TRANSFUSION

BY SEMIRA INDRIS

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 OBJECTIVES
• Blood typing & cross matching
• Blood preparation
• indication
• method
• COMPLICATIONS

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• Blood is very vital as it perfuse oxygen and remove
carbondioxide from the tissues.
• It has two components ,the fluid part which Transport
hemostatic governors like hormones, coagulation factors and
antibodies.
• The formed element comprises the RBC,WBC and PLATELATES.

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 Blood typing & cross matching
• Typing and cross matching of blood is mandatory.
Two groups of antigens on the surface of RBC & are important in
surgical patients
– The ABO system – natural antibodies in the serum.
– The Rhesus system – acquired antibodies after exposure

• Cross matching is mixing of the recipient's serum with the donor’s cells:
– To confirm ABO compatibility
– To test for Rh or any other blood group ag–ab reactions.

• Donor should be screened to prevent any possible infections of the recipient like
hepatites,hiv, syphilis and also we have to be sure that the donating blood have
no harm to the donor.

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• As a rule if patient is RH-VE you should not give rh+ve
blood except for some exceptions.
• Never give rh+ve blood to women of child bearing
age.
• Emergency transfusion could be accomplished by
O-ve blood.(for female & both for males.)

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 Types(preparations)
1) Autologous predeposit transfusion
• Is growing nowadays
• predonate their own blood up to 3 weeks before
surgery for transfusion.
• can donate if hemoglobin is>11g\dl &
hematocrit>34%.

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2)Banked whole blood cells
• This is nowadays rarely available
• With new preservatives its shelf life extend upto 40 to 45 days.
• Changes in RBC during storage are
Decrease in oxygen carrying capacity
Poor source of platelets
All but factor V & VIII stay stable.
After 21 days PH drops from 7 to 6.8, K level rises to 30 meq\
dl, lactic acid from 50 to 680mg\dl , ammonia also rises from 60 to 680 mg\dl.
• Hemolysis from the storage is insignificant.

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3)Fresh whole blood
• Transfusion within 24 hrs of donation.
• Is poor source of platelets and factor 8.
4)Packed RBC
• Prepared by removing the plasma after centrifugation.
• It reduces but doesn’t eliminate rxn cased by plasma
components.
• Each unit has about 330ml.
• Has hematocrit value of 50% to 70% of hematocrit.

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5) Leukocyte reduced(washed RBC)
• Prepared by filtration that removes about 99.9% of WBC &
most of the platelets.
• It prevents almost all febrile , non hemolytic rxn (fever or
rigor).
• Mostly used in patients who have had rxns like fever,
uritticaria, anaphylaxis to unwashed RBCs.
6) Platelet concentrate
• Massive blood loss , inadequate production, qualitative
platelet disorder.

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7) Frozen plasma
• is rich in coagulation factors.
• Prepared from freshly donated blood & stored at –40 0c to –50 0C with
a 2 yr shelf life.(each unit contain 200 to 250ml)
• The risk of infection is the same weather taking FFP, whole blood cell
or RBC.
8) Cryoprecipitate
• Precipitate of FFP and is rich in factor VIII and fibrinogen.
• It is stored at –300C with a 2-year shelf-life.
• It is given in low-fibrinogen states or in cases of factor
VIII deficiency.

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 indications
1) General indication
I. Improvement in oxygen carrying capacity. ( in
symptomatic anemic patient)
II. Volume replacment.
 Measurement of normal volume is inaccurate &
variable specially in those rapidly changing situations
like hemorrhage ,CIP & elderly patients.
 Measurement of hematocrit and hmg levels are
used to estimate blood loss.

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guidelines for transfusion based on the hmg level
– Hemoglobin < 10 gm/dl in patients with a known
increased risk for coronary artery disease or
pulmonary insufficiency ,who have increased risk
of blood loss.
– Hemoglobin < 8gm/dl & patient has ssx of
decreased O2 delivery.
– Hemoglobin <6gm\dl in patients who are not
symptomatic, not undergoing surgery.

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III. Replacment of the clotting factor.
• Transfusion of coagulation factors or proteins responsible for
coagulation may be indicated in specific patients before & during
surgery.
2)Specific indications
 massive transfusion
• Administration of more than 2.5L or 5L over a period of 24hrs.
• Mostly indicated for patients in shock.
• This result significant changes in the bodies metabolic state b\c of administering of
large amount of cold citrate containing blood that undergo several changes during
storage.
hyperkalemia , hypocalcaemia , dilutional thrombocytopenia , changes
in ATP & 2,3 DPG level & hypothermia.

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 Methods to administer blood
 Routine methods.
• Depends on the patients status.
• 5ml per min for the first min after which 10 to 20 ml\min .
• If there is marked oligemia 500ml in the first 10 min then
another 500ml in the next 10 min.
 Other methods
• interaperitoneal , intramedullary cavity of sternum & long
bones.

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 Complications of transfusion.
Hemolytic rxn
• Incompatibility of abo &RH group(mainly ABO)
• Immediate(acute)-within 24 hrs. of transfusion, intravascular destruction
of RBC leading to hemoglobinemia & hemoglobinuria.
• Delayed -2 to 10 days after transfusion, extravascular hemolysis, mild
anemia & unconjugated hyper biluribinmia. (when the individual has low
antibody at first , then it builds up with time)
• Chills , fever, hypotension , renal failure (oliguria),hemoglobinuria &DIC
may present.
MGT
• If immediate ,stop transfusion immmediately.
• Check the blood type of the recipient & the suspected unit of blood.

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• Insert Foley catheter & control the urine out put.
• If it is delayed, usually no intervention is taken.

Febrile & allergic rxn

• Are frequent.
• result in mild uriticaria & fever within 60 to 90 min after the start of
transfusion.
• Rarely anaphylactic shock may develop.
• Is resulted from administration of blood to hypersensitive recipient or
blood containing antibodies of hypersensitive donor .
Treatment
Antihistamines, epinephrine & steroids.
If the rxn is repeated we can prevent by leukocyte depleted(washed) RBC.

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Bacterial sepsis
• Is rare & can be acquired from contaminated collection bag or due
to poor cleaning of the donors skin.(mostly gram –ve)
• Fever ,chills, abdominal cramp, vomiting & diarrhea may present.
mgt
should be discontinued and culture the blood.
 Air embolism
TRALI & pulmonary edema (due to over transfusion
& could be prevented by measuring the central venous
pressure whenever we administer large volume of blood.)

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Superficial thrombophlebitis.(at the site of
prolonged blood infusion , usually if more
than 8 hrs.)
Transmission of infections like hepatites,hiv
malaria.

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THANK YOU!!!!!!

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COAGULATION DISORDERS

SEMHAL GETACHEW

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 Coagulation Disorder
• Is a disorder characterized by bruising that is
unprovoked.
• More commonly precipitated by trivial
incidental or surgical trauma.
• Moderate & Mild coagulopathies may remain
clinically silent.

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 CLASSIFICATION
Hereditary Acquired
• Hemophilia's-A,B&C • Liver disease
• Von willebrands disease • Vitamin K deficiency
• Coagulation deficiency • Anticoagulation Drugs
Factor II
• DIC
Factor V • Massive transfusion of
Factor VII stored blood
Factor XI & XIII • Circulatory inhibitors of
• Idiopathic coagulation
Thrombocytopenic Purpura

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 HAEMOPHILIA

• An inherited disorder of blood

coagulation
• The commonest bleeding disorder
• Characterized by a permanent tendency
to hemorrhages, spontaneous or
traumatic
 
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 HAEMOPHILIA A
• sex-linked recessive
• resulting from a deficiency of factor VIII
• incidence 1:5,000
• occurring almost exclusively in males
• About 30% of patients have no family history
• characterized by
• prolonged clotting time
• decreased formation of thromboplastin
• diminished conversion of prothrombin
• easy bruising
• massive hemorrhage after trauma or operative
procedures 24
 Ctd…

o severe →factor level <1% of normal

o Moderate →factor level 2 to 5% of normal
o Mild →factor level 5 to 50% of normal
» Laboratory features: elevated PTT and normal PT levels
• Treatment: infusions of recombinant factor VIII

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HEMARTHROSES

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 HAEMOPHILIA B
• sex-linked recessive due to factor IX deficiency

• incidence 1:30,000

• In about 15% of these patients, factor IX is present but nonfunctional

• Clinical and laboratory features similar to hemophilia A.

• treated with infusions of recombinant factor IX.

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 Factor XI deficiency

• Referred to as hemophilia C
• Inherited as autosomal recessive trait
• Spontaneous bleeding is rare
• treatment: fresh –frozen plasma(FFP)

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 VON WILLEBRAND DISEASE

• autosomal dominant disorder

• associated with a reduced quantity of circulating vWF
• affecting about 1% of adults in the United States
• bleeding tendency is mild and often goes unnoticed until
some hemostatic stress
• The most common symptoms
• spontaneous bleeding from mucous membranes
• excessive bleeding from wounds
• menorrhagia
• a prolonged bleeding time in the presence of a normal platelet
count.

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 classification
Type 1
• mild to moderate quantitative vWF deficiency,
• 70% of all cases
• is associated with mild disease.
Type 3
• extremely low levels of functional vWF
• severe clinical manifestations
• marked effect on the stability of factor VIII
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Idiopathic Thrombocytopenic Purpura

• Presence of autoantibody directed against

platelet membrane glycoprotein.
• Self-limited in children
• often present after a viral illness.
• ecchymoses ,Petechiae, epistatxis, gum
bleeding, Intracerebral hemorrhage

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 ACQUIRED COAGULATIVE DISORDERS

• Acquired deficiencies usually involve

multiple coagulation factors
simultaneously and can be based on
decreased protein synthesis or a
shortened half-life.

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 Vitamin K deficiency
• impairs production of prothrombin and factors
VII,IX, and X
• vitamin K is a cofactor in the carboxylation of
glutamate residues on prothrombin complex proteins
 Causes: Poor diet
• Recent surgery
• malabsorbition
• obstuctive jaundice
• Multiple antibiotic therapy
• Laboratory features: elevated PT and PTT

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 Liver disease
• Liver is a site for synthesis & clearance of most
procoagulant and natural anticoagulant proteins
• results in deficiencies of all clotting factors except VIII
• Thrombocytopenia is the common presentation in
liver failure
• Failure results in high risk of bleeding

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 Ctd….
• Major causes
– major hepatic injury,
– Cirrhosis
– biliary obstruction
• Laboratory features: elevated PT, normal or elevated
PTT.

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 DISSEMINATED INTRAVASCULAR COAGULATION

• DIC is an acute, subacute, or chronic

thrombohemorrhagic disorder
• the excessive activation of coagulation
• formation of thrombi in the microvasculature of the
body.
• Systemic process producing both thrombosis &
hemorrhage

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 Cause for DIC
1.Infection
I. E.coli
II. N.meningities
III. S.pneumonia
IV. Malaria
2.Cancer- Lung,Pancreas &Prostate
3.Obstetric-placental abruption ,preclampsia

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 Anticoagulant drugs
• Indirect thrombin Inhibitors
.Unfractional heparin(UFH)
.Low molecular weight heparin
.Fundaparinux
• Fibrinolytic drugs
.Streptokinas .Urokinase
• Anti platelet agents
.Asprin .Ticlopidine
•Others
.quanidine .sulfa prepation,
.H2-blockers .antidiabetics agents
.gold salts . rifampin.

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 Hypothermia
• Alteres coagulation in surgical patients
• Open thoracic or abdominal cavity causes
hypothermia
• Hypothermia causes
• increase fibrinolytic activity
• Thrombocytopenia
• impaired platelet function
• decrease in collagen induced platelet aggregration
• increased affinity of hemoglobin for oxygen.
• 30 to 34 °c leads to coagulopathy and acidosis.
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 Other disorders
• fibrinogen deficiency
– liver disease
– L-asparaginase therapy
– rattlesnake bites
• renal failure
• cardiopulmonary bypass
• thrombocytopathy
• defibrinization circulating anticoagulants
• Lymphoma
• SLE
• massive transfusion (dilutional coagulopathy)
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• idiopathic
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