduced into
the pack at the time of blood collection from sources such as donor
skin, donor bacteraemia or equipment used during blood collection
or processing. Bacteria may multiply during storage. Gram positive
and Gram negative organisms have been implicated. Platelets are
more frequently implicated than red cells.
Symptoms: Very high fever, rigors,
profound hypotension, nausea and/or diarrhoea.
Management: Immediately stop the
transfusion and notify the hospital blood bank. After initial
supportive care, blood cultures should be taken and broad-spectrum
antimicrobials commenced. Laboratory investigation will include
culture of the blood pack.
Prevention: Inspect blood products
prior to transfusion. Some but not all bacterially contaminated
products can be recognised (clots, clumps, or abnormal colour).
Maintaining appropriate cold storage of red cells in a monitored
blood bank refrigerator is important. Transfusions should not
proceed beyond the recommended infusion time (4 hours).
Further information: Medilink Newsletter ARCBS Volume 5
No 2 august 2002
Transfusion Related acute Lung Injury (TRALI) is a clinical
diagnosis of exclusion characterised by acute respiratory distress
and bilaterally symmetrical pulmonary oedema with hypoxaemia
developing within 2 to 8 hours after a transfusion. A CXR shows
interstitial or alveolar infiltrates when no cardiogenic or other
cause of pulmonary oedema exists.
Cause: Pulmonary vascular effects are
thought to occur secondary to cytokines in the transfused product
or from interaction between patient white cell antigens and donor
antibodies (or vice versa).
Management: Symptomatic support for
respiratory distress includes oxygen administration and may require
intubation and mechanical ventilation. Symptoms generally resolve
over 24-48 hours.
Cause: Patients with cardiopulmonary
disease and infants are at risk of volume overload especially
during rapid transfusion.
Management: Stop the transfusion,
administer oxygen and diuretics as required.
Prevention: Avoid unnecessary fluids
and use appropriate infusion rates.
Cause: Rapid infusion of large volumes
of stored blood contributes to hypothermia. Infants are
particularly at risk during exchange or massive transfusion.
Prevention and Management:
Appropriately maintained blood warmers should be used during
massive or exchange transfusion. Additional measures include
warming of other intravenous fluids and the use of devices to
maintain patient body temperature.
Cause: Citrate is the anticoagulant
used in blood products. It is usually rapidly metabolised by the
liver. Rapid administration of large quantities of stored blood may
cause hypocalcaemia and hypomagnesaemia when citrate binds calcium
and magnesium. This can result in myocardial depression or
coagulopathy. Patients most at risk are those with liver
dysfunction or neonates with immature liver function having rapid
large volume transfusion.
Management: Slowing or temporarily
stopping the transfusion allows citrate to be metabolised.
Replacement therapy may be required for symptomatic hypocalcaemia
Cause: Stored red cells leak potassium
proportionately throughout their storage life. Irradiation of red
cells increases the rate of potassium leakage. Clinically
significant hyperkalaemia can occur during rapid, large volume
transfusion of older red cell units in small infants and
Prevention: At RCH red cells are
irradiated just prior to issue. Blood less than 7 days old is
generally used for rapid large volume transfusion in small infants
(eg cardiac surgery, ECMO, exchange transfusion)
Cause: Patients may develop antibodies
to red cell antigens. Antibodies can occur naturally, or may arise
as a consequence of previous transfusion or pregnancy. A delayed
haemolytic reaction occurs when a patient develops an antibody
directed against an antigen on transfused red cells. The antibody
may cause shortened red cell survival, with clinical features of
fever, jaundice and lower than expected haemoglobin following
transfusion. Most delayed haemolytic reactions produce few symptoms
and may go unrecognised, however there are reports of serious
consequences in critically ill patients.
Prevention: An antibody screen is
performed as part of pre-transfusion testing. When an antibody is
detected, it is identified and appropriate antigen negative blood
is provided. Sometimes antibodies fall below detectable limits and
may not be detected by pretransfusion testing.
Patients experiencing alloantibody formation are asymptomatic.
The alloantibody is discovered at the time of pretransfusion
testing. Appropriate antigen negative blood will be supplied.
Prevention: alloimmunisation to the D
and K (Kell) antigens is prevented by the provision of Rh(D)
negative and Kell negative blood for Rh(D) negative, Kell negative
patients. This is important for females with child-bearing
potential as these antibodies can cause severe haemolytic disease
of the newborn during pregnancy.
At risk groups: Patients with sickle
cell disease or major haemoglobinopathy syndromes who are
chronically transfused are at greatest risk of alloantibody
formation. Prior to commencing transfusion, patients with these
condition should have extended red cell phenotyping performed (EDTA
sample). Blood matched for the patient's Rhesus and Kell antigens
is usually supplied for transfusion
When thrombocytopenic patients do not achieve the expected
post-transfusion platelet count increment they are said to be
refractory. This usually occurs in patients receiving frequent
platelet transfusions. There are clinical and immunological causes
of platelet refractoriness. Clinical causes include; sepsis, DIC,
bleeding, fever, some drugs, and enlarged spleen.
Cause: Immunological causes include
the development of antibodies to human leucocyte antigens (HLA) or
human platelet antigens (HPA).
refractoriness can be managed by the provision of HLA or HPA
Prevention: Leucocyte reduction of
blood products to levels less than 106/unit reduces the
likelihood of alloimmunisation. This can be achieved through the
use of prestorage or bedside leucocyte reduced blood products.
Cause: Ta-GVHD occurs when donor
lymphocytes in cellular blood products engraft in a susceptible
transfusion recipient. These donor lymphocytes proliferate and
damage target organs especially bone marrow, skin, liver and
gastrointestinal tract. The clinical syndrome comprises fever, skin
rash, pancytopenia, abnormal liver function and diarrhoea and is
fatal in over 80% of cases. The usual onset is 8-10 days post
transfusion, with a longer interval between transfusion and onset
of symptoms in infants.
The most commonly reported setting for Ta-GVHD is
immunocompetent recipients of blood from biologically related
(directed) or HLA identical donors. The disease is also reported in
immunologically compromised patients.
Prevention: Gamma irradiation of
cellular blood products (whole blood, red blood cells, platelets,
granulocytes) for at risk patients.
At risk groups:
Some studies suggest a link between blood transfusion and
increased risk of infection and cancer recurrence. However this is
currently considered unproven.
Cause: Unknown, possibly mediated by
donor white cells or plasma.
Management and Prevention: Not known,
possibly leucocyte depletion of blood products.
Cause: Iron accumulation is a
predictable consequence of chronic RBC transfusion. Organ toxicity
begins when reticuloendothelial sites of iron storage become
saturated. Liver and endocrine dysfunction creates significant
morbidity and the most serious complication is cardiotoxicity which
causes arrhythmias, and congestive heart failure. Patients
receiving chronic transfusion usually have their iron status
monitored and managed by their physician.
Management and Prevention: Iron
chelation therapy is usually commenced early in the course of
chronic transfusion therapy.
A variety of infectious agents may be transmitted by
transfusion. Definitive evidence of transmission by transfusion
requires demonstration of seroconversion or new infection in the
recipient and isolation of an agent with genomic identity from both
the recipient and the implicated donor. Strong presumptive evidence
of transfusion transmission includes recipient seroconversion
within an appropriate interval after transfusion, the recognition
of appropriate infectious markers in an implicated donor on
follow-up investigation, or both. Transfusion transmitted disease
should be reported to the Australian Red Cross Blood Service.
Suspected transfusion-transmitted bacterial or parasitic
infection (malaria) should be reported urgently in order to recall
other potentially infectious blood products from the same
Estimated risk of transfusion transmitted
infection from Medilink, ARCBS October
Point estimates for risk of transfusion transmitted viral
infection from ARCBS donations calculated using data from
July 2000 to June 2003.
The Australian Red Cross Blood Service describes the residual risk estimates for transfusion-transmissible viral infections.