Blood transfusion dr m laban

1
Introduced
by
mohamed sobhy laban
BLOOD
TRANSFUSION
Sunday 12/8/2018

HISTORY OF BLOOD
TRANSFUSIONS
607687
3

1628
1665-’66
1667
Harvey
Discovered Circulation of Blood
Wilkins & Lower
Transfusions from dog to dog
Jean-Baptiste Denis
Performed first recorded blood
transfusions from animals to humans
4
HISTORY OF BLOOD
TRANSFUSIONS

20th Century Transfusions
1901
Karl Landsteiner
Discovers A, B, O Blood
Groups
5

AIMS OF TRANSFUSION
CENTER
6
1. To care forthe donor- ensure
act of donation does not harm
donor.
2. Provision of Blood of the best
possible quality and safety for
the patient receiving it.

SAFETY OF BLOOD
TRANSFUSION
7
Safe blood transfusion means:
Compatible and without transmission
of infection.

SAFETY OF THE TRANSFUSION
CHAIN
FROMVEIN TO VEIN
Right
Blood
Right
Patient
Right
Time
=+ + 
8

The Safest
blood
transfusion is
No
transfusion

BLOOD DONATION
10
Careful donorselection with donor
interview.
Age: not less than 17 years.
Pulse: between 50-100 beat /minute without
irregularities.
Blood pressure: systole<180mmHg, diastolic
<100mmHg.
Temperature: <37.5C
Hemoglobin:>12g/dl, Hct>38%
Site of vein puncture must be free of lesions
and infections.

BLOOD DONATION
11
 ABOgrouping.
 Rh typing.
 Cross matching
 Laboratory screening test for:-
HBsAg.
HCV Ab.
HIV.
HTLV1.
HTLV2.

BLOODGROUPING
12
Blood grouping means:-
• the determination of the antigens of a
specific group on the red cells
•and the antibodies relevant to this
group in the normal serum.

BLOOD TRANSFUSION
13El-Shanshory 2011

Antibodies in
serum
Antigens on red
cells
Blood group
Anti B A A
Anti A B B
Non AB AB
Anti A & anti B O O
14

16
Anindividual's redcellgroupis determinedby
Suspending washed red cells withSuspending washed red cells with
diluted anti-A, anti-B and anti Rh (D).diluted anti-A, anti-B and anti Rh (D).
 Serum is simultaneously incubatedSerum is simultaneously incubated
with group A, B and 0 cells to confirm thewith group A, B and 0 cells to confirm the
presence of the expected naturallypresence of the expected naturally
occurring ABO antibodies.occurring ABO antibodies.
 Agglutination indicates a positive testAgglutination indicates a positive test.

19
The blood must be
•kept in the fluid state.
•living tissue.
•Metabolically viable.
•Free frombacterial infection.
The blood kept in the fluid stat by the
addition of acid citrate dextrose (ACD).

RBC COMPATIBILITY CHART
20
In addition to donating to the same blood group;
type O blood donors can give to A, B and AB;
blood donors of types A and B can give to AB.

PLASMA COMPATIBILITY CHART
22
In addition to donating to the same blood group;
plasma from type AB can be given to A, B and O;
plasma from types A and B can be given to O.

24
Compatibility testing
• Cross-matching entails
suspension of red cells from a donor
pack with recipient serum,
incubation to allow reactions to
occur, and examination for
agglutination.

MODALITIES
OF
TRANSFUSION
26El-Shanshory 2011

27
• Whole blood:- in major blood loss.
• Component therapy : to face an
individual Case needs.

• Whole Blood is rarely given because it is
wasteful and sometimes harmful to give
blood components that are not needed.
• It is only necessary when very large
amounts of blood have been lost,
otherwise blood components are given

BLOOD COMPONENTS AND
PRODUCTS
29

CENTRIFUGING
30El-Shanshory 2011

PLASMA SEPARATION
31El-Shanshory 2011

BLOOD CELL SEPARATOR
32El-Shanshory 2011

BLOOD COMPONENT PREPARATION
+
30M, 4H
1G/DL
PACKED
RED CELLS
Shelf life 45
days at 40
C
Rare group blood
can be frozen in
glycerol.
Shelf Life: 10 years
PLATELET
CONCENTRATE
Shelf life: 3-5 days at
20-240
C on shaker
1 PACK=150250ml
Hct:60-75%
RBC,W,P- warmed
RDP=50-60ML
=35,000,REC,W
SDP=150-300ML=
150,5000,000=
RBC,W
4H, 30-60M
1RDP/10GK=
- ,5 10 000
SDP=30-60,000
1 PACK=450ml
Hct:37-39%
RBC,W,P,F
-Warmed
20 ML/KG
+
30M, 4H
1G/DL
WB
Shelf life 35
days at 4 C
34

CRYOPRECIPITATE
1. Fibrinogen
2. Factor VIII (80
U/bag)
3. von Willebrand’s
Factor
4. Factor XIII
FRESH FROZEN
PLASMA
Stored at minus 300
C
1. All coag factors
2. Fibrinogen
3. Antithrombin
4. Albumin
5. Protein C and S
CRYOSUPERNATE
Factor IX
1 PACK=200=250ML
10-15ml/kg
Water bath 30-37c
6H OF thawing,
2H
-20 30%
1 PACK=20=30ML
1 pack/10kg
Water bath 30-37c
Immediately,
Over 10-15 min
1
PACK=150
-250ml
10-15ml/kg
Water bath
30-37c
6H OF thawing, 2H

Plasma drivativesPlasma drivatives
10ml/min
Human albmin
5%
Human albmin
20%
Factor VIII
CONCENTRATE
Bottle=400 ml
50mg/ml
1g/kg
Bottle=100 ml
200-250mg/ml
1g/kg
0.2-0.4ml/min
1 VIALS=250=500 iu
1UNIT= 2%
ACTIVITY
HL:12H
35

Anti-RhD Ig
Large
amount FXI
FII, FVII, X
HL: 24H
1 VIALA=150-300 ug
50-75 uglkg
Slowly (5 min)
Once 2 weeks
1vials=0.5,1,
2.5, 5 gm
400 mg/kg/day
5 days IVIg
HBIg,rabis,
Tetanus
Varicella
zoster
Once or repeated IMIg
MULTIFACTO
CONCENTRATE

Frozen Red Blood Cells have been frozen to
extend theirstorage period.
Very rare blood types are frozen to insure
they are always on hand.

• Platelet Rich Plasma is an intermediate
stage in the production of platelet
concentrate and plasma components.
• Plasma is the yellow liquid portion of
blood. It is also a source of proteins that
stop bleeding by forming blood clots.
• Frozen Plasma to be manufactured into
derivatives is stored and shipped in the
frozen state.

• Fresh Frozen Plasma must be processed
and frozen within eight hours of the
whole blood donation to preserve the
less stable clotting proteins. It is used
mainly for people with bleeding
complications.
• Cryoprecipitate, a part of the plasma,
contains two important clotting factors
found in whole blood. It is used to treat
two common clotting disorders.

Fractionation
is the process of breaking plasma down into
"fractions."When plasma gets mixed with certain
chemicals, proteins can be separated and
processed into products which are stable and
easily stored. Some of the common fractions are
• Albumin
used in the treatment of certain kidney and liver diseases. Because of
the relative simplicity of storage and administration, it is also used
for emergency cases, such as accident or shock victims, particularly
where facilities for administering blood are not available or where
time does not permit its use.
• PlasmaProteinFraction
similarto albumin; the two products are often used interchangeably.

GammaGlobulin
contains the antibodies in plasma and is
able to modify or prevent measles and other
infectious diseases, such as some varieties
of hepatitis.
HBIg, VZIg
are gamma globulin products prepared from
the plasma of donors with high levels of
specific desirable antibodies.

Lyophilized FactorVIII
- concentrates are used forthe treatment of
Hemophilia A.
OtherClotting FactorDerivatives
-contain concentrated amounts of specific clotting
factors and are used in certain less common
clotting disorders.
- Platelet Concentrates are needed by patients to
control bleeding in thrombocytopenia and platelet
function disorders.

OBSRVATION
• VITAL SIGNS
• COLOROF URINE
• SKIN URTICARIAL RASHES
• SIGNS OF EDEMA OF THE FACE ANDOROPHARNEX
• LUNG WHEEZE ORCRIPITATION
• NECKVEIN DISTENSION
44

Complications
of blood transfusion
45

* TRANSMISSION OF MICROBIAL
DISEASES
• BACTERIAL, E.G. YERSINIA,TREPONEMA,
BRUCELLA, SALMONELLA
• PROTOZOA, E.G. MALARIA,
TOXOPLASMA, MICROFILARIA
• VIRAL
PLASMA-BORNEVIRUSES
• HEPATITIS B,HEPATITIS C.
• HEPATITIS A (RARELY)
• OTHERUNIDENTIFIEDHEPATITIS
VIRUSES
• H1V-1 ANDHIV-2 (ALSO CELLULAR)
• PARVOVIRUS
CELLASSOCIATEDVIRUSES
• CYTOMEGALOVIRUS
• EPSTEIN-BARRVIRUS
• HTLV-I ANDHTLV-II
Complication of the blood transfusion
46

TRANSFUSION REACTIONSTRANSFUSION REACTIONS
DELAYED
REACTIONS
NON IMMUNE
ACUTE
IMMUNE
NON IMMUNE
IMMUNE
47

ACUTE TRANSFUSION
REACTIONS
ImmuneImmune:-:-
1.1.Febrile reactionFebrile reaction..
2.2.Allergic reactionAllergic reaction..
3.3.Anaphylactic reactionAnaphylactic reaction..
4.4.Haemolytic transfusion reactionHaemolytic transfusion reaction..
48

ACUTE TRANSFUSION REACTIONS
NON IMMUNE
1.CIRCULATORY OVERLOAD
2.AIREMBOLISM
3.METABOLIC COMPLICATION
(HYPERKALEMIA,
HYPOMAGNESIMA, ANDCITRATE
TOXICITY)
4.HYPOTHERMIA
5.ACIDBASE CHANGES.
50

DELAYEDTRANSFUSION
REACTIONS
•IMMUNE
IMMUNE SENSITIZATION (ALLO-
ANTIBODIES).
GVHDIN IMMUNOCOMPROMISED.
IMMUNCOMPROMIZING EFFECT.
•NON IMMUNE
 IRON OVERLOADANDHAEMOSIDROSIS.
51

MANAGEMENT OF ACUTE TRANSFUSION
REACTION:
• Stop blood infusion and save the accused
blood bag.
• Keep the intravenous line open and give slow
drip of saline.
• Draw a post-reaction blood sample from the
other vein.
• Record patient’s urine output for the next 6-12
hours.
52

 Send the following items to the transfusionSend the following items to the transfusion
laboratory:laboratory:
• The accused blood bag with the administration setThe accused blood bag with the administration set
• Post-reaction patient’s blood sample for bloodPost-reaction patient’s blood sample for blood
group re-checking and re-cross-matching.group re-checking and re-cross-matching.
• Urine sample voided after the transfusion reaction.Urine sample voided after the transfusion reaction.
53
MANAGEMENT OF ACUTE TRANSFUSION REACTION:

LABORATORY PROCEDURES FOR
AHTR
• Check the identifying information on: The blood
bag , pretransfusion blood sample and label on the
post-reaction samples
• Re-check blood grouping of the pre-transfusion,
post-reaction samples , blood bag and re-check
cross-matching.
• Look for hemolysis in the post-reaction blood
sample.
54

LABORATORY PROCEDURES FOR
AHTR:• Perform DAT on patient’s RBC in the pretransfusionPerform DAT on patient’s RBC in the pretransfusion
and post-reaction blood samples. Examineand post-reaction blood samples. Examine
microscopically .microscopically .
• Examine urine sample for hemoglobinuria and necroticExamine urine sample for hemoglobinuria and necrotic
tubular cells.tubular cells.
• Estimate serum bilirubin ,LDH, creatinine, electrolytes.Estimate serum bilirubin ,LDH, creatinine, electrolytes.
N.B.Negative results for re-checking, DAT, hemolysis andN.B.Negative results for re-checking, DAT, hemolysis and
hemoglobinuria rule out ABO incompatibilities.hemoglobinuria rule out ABO incompatibilities.
55

THERAPYOFAHTR
The main lines of therapy are:The main lines of therapy are:
• Supportive therapy for theSupportive therapy for the
cardiovascular system and renalcardiovascular system and renal
system by IV fluids and diureticsystem by IV fluids and diuretic
such as mannitol.such as mannitol.
• Bronchodilators and low-doseBronchodilators and low-dose
dopamine.dopamine.
• Replacement for coagulation such asReplacement for coagulation such as
FFP, platelets and cryoprecipitate ifFFP, platelets and cryoprecipitate if
there is impending DIC.there is impending DIC.
56

THERAPYOFAHTR
Monitoring of therapy for AHTRMonitoring of therapy for AHTR
• Renal status by creatinine and urine output.Renal status by creatinine and urine output.
• DIC by PT, PTT, platelet and fibrinogen.DIC by PT, PTT, platelet and fibrinogen.
• Degree and progress of hemolysis by LDH.Degree and progress of hemolysis by LDH.
57

ALLERGIC REACTIONS RELATED
TO BLOOD TRANSFUSION
58El-Shanshory 2011
It is one of the common reactions and
ranges from:
1.Severe fatal reaction (anaphylactic
allergic reaction) .
2.To very mild skin (urticarial) reaction.

ALLERGIC URTICARIAL
REACTION• It is a common reaction (1% of transfusion) and is
manifested by a sense of itching, with urticarial rash.
• Pathogenesis: it is an immunological reaction
between soluble antigen in the transfused blood
units and antibodies in the patient.
• Treatment:
– Transient stopping of transfusion, give
antihistamines.
– Restart transfusion with slow rate.
• Prevention: use of washed RBCs and pre-
transfusion of antihistamines.
59

ANAPHYLACTIC TRANSFUSION REACTION
60
Definition:
it is acute onset of hypotension, bronchospasm,
chills, fever, and urticarial following transfusion
blood , plasma or products of blood.
Pathophysiology:
it is the result of massive release of vasoactive
and smooth muscle-reactive mediators following
acute antigen-antibody interaction.
Commonly, it occurs in IgA deficient patients who
developed anti-IgA (Ag)
The incidence of anaphylatic reaction:
it is reported to occur in 1 in 20,000 or to 50,000
recipients.
Clinical picture of anaphylactic reaction: Most
patients show sudden :-
* severe hypotension. * Flushing.
* bronchospasm, dyspnea. * Chills.
* vomiting ,diarrhea. * wide-spread oedema,
urticarial rash .

LABORATORY DIAGNOSIS OF ANAPHYLACTIC REACTION:
TREATMENT OF ANAPHYLACTIC
REACTION:
PREVENTION OF ANAPHYLACTIC
REACTION:
• Detection of IgA.
• Detection of anti-IgA by passive hemagglutination assay
utilized IgA coated RBCs.
• Stop transfusion immediately.Stop transfusion immediately.
• Antihistamines.Antihistamines.
• Epinephrine.Epinephrine.
• Fluid therapy to maintain the blood pressure.Fluid therapy to maintain the blood pressure.
• Use washed RBCs in suspected patients.Use washed RBCs in suspected patients.
62

DELAYEDHEMOLYTIC TRANSFUSION REACTION IN SOME
CLINICAL CONDITIONS
DHTR in solid organ transplantation
 In minor incompatibilityIn minor incompatibility :-:-
• the contaminant lymphocytes in the transplanted organ (liver,the contaminant lymphocytes in the transplanted organ (liver,
kidney, heart) may produce antibodies against the recipientkidney, heart) may produce antibodies against the recipient
RBCs (for example O liver donor and A recipient).RBCs (for example O liver donor and A recipient).
• These antibodies may produce DHTR within 7 days afterThese antibodies may produce DHTR within 7 days after
transplantation and may last for 1 month.transplantation and may last for 1 month.
• It may be complicated by renal failure.It may be complicated by renal failure.
• The patient is given O Rh negative RBCs.The patient is given O Rh negative RBCs.
 In major incompatibility:In major incompatibility:
• The donor’s organ carrying ABO antigens that can beThe donor’s organ carrying ABO antigens that can be
agglutinated by the recipient antibodies .agglutinated by the recipient antibodies .
• It is recommended to carry pre-transplant plasmapheresis .It is recommended to carry pre-transplant plasmapheresis . 63

DHTR following hemopoietic stem cell transplantation(HSDT)
 In minor-incompatibilityIn minor-incompatibility::
• The contaminant cells of the donor (lymphocytes) in theThe contaminant cells of the donor (lymphocytes) in the
HSCT may produce antibodies.HSCT may produce antibodies.
• Treatment:Treatment:
 Transfusion of O cells to dilute the patients RBCs.Transfusion of O cells to dilute the patients RBCs.
 In severe cases, RBCs exchange with blood group OIn severe cases, RBCs exchange with blood group O
RBCs if there is rapid bone marrow engraftment .RBCs if there is rapid bone marrow engraftment .
 InIn major incompatibilities:major incompatibilities:
• The donor’s BM RBCs are hemolysed by the patient’sThe donor’s BM RBCs are hemolysed by the patient’s
antibodies.antibodies.
1)Depletion of the donor’s bone marrow from RBCs1)Depletion of the donor’s bone marrow from RBCs
2)Pre-transplantation plasmapheresis.2)Pre-transplantation plasmapheresis.
 In minor-incompatibilityIn minor-incompatibility::
• The contaminant cells of the donor (lymphocytes) in theThe contaminant cells of the donor (lymphocytes) in the
HSCT may produce antibodies.HSCT may produce antibodies.
 Transfusion of O cells to dilute the patients RBCs.Transfusion of O cells to dilute the patients RBCs.
 In severe cases, RBCs exchange with blood group OIn severe cases, RBCs exchange with blood group O
RBCs if there is rapid bone marrow engraftment .RBCs if there is rapid bone marrow engraftment .
 InIn major incompatibilities:major incompatibilities:
• The donor’s BM RBCs are hemolysed by the patient’sThe donor’s BM RBCs are hemolysed by the patient’s
antibodies.antibodies.
1)Depletion of the donor’s bone marrow from RBCs1)Depletion of the donor’s bone marrow from RBCs
2)Pre-transplantation plasmapheresis.2)Pre-transplantation plasmapheresis.
64

DHTRFOLLOWING BLOODTRANSFUSION IN SICKLE CELL
DISEASE
• The frequency of alloimmunization in sickle cell disease afterThe frequency of alloimmunization in sickle cell disease after
repeated transfusion is about 20-30%.repeated transfusion is about 20-30%.
• Some patients may develop warm-reacting auto-antibodies.Some patients may develop warm-reacting auto-antibodies.
• Clinically, DHTR in sickle cell disease:Clinically, DHTR in sickle cell disease:
• Signs of sickle cell crisis.Signs of sickle cell crisis.
• Development of more anemia.Development of more anemia.
• Reticulocytopenia secondary to suppression ofReticulocytopenia secondary to suppression of
erythropoiesis by blood transfusion and hemolysis oferythropoiesis by blood transfusion and hemolysis of
reticulocytes.reticulocytes.
• Prevention and treatment:Prevention and treatment:
• RBCs phenotyping for Kell, kid ….. and Rh areRBCs phenotyping for Kell, kid ….. and Rh are
recommended before the start of long term bloodrecommended before the start of long term blood
transfusion.transfusion.
• Corticosteroid and immunoglobulin during DHTR.Corticosteroid and immunoglobulin during DHTR.
65El-Shanshory 2011

POST-TRANSFUSION PURPURA
(PTP(
• Definition:Definition: It is acute episode of severe thrombocytopeniaIt is acute episode of severe thrombocytopenia
occurring about one week after blood transfusion.occurring about one week after blood transfusion.
• It usually affectsIt usually affects :-:-
 HPA-1aHPA-1a (Human Platelet Antigen)(Human Platelet Antigen) negative pregnant womennegative pregnant women
 or HPA-1a negative persons who were repeatedly transfused withor HPA-1a negative persons who were repeatedly transfused with
HPA-1a positive blood componentsHPA-1a positive blood components..
• Incidence:Incidence: It is a very rare complication 1:400,000It is a very rare complication 1:400,000
transfusions as the prevalence of HPA-1a negative persons istransfusions as the prevalence of HPA-1a negative persons is
very low.very low.
• Definition:Definition: It is acute episode of severe thrombocytopeniaIt is acute episode of severe thrombocytopenia
occurring about one week after blood transfusion.occurring about one week after blood transfusion.
• It usually affectsIt usually affects :-:-
 HPA-1aHPA-1a (Human Platelet Antigen)(Human Platelet Antigen) negative pregnant womennegative pregnant women
 or HPA-1a negative persons who were repeatedly transfused withor HPA-1a negative persons who were repeatedly transfused with
HPA-1a positive blood componentsHPA-1a positive blood components..
• Incidence:Incidence: It is a very rare complication 1:400,000It is a very rare complication 1:400,000
transfusions as the prevalence of HPA-1a negative persons istransfusions as the prevalence of HPA-1a negative persons is
very low.very low.
66

PATHOPHYSIOLOGY OF PTP
• The pathophysiology is similar to HDN Hemolytic
disease of the newborn.
• Blood transfusion of HPA-1a positive platelets or
blood donor in a previously expose HPA-1a
negative patient (pregnancy ….) will cause
secondary immune response with marked rise in
anti-HPA-1a antibodies which is followed by
destruction of the patient’s HPA-1a negative
platelets by unknown mechanism. 67

• Clinical picture of PTP:
• Most patients are persons who have had previous
transfusion.
• The platelet-count usually drop rapidly within 5-10
days after transfusion with severe hemorrhage
(purpura and GIT bleeding).
• Platelet count rises again within 2-4 weeks.
• Prognosis of PTP: mortality is about 5% from
intracranial hemorrhage.
• Differential diagnosis of PTP
• Auto-immune and drug-induced thrombocytopenia.
• DIC and TTP.
68

• Laboratory investigation of PTP:
• Performance of platelet-count.
• Detection of HPA-1a antigen.
• Detection of HPA-1a antibodies.
• BM to exclude bone marrow aplasia.
• Treatment:
• High dose IVIgG.
• Corticosteroids.
• Plasmapheresis.
• Platelet concentrates are of little value and indicated in
severe bleeding. It may cause transfusion related acute
lung injury .
• Prevention:
The patient should be transfused from HPA-1a
negative donor. 69

IMMUNOMODULATION EFFECTS OF BLOOD
TRANSFUSION
• Blood transfusion leads to both activation of
immune system (production of alloantibodies)
and suppression of immune-mediated
activities .
• The suppressor effects on the immune system
are :
1.Reduction in CD4/CD8 ratio and natural killers.
2.Impaired lymphocyte mitogenic response.
3.Suppression of delayed hypersensitivity reaction.
4.Induction of state of anergy.
5.Inhibition of neutrophil function.
71

CLINICAL EFFECTS OF
IMMUNOMODULATION:
• The adverse post-transfusion
immunomodulation is the result of leucocyte
chimerism and cytokine production:
• Increase cancer recurrence.
• Increase post-operative infection.
• Transfusion-associated graft-versus host
disease.
72El-Shanshory 2011

Minimizing the blood transfusionMinimizing the blood transfusion
74
 Maintenance of cardiac output by:
• Crystalloid solutions.
• Colloid solution :-
 Dextran
 Delatin
 Hydroxylethy Starch)
• Act from 4-24 hours.

BLOOD transfusion alternatives
Hydroxy ethystarchHydroxy ethystarch
(metastarch)(metastarch)
Cool placesCool places
-
45 min
Normal salineNormal saline
ringer lactateringer lactate
Cool placesCool places
Gelatin (hemocel)Gelatin (hemocel)
At room temp<25At room temp<25
5 years5 years
Dextran 60, 70Dextran 60, 70
At room temp<25At room temp<25
1 bootle=
500ml
3 times
Blood lost
4% in 0.9
NaCl
4H
3%dextran 60
in NaCl 0.9%
6% dextran 70
In 5% glucose
Not exceed
25-50ml/kg/24h
12h
6%metastarch
in
NaCl 0.9%
Not exceed
20ml/kg/24h
20-24h
75El-Shanshory 2011

Minimizing the blood
transfusion
76
 Do not delay an emergency operation
( bleeding case) regardless of preoperative
Hb level

77
transfusion
 Minimizing blood loss by:-
 Preoperative planning.
 Induced hypothermia
 Hypotensive anesthesia
 Meticulous hemostasis.
 Minimizing the oxygen consumption by:-
 Mild hypothermia.
 Neuromuscularblocking agent.
 Minimizing phlebotomies by:-
 Transcutaneous pulse oximeter.
 Pediatric microsampling.
 Multiple test persample.

78
 Drug modifiers:
1. Hydroxyurea to increase fetal
hemoglobin in sickle cell
anemia.
2. Desmopressin in Von-
Willbrand disease.
 Maximizing blood production by
growth factors as:
1. GM-CSF, G-CSF for
neutropenia.
2. Erythropoietin hormone for
anemia.
3. IL11: thrombocytopenia.
transfusion

REFERENCES
• BLOOD TRANSFUSION LECTURE
DR MOHAMED EL SHANSHORY
PROF. OF PEDIATRIC HEMATOLOGY
TANTA UNIVERSITY HOSPITAL

Blood transfusion dr m laban

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