BLOOD COMPONENTS TRANSFUSION AND ITS COMPLICATIONS.pptx

BLOOD COMPONENTS-
TRANSFUSION AND ITS
COMPLICATIONS
SPSSP
SPEAKER
KHUSHBOO GARG

BLOOD COLLECTION
• Blood components prepared from Whole blood collection or apheresis.
• Apheresis is a process by which blood being removed from a subject is continuously
separated into component parts, usually to allow a desired component(s) to be retained
while the remainder is returned to the subject.
• Advantages of Apheresis
Can collect multiple unit -equivalents of platelets, plasma or RBCs from one donation.
This minimizes possible recipient exposure to infectious agents.
Also used for therapeutic plasma exchange(TPE) and for collection of peripheral blood
hematopoietic progenitor cells(HPEs) or donor lymphocytes
Wintrobe’s Clinical Hematology 13th ed

Preparation of components from whole blood
donation

Blood Components -
From one unit of whole blood one can make
• PRBC
• Platelet pack(random donor)
• Fresh plasma
• Granulocyte pack
• Fresh plasma →frozen at -30°C→FFP
• Cryoprecipitate
• Plasma
Albumin
Gamma globulins
Plasma proteins

WHOLE BLOOD
350 ml blood + 49ml anticoagulant (CPDA1) .
Hematocrit 35% (depends upon the donor).
Rarely indicated-
- Acute blood loss
- Exchange transfusion
10cc/kg body weight of whole blood will raise Hct. by 3-5% and hemoglobin
by 1 to 1.5 gm%.
 Transfusion completed within 4hr of commencement

Stored at 1-4˚C
 Shelf life of 35-42 days.
First 4-6 hrs -100% of all the components.
Changes with time
 Platelets fall to less than 1% by 4-48hrs.
Labile clotting factors V and VIII also disappear in same time.
 other clotting factors II,VII,IX,X thereafter.
K+ level ↑,ATP level ↓
2-3DPG and PH ↓ especially after 5-7 days of storage

Why not whole blood and why components ?
Each component has a specialized function.
All functions are not deranged in all the patients and so all the
components are not required all the time.
Making components from one unit of whole blood will satisfy the
needs of more than one patient from the same unit of blood

Whole blood will lead to harmful effects:
• plasma overload
• Lymphocyte mediated toxicities
• Allosensitization etc.
Some components-effective as component only
eg: platelets which are otherwise destroyed in stored whole blood.
Some components-better given as components
eg: clotting factors

Packed Red Blood Cells
The main indication of RBC transfusion is inadequate oxygen delivery as a result
of anaemia
WHEN TO TRANSFUSE RBCs
• Multiple factors related to patient’s clinical status
• Transfusion should be given for symptoms of anaemia and should not be based on
haemoglobin concentration alone.
• AABB clinical practice guidelines suggest that patients should not be transfused
with red blood cells, in the absence of symptoms/signs of anemia, unless the Hgb
concentration is less than 7 to 8 g/dl, or less than 8 g/dl for patients with
symptoms or known to have cardiovascular disease

• Nutritional Deficiencies:
 Rarely indicated in these patients if there is time to correct anaemia with
alternative therapies.
 Life threatening anaemia (Hgb <6.5 g/dl) by WHO criteria may require
transfusion.
 Elderly patients particularly with angina or CHF.
 Iron-deficient patients who are also bleeding actively (e.g. , from the G.I.
tract)
(Wintrobe’s Clinical Hematology 13th ed.)

• Hemolytic Anemias:
 At a haemoglobin < 6 gm/dl, most patients require transfusion.
 Transfusion of crossmatch- compatible blood is indicated in severe AIHA . But,
this may pose a special problem because, if the antibody involved is
nonspecific, all of the blood units cross-matched will be incompatible.
In these cases, it is often correct, paradoxically, to transfuse incompatible
blood, with the rationale being that the transfused red cells will be destroyed
no less but no more than the patient’s own red cells, but in the meantime, the
patient stays alive.
 The risk of complications is increased if the patient has brisk hemolysis or if
the patient has an undetectable alloantibodies in addition to autoantibody.
(Wintrobe’s Clinical Hematology 13th ed.)

• Thalassemia
A transfusion program generally requires monthly transfusions, with the pre-
transfusion haemoglobin level >9 and<10.5 g/dl.
Chronic hyper-transfusion therapy designed to maintain a hematocrit of
at least 27–30% to suppress extra-medullary erythropoiesis and skeletal
changes (caused by expanded marrow). [Harrison’s principles of internal medicine19th
edition].
Best is to use washed PRBC and if affordable, WBC filtered PRBC to decrease
leuko-contamination and alloimmunization.
Meticulous record of the amount transfused should be kept in order to
calculate the iron intake of the patient.
Chelation should be started once serum ferritin is more than 1000 ng/ml .

• Sickle cell disease
Severe, symptomatic acute chest syndrome (O2 sat. <90% despite
supplemental O2 therapy)
 Acute splenic sequestration with severe anemia
Children or adults with acute stroke (begin prophylactic transfusion
regimen to maintain a Hgb S level below 30%of the total Hgb)
 Multisystem organ failure
 Aplastic crisis
 Symptomatic anemia
American Red Cross guidelines 2017

RANDOM DONOR PLATELETS
• Derived from SINGLE UNIT of whole blood.
• Contains platelets ≥5.5 x 1010/RD unit in 50-60ml of plasma per pack.
• Usual dose is one unit for each 10 Kg body weight.
• It should be transported quickly and infused rapidly over 20-30 minutes to prevent
loss of platelets due to aggregation
• ADVANTAGE
Less costly and easily available.
DISADVANTAGE
• Expose recipient to more no. of donors.
• One cannot use specific donor like CMV negative or HLA matched

APHERESIS ( Single Donor Platelets/SDAP )
• Apheresis Platelets must contain at least ≥3.0 x 1011 / SDAP unit in 300ml of
plasma by AABB standards.
• Equal to about 6 whole blood platelet concentrates.
ADVANTAGE:
• More concentrated hence more effective.
• Exposing recipient to only a single donor.
• One can use same donor again after 2-3 weeks.
• One can select specific donor.
DISADVANTAGE:
• Extremely costly.
• Needs sophisticated equipments.
• Donor has to wait for longer periods in blood bank

Indication of platelet transfusion
The risk of significant spontaneous haemorrhage increases gradually as the
platelet count drop to <50000/µl and high at counts<5000/µl
Current guidelines from the European Union and United States recommended
a transfusion trigger of 10000/µl for prophylactic transfusion.
Prophylactic PLT Transfusion Thresholds (AABB guidelines)

Therapeutic indication of platelet transfusion.
Most useful in thrombocytopenic patients with microvascular bleeding(e.g;
oozing or mucous membrane or gastrointestinal bleeding).
In case of massive bleeding bypass– induced platelet dysfunction after cardiac
surgery.
Transfusion is recommended in bleeding patients with platelet dysfunction,
regardless of platelet counts.
In all situations, the clinical decision regarding platelet transfusion depends
on-
-Estimation of platelet count and function
-Cause of thrombocytopenia
-State of the coagulation system
- Presence of likelihood of bleeding
- Hazards of transfusion

• Platelet transfusion is generally not recommended in patients with
platelet consumption disorders and may even harmful.
-idiopathic thrombocytopenic purpura(ITP)
-Thrombotic thrombocytopenic purpura(TTP)
• However, platelet transfusion may be used to life threatening bleeding in
patients with ITP and TTP.( Wintrobe’s Clinical Hematology 13th ed.)

Expected response after platelet transfusion
• May be calculated as CCI (corrected count increment)
• CCI = (post T C- Pre T C ) × BSA (m.sq)/ no. of platelets administered
• CCIs measured between 10 and 60 minutes post-transfusion are expected
to be >7,500/µl.
• In the absence of a consumptive process or decreased production, post-
transfusion counts may be somewhat lower than the dose administered
because approximately 7,100 platelets/μL (equivalent one RDP per day) are
consumed daily in endothelial support functions
. Wintrobe’s Clinical Hematology 13th ed

Platelet refractoriness
• Defined as an unacceptable recovery of transfused platelets on two or more
occasions
• After an apheresis platelet (SDP) transfusion, containing the minimum of
300000/µl platelet maximum achievable CCI is appx. 25000/µl and minimum
should be 7500/µl
• A CCI of <5 to 7.5 × 109/L measured at 10 minutes to 1 hour after the transfusion
is a commonly used definition of an unacceptable response.
• Or as a general rule of thumb , an absolute increment of < 13000/µl after
transfusion of six units of platelets to a 70-Kg adult

Factors associated with platelet refractoriness
• Immune Factors
Alloantibodies
Anti-HLA
Antiplatelet glycoprotien
ABO
Autoantibodies
ITP, drug-related
• Nonimmune Factors
Splenomegaly
Fever, infection, DIC
Immune complexes
Bone marrow transplantation

Fresh Frozen Plasma - FFP
• Prepared by separating citrated plasma from whole blood and freezing it within 8
hours of collection or by freezing citrated apheresis plasma within 6 hours of
collection.
• FFP may be stored at -18ºC or below for up to 1 year.
• FFP contains plasma proteins including albumin, gamma-globulins ,fibrinogen
and also the labile coagulation factors VIII and V.
• The typical dose of plasma is 10 to 20 ml/kg. 1 unit of FFP increases coagulation
factors about 2%
• After thawing, FFP may be stored in refrigerator for up to 24 hours before use

FFP Indications
• Active bleeding or risk of bleeding due to deficiency of multiple coagulation factors
e.g liver disease.
• Severe bleeding due to warfarin therapy or urgent reversal of warfarin effect.
• Bleeding or prophylaxis of bleeding for a known single coagulation factor deficiency
for which no concentrate is available e.g. FV, XI deficiency, protein C and S ,
antithrombin deficiency.
• Thrombotic thrombocytopenic purpura(deficiency of , or antibodies to ADAMTS13,
that cleaves VWF).
• DIC-Only indicated for bleeding patients with DIC
- Not indicated if there is no bleeding, whatever the result of laboratory tests, and
there is no evidence for prophylaxis with plasma

FFP contraindications
• Should not be used when
-coagulopathy can be corrected more effectively with specific therapy, such
as vitamin K, cryoprecipitate, or Factor VIII concentrates.
- normalizing abnormal coagulation screen results in the absence of bleeding.
-when the blood volume can be replaced with other volume expanders such as
0.9% sodium chloride, lactated ringer’s, albumin.

Cryoprecipitate (Cryo)
• Cryoprecipitate is prepared by thawing fresh frozen plasma at a temperature
between 1°C and 6°C.
• After centrifugation, the supernatant plasma is removed and the insoluble
cryoprecipitate is refrozen.
• It contain concentrated level of factor VIII, VWF (von Willebrand factor) , factor
XIII, and fibrinogen.
• On average, each unit of cryoprecipitate contains 80 to 120 IU Factor VIII and at
least 150 mg of fibrinogen in 5-15 ml of plasma.
• Indications - Congenital fibrinogen deficiency, Hemophilia A, Factor XIII
deficiency, Von Willebrand disease when specific deficient concentrate is not
available.

BLOOD COMPONENTS MODIFICATION
1. LEUKOCYTE REDUCED COMPONENTS
• Leukoreduction is a process through which the white blood cell content of cellular
blood components is reduced.
• This may be accomplished in-process during apheresis collection or by filtration
of the blood product either in the manufacturer’s laboratory (pre-storage), or at
the patient’s bedside (post-storage).
• Prestorage leukocyte reduction is preferable to post-storage as it removes
leukocytes prior to the release of cytokines, cellular debris, and intracellular
microorganisms

• Indications –
To reduce the incidence of recurrent febrile non-hemolytic transfusion reactions
(FNHTR) (incidence reduced by up to 60%.)
To reduce HLA alloimmunization and HLA-mediated platelet refractoriness
(incidence reduced by 50–80%).
To prevent transmission of intracellular pathogens such as cytomegalovirus and
Human T-Lymphotropic Virus, types I and II (HTLV- I/II).
NOTE-
Leukoreduction does not eliminate the presence of all white blood cells. The presence of
residual donor leukocytes may result in microchimerism, which can lead to transfusion
associated graft-versus-host disease (TA-GVHD). For patients at risk of TA-GVHD, cellular
products must be irradiated.

2. IRRADIATED COMPONENTS
• Inactivation of donor lymphocytes by gamma- or X-irradiation (25 Gy) can
prevent the proliferation of transfused lymphocytes and the development of
TA-GVHD.
• INDICATIONS -
Intrauterine transfusion (IUT) and infants who have received IUTs
 Congenital cellular immunodeficiency, for example, severe combined
immunodeficiency (SCID), DiGeorge syndrome.
 Hodgkin disease
 Granulocyte transfusions
Blood product from a related donor (any degree relation)
 Recipients undergone marrow transplantation

• Saline washing with automated cell washers. Capable of removing 99% of plasma proteins
from red cell products. Usually performed in an open system ,so the red cells have only 24
hours self life after washing.
• Indications –
Anaphylactic and recurrent significant allergic transfusion reactions that are unresponsive to
pre-medication.
For recipients with IgA deficiency, particularly those with a prior anaphylactic reaction, when
the need is urgent and a product from an IgA-deficient donor cannot be located.
 Avoidance of hyperkalemia in patients predisposed to arrhythmia from rapid transfusion
and/or large volumes (for example, neonates, patients with renal disease).
An alternative to washing RBC units when potassium is an issue is the use of fresher (e.g.,
<5-day-old) products
Recurrent febrile non-hemolytic transfusion reactions (FNHTRs) in patients unresponsive to
leukocyte-reduced products and anti-pyretic pre-treatment
3. WASHED CELLULAR COMPONENTS.

For safer transfusion we should strictly maintain
• Proper donor selection.
• Screening of donor to TTI i.e. HIV , HBV , HCV , malaria and syphilis
• Compatibility testing.
• Rational use of blood component therapy.
• Transfusion and monitoring

Administration of Blood Products
 When blood is transfused, it is important to keep detailed records including
the following in the patient’s notes:
• Type and volume of each unit transfused.
• Unique donation number of each unit transfused.
• Blood group of each unit transfused.
• Time at which the transfusion of each unit commenced.
• Signature of the individual responsible for administration of the blood.
• Monitor the patient before, during and on completion of the transfusion.
• Record the time of completion of the transfusion.
• Identify and respond immediately to any adverse effect, by stopping the
transfusion.
• Record the details of any transfusion reaction
WHO clinical transfusion practice guidelines

Blood request form-
 The blood request form should always be accompanied by the patient’s blood
sample. The sample is placed in a sample tube that is correctly labelled and is
uniquely identifiable with the patient.
 The prescribing clinician should sign the request form and complete all the details
accurately and legibly.
 The blood sample collected must include the following information
• Patient’s full name, age and sex.
• Registration number.
• Ward/bed number
 Use positive patient identification to identify the patient. NEVER pre‐label the
sample tube before phlebotomy.
Errors at the patient’s bedside, such as mislabeling the sample, are responsible for the
majority of hemolytic transfusion reactions

 Pre transfusion testing
Red cell compatibility testing includes –
• ABO and RhD grouping on patient and donors.
• Antibody screening on patient.
• Cross matching between serum of patient and red cells of donor.
Purpose of compatibility testing:
• To select blood components that will cause no harm to the recipient and will
have acceptable survival rates when transfused.
• Compatibility tests will confirm ABO compatibility between component and
recipient and will detect the most clinically significant unexpected antibodies
Harrison’s Principle of Internal Medicine, 19th edition

Before transfusion we must determine WHAT for any procedure
Whether required
How much required
Actual component required
Time of duration of transfusion

 Performing the transfusion
• The final check of the patient’s identity and the blood bag before transfusion
should be undertaken at the patient’s bedside, as is the last opportunity to
detect an identification error and prevent a potentially incompatible transfusion,
which may be fatal.
• Transfusion rate depends on clinical circumstances and may vary from 3‐5
mL/kg/hour to greatly increased rates for individuals in hypovolaemic shock

Continued…
• Time limits for transfusion
There is a risk of bacterial proliferation or loss of function in blood products
once they have been removed from the correct storage conditions

 Monitoring the transfusion
• Before commencing the transfusion, it is essential to encourage the patient to notify a
nurse or doctor immediately if he or she becomes aware of any discomfort such as
shivering, flushing, pain or shortness of breath or begins to feel anxious.
• For each unit of blood transfused, monitor the patient:
- Before starting the transfusion (baseline observation).
- 15 minutes after starting the transfusion.
- At least every hour during transfusion.
- Carry out a final set of observations 15 minutes after each unit has been transfused.
• Severe reactions most commonly present during the first 15 minutes of a transfusion. All
patients and in particular, unconscious patients should be monitored during this period
and for the first 15 minutes of each subsequent unit.
In an unconscious or anaesthetized patient, hypotension and uncontrolled bleeding
may be the only sign of an incompatible (mismatched) transfusion

 Adverse Reactions of Blood Transfusion
• Acute reactions may occur in 1% to 2% of transfused patients. Rapid recognition and
management of the reaction may save the patient’s life.
• Errors and failure to adhere to correct procedures are the common causes of
life‐threatening acute haemolytic transfusion reactions.
• Bacterial contamination in red cells or platelet concentrates is an under‐recognized
cause of acute transfusion reaction.
• Patients who receive regular transfusions are particularly at risk of acute febrile
reactions. These should be recognized so that transfusion is not delayed or stopped
unnecessarily.
.

• TTI’s are the serious delayed complications of transfusion. Since a delayed
transfusion reaction may occur days, weeks or months after the transfusion,
the association with the transfusion may not be recognized.
Transfusion reaction (TR)
 Acute TR (<24 hours)
- Wrong blood, primed immunological recipient
- Poor quality blood, faulty assessment
Delayed TR (>24 hours)
- Diseases, other delayed immunologic reactions, metabolic effect (5‐10
days)

Blood Transfusion Reactions
Immunologic
• Alloimmunization to: Red cell antigens , HLA
antigens , Platelet-specific antigens, Neutrophil-
specific antigens
• Hemolytic transfusion reactions
Acute
Delayed
• Febrile nonhemolytic transfusion reactions
• Transfusion-related acute lung injury (TRALI)
• Allergic transfusion reactions
• Posttransfusion purpura (PTP)
• Transfusion-associated graft-versus-host disease
(TA-GVHD)
Nonimmunologic
• Transfusion-associated circulatory overload
(TACO)
• Massive transfusion
Metabolic
Hypothermia
Dilutional
• Miscellaneous - Transfusion hemosiderosis
Infectious
Hepatitis: B, C
Human immunodeficiency virus-1/-2
Human T-lymphotropic virus-I/-II
Syphilis
Cytomegalovirus
West Nile virus
Parasites: malaria, Babesia, trypanosomes
Bacterial contamination
Wintrobe’s Clinical Hematology 13th edition

Immune - Mediated Reactions
• Acute Hemolytic transfusion Reactions
 Recipient has preformed antibodies (mostly ABO isoagglutinins) that lyse donor
erythrocytes.
 Alloantibodies directed against other RBC antigens, i.e., Rh, Kell, and Duffy, are responsible
for more fatal hemolytic transfusion reactions.
 It may present with hypotension, tachypnea, tachycardia, fever, chills, hemoglobinemia,
hemoglobinuria, chest and/or flank pain, and discomfort at the infusion site.
The immune complexes that result in RBC lysis can cause renal dysfunction and failure. Tissue
factor released from the lysed erythrocytes may initiate DIC .
 Errors at the patient’s bedside, such as mislabeling the sample or transfusing the wrong
patient, are responsible for the majority of these reactions.

• A correctly labeled posttransfusion blood sample and any untransfused blood should be
sent to the blood bank for evidence of hemolysis which includes the measurement of
serum haptoglobin, lactate dehydrogenase (LDH), and indirect bilirubin levels.
• Analysis also includes repeat typing and cross-matching of the blood components , direct
antiglobulin test(detect the presence of antibody or complement bound to RBCs in vivo).

Delayed hemolytic transfusion reactions
 Occur 5-10 days after transfusion.
 These reactions occur in patients previously sensitized to RBC alloantigens who have a negative
alloantibody screen due to low antibody levels. When the patient is transfused with antigen-positive
blood, an anamnestic response results in the early production of alloantibody that binds donor
RBCs.
Pre- transfusion testing

• Febrile nonhemolytic transfusion reaction
It is the most frequent reaction associated with the transfusion of cellular blood
components, characterized by chills and rigors and a ≥1°C rise in temperature.
Antibodies directed against donor leukocyte and HLA antigens may mediate these
reactions; thus, multiply transfused patients and multiparous women are felt to be at
increased risk.
Although anti-HLA antibodies may be demonstrated in the recipient’s serum,
investigation is not routinely done because of the mild nature of most FNHTR.
The use of leukocyte-reduced blood products may prevent or delay sensitization to
leukocyte antigens and thereby reduce the incidence of these febrile episodes.
Cytokines released from cells within stored blood components may mediate FNHTR;
thus, leukoreduction before storage may prevent these reactions.

• Allergic and Anaphylactic reaction
Urticarial reactions are related to plasma proteins found in transfused components.
 Mild reactions may be treated symptomatically and the transfusion may be completed after
the signs and/or symptoms resolve.
Cellular components can be washed to remove residual plasma for the extremely sensitized
patient.
Anaphylactic Reaction
 Present with difficulty breathing, coughing, nausea and vomiting, hypotension,
bronchospasm, loss of consciousness, respiratory arrest, and shock.
 Treatment includes stopping the transfusion, maintaining vascular access, and administering
epinephrine (0.5–1 mL of 1:1000 dilution subcutaneously). Glucocorticoids may be required
in severe cases.
Patients who are IgA-deficient, <1% of the population, are at risk for anaphylactic reactions
associated with plasma transfusion.
Patients who have anaphylactic or repeated allergic reactions to blood components should be
tested for IgA deficiency

Graft-versus-host disease
 It is mediated by donor T lymphocytes that recognize host HLA antigens as foreign and
mount an immune response, manifested clinically by the development of fever, cutaneous
eruption, diarrhea, pancytopenia and liver function abnormalities.
 Clinical manifestations appear at 8–10 days, and death occurs at 3–4 weeks after
transfusion.
It can be prevented by irradiation of cellular components (minimum of 2500 cGy) before
transfusion to patients at risk include
 fetuses receiving intrauterine transfusions,
selected immunocompetent recipient (e.g., lymphoma patients)
immunocompromised recipients,
 recipients of donor units known to be from a blood relative, and
recipients who have undergone marrow transplantation.

• Transfusion – related acute lung injury (TRALI)
It is the most common cause of transfusion related fatalities.
It results from the transfusion of donor plasma that contains high-titer anti-HLA antibodies that
bind recipient leukocytes, which aggregate in the pulmonary vasculature and release mediators
that increase capillary permeability.
Presented with symptoms of hypoxia (Pao2/FIo2 <300 mmHg) and signs of noncardiogenic
pulmonary edema, including bilateral interstitial infiltrates on chest x-ray, either during or
within 6 h of transfusion .
Treatment is supportive, and patients usually recover without sequelae.
• Posttransfusion Purpura
This reaction presents as thrombocytopenia 7–10 days after platelet transfusion.
 Platelet-specific antibodies found in the recipient’s serum, recognized the antigen HPA-1a
found on the platelet .
Additional platelet transfusions can worsen the thrombocytopenia and should be avoided

Non immune – mediated reactions-
• Transfusion associated circulatory overload (TACO)
It can result in dyspnea with PaO2 <90% on room air, bilateral infiltrates on chest x-ray, and
systolic hypertension. Brain natriuretic peptide (BNP) is often elevated (>1.5) compared with
pretransfusion levels.
 May occur when:
Too much fluid is transfused.
The transfusion is given too rapidly.
Renal function is impaired.
Underlying cardiovascular disease
• Transfusion induced hemosiderosis
Symptoms and signs of iron overload affecting endocrine, hepatic, and cardiac function are
common after 100 units of RBCs have been transfused (total-body iron load of 20 g).
 Preventing this complication by using alternative therapies (e.g., erythropoietin) and
judicious transfusion is preferable and cost effective.

• Massive transfusion
defined as –
Replacement of a blood volume equivalent within 24 hours.
>10 units within 24 hours.
Transfusion >4 units in 1 hour.
Replacement of 50% of blood volume in 3‐4 hours
Effects of massive transfusion
Acidosis
Hypothermia
Hyperkalemia
Hpocalcemia due to citrate toxicity
Dilutional coagulopathy
Mortality is high in massive transfusion and its aetiology is multifactorial, which includes
hypotension, acidosis, coagulopathy, shock and the underlying condition of the patient.

 Investigating Acute Transfusion Reactions –
The very first step is to stop the transfusion immediately. If the reaction is severe, the
needle should be removed to prevent any further transfusion of blood .
 All suspected acute transfusion reactions should be reported immediately to the blood
transfusion centre and to the doctor responsible for the patient. With the exception of
urticarial allergic reactions and febrile non‐haemolytic reactions, all are potentially fatal
and require urgent treatment.
Record the following information on the patient’s notes:
– Type of transfusion reaction.
– Time lapse between start of transfusion and when reaction occurred.
– Volume, type and bag number of blood products transfused.

Immediately take post‐transfusion blood samples (1 clotted and 1 anti‐coagulated)
from the vein opposite the transfusion site and forward to the blood centre for
investigation of the following:
– Repeat ABO and RhD group.
– Repeat antibody screen and cross match.
– Full blood count.
– Coagulation screen.
– Direct antiglobulin test.
– Urea and creatinine , Electrolytes.
Blood bag and transfusion set containing red cell and plasma residues from the
transfused unit return to the blood centre.

Anticoagulant /Preservative Solutions
Solution PURPOSE WB or
RBCs
Storag-
e
Additive Performances
CPD Anticoagul-
ant and
storage
21 days Sodium Citrate( dihydrate),
Citric acid(monohydrate),
Dextrose( monohydrate),
Monobasic sodium
Biphoshate (monohydrate)
•Prevents coagulation of blood as citrate
ion chelates the calcium.
• Nutrition source for RBCs
•Adjust PH.
CPDA1 Anticoagul-
ant and
storage
35 days Sodium Citrate( dihydrate),
Citric acid(monohydrate),
Dextrose( monohydrate),
Monobasic sodium,
Biphosphate (monohydrate)
Adenine
•Prevents coagulation of blood as citrate
ion chelates the calcium.
• Nutrition source for RBCs
•Adjust PH.
•Supports to maintain ATP level in RBCs.
SAGM Red cell
preservation
42 days Dextrose(monohydrate), sodium
chloride,adenine
D-Mannitol
•Nutrition source for RBCs.
•Adjust osmotic pressure.
•Supports to maintain ATP level in RBCs.
•Supports integrity of RBC membrane(to
avoid hemolysis).

BLOOD COMPONENTS TRANSFUSION AND ITS COMPLICATIONS.pptx

BLOOD COMPONENTS TRANSFUSION AND ITS COMPLICATIONS.pptx

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