BLOOD THERAPY
BYMOHAMED E. ABDEL-GHAFFAR, MD.
Professor & Chairman,Department of Anesthesia &
Intensive Care, FOM, Suez Canal University.
HISTORICAL REVIEW
• Initial attempts by Lower and Denys to affect
transfusion from one animal to another led
eventually to transfusions from animals to
humans with catastrophic results leading to
legal sanctions against the practice for about
two centuries.
• In 1818 Blundell and others used humans as
both donors and recipients with occasional
though unpredictable success.
HISTORICAL REVIEW• The real breakthrough was the discovery of
human ABO blood groups by Karl
Landsteiner in 1900.
• Later Landsteiner and Levine discovered M,
N, & P groups.
• Further work by Landsteiner and Wiemer
discovered the Rhesus groups in 1939.
• In spite of all this, lack of a safe anticoagulant
remained a major transfusion problem until
1943 when Loutit and Mollison developed an
acid citrate soln.(ACD) to be mixed with
blood.
Blood groups
• 85% of the population have the D antigen and
designated Rh +ve.
• Other minor and rare blood groups include M, N, P and S
groups and they are cold agglutinins i.e. giving strong
reactions at about 20 C with little or no reactivity at 37 C.
Group Antigen on
RBCs
Antibodies
in serum
% of
population
O None Anti A, Anti
B
47
A
A Anti B 42
B
B Anti A 8
AB
A & B None 3
BLOOD THERAPY, Cont.
Compatibility testing
• The ABO - Rh type, cross match and antibody screen
were designed to demonstrate harmful antigen -
antibody interactions in vitro, so that harmful in vivo
interactions could be prevented.
Blood storage
• Banked blood contains CDP-A ( citrate, dextrose,
phosphate and adenine ) and is stored at 4-6 C to
prevent bacterial growth. This blood is valid to be
used for up to 35 days.
BLOOD THERAPY, Cont.
Indications for whole blood transfusion
• Blood transfusions are given to increase O2
carrying capacity and intravascular volume (IVV),
thus tissue hypoxia & Hb < 7 g/dl or Hct < 21 are
the only two absolute indications for whole blood.
• Additional factors that must be considered are:
• Age of the patient
• Cause of anemia & chronicity of anemia
• Hemodynamic status and presence of coexisting
cardiac, pulmonary or vascular disease.
BLOOD COMPONENT THERAPY
1- Packed Red Blood Cells ( PRBCs )
• PRBCs are made by removing 2/3 of plasma from
a unit of whole blood. Plasma removed is utilized
for other component therapy.
• PRBCs are used to restore O2 carrying capacity.
• One unit of PRBCs Hct 3 units.
BLOOD COMPONENT THERAPY Cont.
2- Fresh Frozen Plasma ( FFP )• FFP is formed when the plasma portion is removed from a
unit of whole blood and then frozen.
• FFP contains factor V, factor VIII, and prothrombin as well
as antithrombin III, protein C and protein S.
• FFP is indicated for :
1- Treatment of dilutional coagulopathy in a massively
transfused patient.
2- Correction of warfarin anticoagulation ( one unit of FFP ↓
PT by 2 sec. ).
3- Treatment of congenital or acquired coagulation factor
deficiencies.
4- Treatment of antithrombin III deficiency.
BLOOD COMPONENT THERAPY Cont.
3- Cryoprecipitate (CP )
• CP is formed when the plasma is rapidly frozen, then
allowed to rewarm.
• CP contains most of factor VIII and fibrinogen of the
original unit of blood. CP also contains factor IX,
factor VIIIa and Von Willebrand’s factor
• CP is indicated for:
1- Hemophilia A
2- Von Willebrand’s disease.
3- Hypofibrinogemic states.
4- Bleeding from thrombolytic therapy.
COMPLICATIONS OF BLOOD THERAPY
• It is always stressed that every Blood Transfusion (BT)
carries an element of risk and never be given without a
definite indication.
1- Mortality :
• Mortality as a result of BT is about 0.1 - 1.0 % and
is to be comparable with that of appendectomy.
• 3000 persons die annually in USA due to BT.
COMPLICATIONS OF BLOOD THERAPY Cont.
2- TRANSFUSION REACTIONS :A- Hemolytic transfusion reaction ( HTR ) :
• Incidence is 1/4000 to 1/6000 . The incidence of a fatal HTR is 1/100,000 .
• Mechanism : two mechanisms are recognized.
1- The most catastrophic with a mortality of 20 -60% is intravascular hemolysis when there is a direct attack on transfused donner cells by recipient antibodies and complement and usually results from ABO blood group incompatibility.
2- Extravascular hemolytic reaction is usually less serious than the iv variety.
Here recipient antibodies coats but don’t immediately hemolyse the transfused RBCs.
Destruction occurs primarily in the reticuloendothelial system ( RES ).
COMPLICATIONS OF BLOOD THERAPY Cont.
SIGNS AND SYMPTOMS :
Chills, fever, chest and flank pain,
nausea, flushing, hypotension,
dyspnea, hemoglobinuria, oliguria or
anuria, and increased bleeding from
the surgical field.
The clinical presentation is quite
variable
COMPLICATIONS OF BLOOD THERAPY Cont.
TREATMENT :
1 - STOP transfusion and return unused blood to blood
bank for recrossmatch.
2- Enforce forced alkaline diuresis to a minimum urine
output of 75 - 100 ml/hr by:
a- Generous iv fluids + Mannitol 0.5 - 1.0 g/kg over 10 -
15 min., if not enough give iv furesemide 20 - 40 mg.
b- Alkalinize urine : 0.5 -1.0 mEq/kg NaHCO3 is usually
sufficient to raise urine pH to 8. High urine pH ensures
rapid clearance of hemoglobin
3- Assay urine & blood Hb conc, platelet count, PTT and
serum fibrinogen levels .
4- Send patient blood to blood bank for antibody screen 5-
Prevent hypotension to ensure adequate renal blood
flow.
COMPLICATIONS OF BLOOD THERAPY Cont.B- Delayed hemolytic transfusion reaction :
• In many cases of HTRs, the transfused donner cells may
survive well initially, but after a variable delay ( 2 - 21 days )
will be hemolysed.
• This reaction is common in people who had received
multiple blood transfusions and in females who had
multiple pregnancies.
• In this type of reaction the antibody level at the time of
transfusion is too low to be detected or too low to cause
RBC destruction.
• RBCs destruction occurs only when the level of antibody is
increased after a secondary immune response ( anamnestic
response ).
• These reactions are usually manifested by a decrease in the
post-transfusion Hct.
• Unlike the immediate reactions Rh and Kidd system rather
than ABO system are implicated.
COMPLICATIONS OF BLOOD THERAPY Cont.C- Non hemolytic transfusion reactions :
• These reactions are usually not serious and are of either
febrile or allergenic nature.
• Most allergic reactions are anaphylactoid and are caused
by the presence of foreign protein in the transfused blood.
• The most common symptoms are urticaria and itching ,
some patients develop facial swelling, chills, fever,
headache, nausea and myalgia.
• Incidence is around 3% and they usually respond to H-1
blockers.
• Infrequently a more severe form of allergic reaction
involving anaphylaxis occurs and causes dyspnea, chest
pain and shock.
• This type of reaction does not involve RBCs destruction
and occurs rapidly after transfusion of few mls of blood or
plasma. Adrenaline must be given SC, IM or IV.
COMPLICATIONS OF BLOOD THERAPY Cont.
3- Transmission of disease :
1- Hepatitis A, B and C
2- HIV.
3- Human T Cell Leukemia Virus type-1 ( HTLV-1 ).
4- Cytomegalovirus ( CMV ).
5- Syphilis and malaria.
6- Others are much less common e.g., Herpes,
infectious mononucleosis, toxoplasmosis,
brucellosis, trypanosomiasis, leishmaniasis,
salmonillosis, typhus and filariasis.
COMPLICATIONS OF BLOOD THERAPY Cont.
4- Citrate intoxication :
• Stored blood contains citrate as an
anticoagulant and if transfused rapidly at
a rate > 70 ml/kg/min. may lead to S&S of
citrate intoxication which are essentially
those of hypocalcemia, since citrate binds
Ca thus decreasing serum Ca leading to
tremors, hypotension and cardiac
arrhythmias.
• Citrate is rapidly metabolized by the liver
to HCO3 .
COMPLICATIONS OF BLOOD THERAPY Cont.
5- Dangers of cold blood :
• Transfusion of unwarmed stored
blood at 4 C can lower the recipient
temp. markedly leading to shivering,
ventricular arrhythmias or even
sudden arrest.
• Proper warming of blood using
thermostatically controlled devices is
a good and safe practice.
COMPLICATIONS OF BLOOD THERAPY Cont.
6- Changes in O2 transport :
• The respiratory function of RBCs may impaired during
preservation, making it difficult for stored RBCs to
release O2 to tissues immediately after transfusion.
O2 dissociation curve of stored blood is shifted to
the left.
• This may be manifest for 24 hr following BT.
7- Coagulation abnormalities :
• More pronounced after massive BT and include:
1- Dilutional thrombocytopnea.
2- Low factors V and VIII.
3- Disseminated Intravascular Coagulation ( DIC ).
COMPLICATIONS OF BLOOD THERAPY Cont.
8- Circulatory overload :• Neonates, elderly and patients with limited cardiac reserve
are more likely to suffer.
• HR, BP and CVP are increased. Lung bases may show
crepitations.
9- Infusion of microaggregates :• It has been demonstrated that amounts of clot and debris in
bank blood increases with duration of storage, and some of
this particulate matter is not filtered by the standard 170 um
filter during routine transfusion and enters the recipient blood
stream.
• Some authors believe that this contributes to posttransfusion
pulmonary dysfunction and posttransfusion kidney
dysfunction.
• These authors advocate the use of 40 um blood filter for
patients undergoing massive BT.
RECENT CHANGES IN ATTITUDES AND PRACTICES TOWARDS BLOOD TRANSFUSION
Because we know now more about the hazards and
complications of BT, there are now significant changes in
the attitudes and practices of BT. So that
1- Autologous blood :is more widely used than ever where up to 6 units of patient’s blood
can be withdrawn over three weeks to be retransfused during
surgery and postop. This practice markedly reduced the need for
homologous blood for elective surgeries.
2- Use of cell savers :These machines essentially take sequestered and collected patient’s
blood in the surgical field, wash RBCs, filter them and return
washed viable RBCs to the patient.
3- Use of component blood therapy when applicable:
So that, only the needed component is given to the patient e.g., factor
VIII and the rest of the blood is used for other patients.