Safe Use of Blood

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Before transfusing check the compatibility report, the label
attached to the blood bag for the following:
• IP number
• Name of the patient including middle name and surname.
• The name and IP number should tally.
• Blood group.
• Donor registration number.
• Date of collection and date of expiry.
At the bedside confirm the patient’s identity which should be
checked from:
• The records of the patient.
• The patient himself verbally.
• In unconscious patients identify the patient from wrist band.
Following are the most important points:
1. Do not infuse any other medication along with blood.
2. A doctor should supervise the event.
3. When transfusing blood, watch the patient for first 15 minutes
for vitals. Then watch every 30 minutes till transfusion is
completed.
4. Rate of transfusion for whole blood/PRBCs should be 1 mL/
minute and transfusion should be completed within 4 hours.
5. Avoid transfusion from family members in view of graft
versus host disease (GVHD).
Blood transfusion is not without risks. Hence overweigh the
benefits for the patient.
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Safe Use of Blood
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Essentials of Blood Banking and Transfusion Medicine
The reason for this is:
• Blood cannot be manufactured. It has to come only from donors.
• The red cells have antigens on their surface.
• In routine practice, it is necessary to determine the
compatibility of certain red cell antigens between the donor
and the recipient.
• Blood can be a source of blood transmitted infectious diseases.
There are many blood group systems. Amongst these, the
two most important blood groups in blood transfusion are:
• ABO System
• Rh System
ABO and Rh compatible blood is mandatory requirement.
Testing for rare blood groups can be sometimes encountered.
Do not transfuse unless clear indication is present. Some of
the indications of blood transfusion are given below.
• Chronic anaemias with Hb less than 6 gm/dL.
• Less than 7 gm/dL when patient is symptomatic and under-
going surgery.
• Less than 8 gm/dL with CVS problems.
• With 6–10 gm/dL only when severe bleeding or complica-
tions of inadequate hypoxia are expected.
• Blood loss of 30–40% of circulating blood volume (CBP).
• In anaemia/severe heart or pulmonary disease/when
bleeding continues with blood loss of 15–30% of CBP.
• In obstetrics patients Hb less than 7 gm/dL, not amenable
to timely therapies antenataly.
• In concealed haemorrhage with abruptio placenta, to
replenish the concealed blood loss irrespective of symptoms.
Points to keep in mind for neonates:
• In neonates 10–20 mL/kg body weight blood can be given.
• Blood less than 7 days is preferred for neonatal transfusion.
• In neonates only antigen grouping is done.
• Blood to be given to neonate should be compatible with
mother’s serum.
• If mother’s and baby’s group are the same, use Rh negative
blood of baby/mother’s ABO group. If not the same, use
‘O’ Rh negative blood.

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Safe Use of Blood
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• In neonates, rate of transfusion should be 10–20 mL/kg to
be given over 4 hours.
Points to keep in mind regarding transfusion
• One unit of whole blood will increase Hb by 1 gm/dL and
PCV by 3%. 1 unit of packed red cells has 250 mg of iron.
• Iron that can be removed by the body is 1 mg/day.
• One unit of single donor platelets (SDP) will increase platelet
count by 30,000–60000 platelets/cmm.
• One unit of random donor platelets (RDP) will increase the
platelet count by 4,000–6000 platelets/cmm.
• Preserve the platelets at 22–24 degree C in agitator.
• Transfuse platelets, if platelet count is less than 10,000 cells/
cmm. With antibodies to platelets, platelet transfusion may
not be of use.
• Platelet increase is observed after 1 hour and again at
20–24 hours of platelet transfusion.
• Preserve the whole blood/PRBCs at 1–6 degree C.
• FFP once collected from the Blood Bank, can be preserved
at 1–6 degree C and has to be used within 6 hours.
Observe for transfusion reactions (TR). These can be due to
many reasons, e.g. alloantibodies, autoantibodies, complement
activation, GVHD, etc. These can be classified as:
Acute transfusion reactions—immunological
• Febrile non-haemolytic transfusion reaction (FNHTR)
allergic reactions
• Anaphylactic and anaphylactoid reactions
• Acute haemolytic transfusion reactions (AHTRs)
• Transfusion related acute lung injury (TRALI)
Acute transfusion reactions—non-immunological
• Bacterial contamination
• Transfusion—associated circulatory overload (TACO)
• Physical and chemical haemolysis
• Metabolic derangements
Delayed transfusion reactions—immunological
• Delayed haemolytic transfusion reaction (DHTR)

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Essentials of Blood Banking and Transfusion Medicine
• Transfusion associated graft-versus-host disease (TA-GvHD)
• Post-transfusion purpura
Delayed transfusion reactions—non-immunological
• Iron overload
• Transfusion transmitted diseases
Immediate adverse effects of transfusion and their management
features
Category 1: Mild reactions
Signs
Symptoms
Possible cause
Immediate management
Urticaria/
Pruritis
Allergic
1. Stop transfusion
rash
(itching)
2. Assess patient
3. An antihistamine may
be required
4. Transfusion may be
restarted if no other
signs/symptoms are
present
5. If signs/symptoms
worsen, 
treat 
as
Category 2.
Category 2: Moderately severe reactions
Signs
Symptoms
Possible cause
Immediate management
Flushing
Anxiety
Allergic (mode-
1. Stop transfusion and
rately-severe)
maintain IV line with
Urticaria
Pruritis
Febrile non-haemo-
normal saline
lytic transfusion
2. Contact medical officer
Rigors
Palpitations reaction: Antibodies 3. Patient may require
to white cells or
antihistamine medica-
Fever
Mild
platelets
tion and/or paraceta-
dyspnea
Antibodies to pro-
mol
teins including
4. Further investigation
IgA
and management
Restlessness Headache
Possible contamina-
according to clinical
tion with pyrogens
features
Tachycardia
and/or bacteria
If investigation required:
Complete transfusion
reaction form and send
blood pack, form and
samples to blood bank
(Contd.)

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Safe Use of Blood
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Category 3: Life-threatening reactions
Signs
Symptoms
Possible cause
Immediate management
Rigors
Anxiety
1. Acute intra-
1. Stop transfusion and
Fever
Chest pain
vascular
maintain IV line with
Restlessness Pain at
haemolysis
normal saline
Hypotension infusion site
(wrong blood)
2. Contact medical officer
on duty
Tachycardia Respiratory 2. Bacterial conta- 3. Manage immediate
Dark
distress
mination and
needs:
Urine
Loin/back
septic shock
a. Fluid for hypotension
Unexplained pain
3. Fluid overload
b. Oxygen
bleeding
Headache
4. Anaphylaxis
c. Adrenaline for ana-
(DIC)
Dyspnea
Transfusion related
 phylaxis
acute lung injury
d. Diuretic for fluid
(TRALI)
 overload
4. Further management
according to likely cause
5. Bedside clerical checks
of all forms, labels and
patient identification
for correctness of the
unit and the intended
recipient are required.
Reconfirm ABO, Rh
and antibody screen
and crossmatch tests.
6. Complete transfusion
reaction form and the
unit and all tubing
should be returned to
the blood bank, along
with post-infusion
blood 
and 
urine
samples (DCT, urine
h e m o g l o b i n u r i a ,
serum bilirubin, hemo-
globinaemia, urea,
creatinine, electrolytes,
urine output, coagula-
tion screen
(Contd.)

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Essentials of Blood Banking and Transfusion Medicine
ACUTE HAEMOLYTIC REACTIONS
Causes
• The majority of haemolytic reactions are caused by trans-
fusion of ABO incompatible blood, e.g. group A transfused
to group B patient or vice versa.
• Antibodies in the patient’s plasma will hemolyse the
incompatible red cells.
Even a small volume of incompatible blood (5–10 mL) can
cause severe reactions and large volumes increase the risk.
Symptoms: Chills, fever, pain (along IV line, back, chest), hypo-
tension, dark urine, uncontrolled bleeding due to DIC.
The common cause of AHTR is transfusion of ABO incompa-
tible blood and this can be due to:
• Errors in blood request form
• Taking wrong sample into prelabeled sample tube
• Incorrect labeling of the sample tube sent to the blood bank
• Inadequate checks of the blood against the identity of the
patient while starting a transfusion
• In a conscious patient signs and symptoms appear within
minutes of starting the transfusion; sometimes even less than
10 mL have been given.
7. Additional samples
sometimes required
for (a) Blood cultures,
(b) HLA or neutrophil
antibodies, (c) Anti-
IgA antibodies and
(d) HLA typing
8. The reaction should
be documented in the
patient’s chart. Once
these initial measures
have been implemen-
ted, the investigation
of the reaction by the
transfusion service can
proceed

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Safe Use of Blood
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• In an unconscious or anaesthetized patient, hypotension and
uncontrolled bleeding (DIC) may be the only signs.
• Hence monitor the patient at the start of transfusion.
Prevention of Errors
1. Correctly label the blood samples and request forms.
2. Place the patient’s blood sample in the sample tube.
3. Always check the blood against the identity of the patient at
the bedside before transfusion.
4. Proper identification of the patient from sample collection
through to blood administration, proper labeling of samples
and products are essential. Prevention of non-immune
haemolysis requires adherence to proper handling, storage
and administration of blood products.
Management: Immediately stop transfusion. Notify hospital
blood bank immediately (another patient may also have been
given the wrong blood!). These patients usually require ICU
support and therapy includes vigorous treatment of hypo-
tension and maintenance of renal blood flow.
FEBRILE REACTIONS
This is the most common cause of TR.
Cause: 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 than red cell
transfusion.
It is important to distinguish from fever due to the patient’s
underlying disease or infection (check pre-transfusion
temperature). Fever may be the initial symptom in a more
serious reaction such as bacterial contamination or haemolytic
reaction and should be taken seriously.
Management
• If fever is present, give paracetamol.
• Follow the steps of ‘immediate management’ of an acute
transfusion reaction. For isolated fever or chills in some

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Essentials of Blood Banking and Transfusion Medicine
patients, the treating doctor may choose to restart the trans-
fusion. 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
reactions.
Prevention: A proportion of patients who have febrile reactions
will have similar reactions to subsequent transfusions. Many
are prevented by pre-storage leucocyte filtration.
URTICARIAL (ALLERGIC) REACTIONS
Cause: Caused by foreign plasma proteins. On rare occasions,
this is 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 mild, administer anti-histamine medication
before restarting the transfusion. If associated with other
symptoms, cease the transfusion and proceed with
investigation.
Investigation
In 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 trans-
fusion. Such a decision should be made after assessment by
the treating doctor.
ANAPHYLACTIC/ANAPHYLACTOID REACTIONS
Anaphylactic and anaphylactoid reactions have signs of cardio-
vascular instability including hypotension, tachycardia, loss of
consciousness, cardiac arrhythmia, shock and cardiac arrest.
Sometimes respiratory involvement with dyspnea and stridor
are prominent.
Cause: In some cases, patients with IgA deficiency, who have
anti-IgA antibodies can have these reactions.

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Management
• Immediately stop transfusion, supportive care including
airway management may be required. Adrenaline may be
indicated. Usually given as 1:1000 dilution, 0.01 mg/kg
subcutaneously/IM or slow IV.
• Investigate for IgA levels and anti-IgA antibodies.
Prevention: Patients with anti-IgA antibodies require special
blood products such as washed red blood cells and plasma
products prepared from IgA deficient donors.
BACTERIAL CONTAMINATION
Cause: Bacteria may be introduced into the blood 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.
Some contaminants, particularly pseudomonas species grow
at 2–6 degree C and staphylococci grow at 20–24 degree C.
Signs and symptoms appear rapidly after starting the
infusion, but may be delayed for a few hours.
Symptoms: Common symptoms are very high fever, rigor,
profound hypotension, nausea and/or diarrhoea. A severe
reaction may be characterized by sudden onset of high fever,
rigors and hypotension.
Management
• Immediately stop the transfusion and notify the hospital
blood bank. After initial supportive care, blood cultures
should be taken and high dose broad-spectrum anti-
microbials need to be administered.
• 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).

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Essentials of Blood Banking and Transfusion Medicine
• Maintaining appropriate cold storage of red cells in a blood
bank refrigerator is important.
• Transfusions should not proceed beyond the recommended
infusion time (4 hours).
FLUID OVERLOAD
1. Fluid overload can result in heart failure and pulmonary
oedema
2. May occur when:
• Too much fluid is transfused.
• The transfusion is too rapid.
• Renal function is impaired.
3. Fluid overload is likely to occur in patients with
• Chronic severe anaemia
• Underlying cardiovascular disease
TRANSFUSION-RELATED ACUTE LUNG INJURY
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 chest X-ray 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’s 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.
HYPOTHERMIA
Cause: Rapid infusion of large volumes of stored blood
contributes to hypothermia. Infants are particularly at risk
during exchange or massive transfusion.

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Safe Use of Blood
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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.
HYPERKALEMIA
Cause: Stored red cells leak potassium proportionately
throughout their storage life. Irradiation of red cells increases
the rate of potassium leakage. Clinically significant hyper-
kalemia can occur during rapid, large volume transfusion of
older red cell units in neonates and children.
Prevention: Red cells are irradiated just prior to issue especially
in neonates and children. Blood less than 7 days old is generally
used for transfusion in neonates (e.g. cardiac surgery, ECMO,
exchange transfusion).
DELAYED HAEMOLYTIC TRANSFUSION REACTION (DHTR)1
DHTR commonly occurs after 24 hrs, may occur several days
after administration of red cells usually from 2 to 14 days.
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.
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.

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Essentials of Blood Banking and Transfusion Medicine
TRANSFUSION ASSOCIATED GRAFT-VERSUS-HOST DISEASE
(TA-GvHD)
Cause: TA-GvHD occurs from donor lymphocytes 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 about 12 days of post-transfusion period.
Also, can occur in immunocompetent recipients of blood
from a 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
patients of risk group has to be given.
Risk groups
• Recipients of blood from biologically related (directed) or
HLA matched donors.
• Patients with congenital immunodeficiency
• Patients receiving granulocyte transfusions
• Patients with Hodgkin’s disease
• Allogeneic and autologous peripheral blood stem cell (PBSC)
and bone marrow transplant recipients
• Patients with aplastic anaemia receiving immuno-
suppression
• Patients treated with purine analogue drugs
Post-transfusion purpura: For details refer to transfusion
reactions.
TRANSFUSION RELATED IMMUNE MODULATION (TRIM)
Allogenic blood transfusion may be associated with immuno-
suppression, increased risk of infection and cancer recurrence.
Cause: Unknown, possibly mediated by donor white cells or
plasma.

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IRON ACCUMULATION
Cause: Iron accumulation is a predictable consequence of
chronic RBC transfusion. Organ toxicity begins when reticulo-
endothelial 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 should monitor their iron status monitored
and managed by their physician.
Management and pevention: Iron chelation therapy is usually
commenced early in the course of chronic transfusion therapy.
INFECTIOUS DISEASE TRANSMISSION
A variety of infectious agents may be transmitted by
transfusion. Hence proper screening is essential.
ALLOIMMUNISATION
In this, the antibodies are formed to the antigens those are not
present on the person’s blood cells.
Red cell alloimmunization: Patients experiencing alloantibody
formation are asymptomatic. The alloantibody is discovered
at the time of pre-transfusion testing. Appropriate antigen
negative blood should 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
respectively. This is important for females with child-bearing
potential as these antibodies can cause severe haemolytic
disease of the newborn during pregnancy.
Risk groups: Patients with sickle cell disease or major haemo-
globinopathy syndromes who are chronically transfused are
at greatest risk of alloantibody formation. Prior to commencing
transfusion, patients with these conditions should have extended
red cell phenotyping performed. Blood matched for the patient’s
Rhesus and Kell antigens is usually supplied for transfusion

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Essentials of Blood Banking and Transfusion Medicine
Platelet alloimmunization: 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.
Causes: There are clinical and immunological causes of platelet
refractoriness. Clinical causes include sepsis, DIC, bleeding,
fever, some drugs, and enlarged spleen.
Immunological causes include the development of antibodies
to human leucocyte antigens (HLA) or human platelet antigens
(HPA).
Management: Immunological refractoriness can be managed
by the provision of HLA or HPA matched platelets.
Prevention: Leucocyte reduction of blood and blood products
to levels less than 106/unit reduces the likelihood of
alloimmunisation. This can be achieved through the use of pre-
storage or bedside leucocyte reduced blood products.