BLOOD TRANSFUSION THERAPY

BY

DR ARUN RAJ & DR RAVI

UNDER GUIDENCE OF

DR R D PATEL
DR SUNIL
TRANSFUSION TRIGGER

Hemoglobin level below which transfusion of RBCs are

indicated
General consideration for transfusion
Age
blood volume
blood loss
cardiac output
cardiovascular status
oxygen extraction ratio
ASA 1996 guidelines
rarely required if Hb >10 gm%

always indicated if Hb < 6 gm%

Hb between 6 and 10 g% transfusion depends on

complications of inadequate oxygenation and
cardiovascular status
Whenever possible use:
Acute normovolemic hemodilution
Preoperative autologous blood donation
Postoperative modifications to reduce blood loss
Habibi Recommendations

• Hb ≤ 8 g% in all patients

• Hb ≤ 10 g% in ischemis heart disease and

emphysema

• Hb ≤ 10 g% if autologous blood transfusion

• Hb ≤ 12 g% in ventilator dependant patient
If blood loss ≥ 20% blood volume
 Blood loss ≥ 100 ml in pediatric patients.
 Herbert Recommendations
 If Hb ≤ 10 g% in unstable angina and anterior wall MI

Hb between 10 and 12 g% in critically ill patients.

Blood Components

Erythrocyte preparations:
PRBCs
Washed RBCs
Leukocyte poor RBCs
Frozen RBCs
Leukocyte preparations:
Granulocytes
Mononuclear cells
Platelets
.
Plasma fractions:
FFP
Cryoprecipitate
Platelet rich plasma
Fractionated plasma:
Factor VIII concentrate, factor IX concentrate
Autithrombin III concentrate
Prothrombin complex
Albumin
Intravenous immunoglobins
 BLOOD COMPONENT THERAPY

aimed at correcting deficiency of specific component of

whole blood by

administration of that specific component instead of

giving whole blood.
 ERYTHROCYTE PREPARATIONS
Packed Red Blood Cells
Obtained by apheresis collection or prepared from
anticoagulated whole blood.
Following centrifugation, plasma is removed and
100 ml of additive solution is added.
Each unit contains:
200 ml RBCs
Plasma < 50 ml
Hematocrit of 55–60%
Shelf Life
21–42 days (at 1–6C)
Dosage
Each 2 units or 15 ml/Kg increases Hb by 2 g/dl.
Leukocyte Poor Red Cells
Indications
Patients with recurrent febrile reactions to prevent
nonhemolytic febrile reactions

Frequently transfused patients to reduce HLA

antigen alloimmunization

Prevent transmission of CMV and TA-GVHD

PLATELET PREPARATIONS
Types
Apheresis platelets (collecting more platelets from 1 donor
to avoid multiple donors)

Platelet concentrates (from multiple donors)

Lymphocyte depleted platelets

Ultraviolet B irradiated platelets.

Manufacture
Platelet concentrates:

Manufactured from whole blood by centrifugation

Stored at 20–32 C under constant agitation for 5 days

Only blood product to be stored at room temperature

It is lymphocyte contaminated
5–6 platelet concentrates pooled to obtain adult dose
1 unit of platelet concentrate increases platelet
count by 7000–10000 cells/mm3 one hour after
transfusion in a 70 kg adult.
Apheresis platelets:
From single donor by apheresis
known as Single Donor Platelets (SDP)

Stored at 20–22 C under constant agitation for 5 days

1 unit SDP increases platelet count by 30,000 to 60, 000
cells/mm3
Each SDP unit is equivalent to ‘6 pack’ platelet
concentrate.
Indications
ASA 2006 Guidelines
Platelet count < 10, 000/mm3 in non-bleeding
patients without other abnormalities of hemostasis

Platelet count 10,000 to 50,000/mm3 for:

Lumbar puncture/epidural anesthesia
Central venous access
Endoscopy with biopsy
Liver biopsy
Vaginal delivery
Laparotomy

To maintain same platelet count or > 50,000/mm3 during DIC with

ongoing blood loss.
To maintain > 75, 000/mm3 during management of massive
blood loss
Platelet count 1,00, 000/mm3: neurosurgery

Microvascular bleeds due to platelet dysfunction in:

–– Uremia
–– Cardiopulmonary bypass
–– Massive blood transfusion.
Shelf Life 5 days.
Contraindications
Diseases associated with platelet activation:
–– Thrombotic thrombocytopenic purpura
–– Heparin induced thrombocytopenia
–– Administration of platelet concentrates may increase
thrombosis
• Idiopathic Thrombocytopenic Purpura: Unless life
threatening bleeding
Prophylactic administration:
–– Massive blood transfusion
–– After cardiopulmonary bypass.
Dosage
• 5 ml/kg or 6 units of platelet concentrates increases
count by 50,000 cells/mm3
• 1 unit of apheresis platelets increases count by 40 to
60,000 cells/mm3
• Use ABO compatible platelet concentrates where possible
• Platelet concentrates/RDP need not be group specific
• ABO incompatible platelet concentrates also produce
effective hemostasis
Side Effects
• Infection:
As it is stored at room temperature, especially
for than 5 days

Suspect sepsis from platelet concentrates if fever within 6

hours of transfusion
Platelet refractoriness:
Suspected if poor increment in platelet count 60 minutes
after transfusion
Clinical causes:
Hypersplenism
Fever
Disseminated intravascular coagulation
Immunological causes:
Antibodies to platelet specific antigens.
Fresh Frozen Plasma
Types
FFP: When fluid position of centrifuge is frozen within 6 to 8 hours

FP24:
Plasma frozen 24 hours after phlebotomy

Manufacture
Obtained by separation of plasma from centrifuged whole blood
Plasma is frozen at –20 C within 6 and 8 hours of
collection (FFP) or

within 24 hours (FP24)

Each unit of FFP prepared from 1 unit of blood will

have 200 to 250 ml.
Shelf Life
1 year frozen and 24 hours thawed.
Contents
Factors IV, V, VII, VIII, IX
Especially rich in factors V and VIII (contains 1 IU/ml of each
factor)
Protein C, S and antithrombin III
Electrolytes, albumin, immunoglobulins and complement.
ASA Task Force Recommendations
Urgent reversal of warfarin therapy
In patients requiring heparin when antithrombin III concentrates are not
available.
Replacement of isolated factor deficiencies:
Used when the specific concentrates are unavailable
–– Factor II, V, VII, VIII, IX, X
–– Protein C and S
–– C1 esterase inhibitors
––Antithrombin III deficiency.

• Treatment of:
–– Disseminated Intravascular Coagulation (DIC)
–– Thrombotic Thrombocytopenic Purpura (TTP).

• Massive blood transfusion, if PT/APTT > 1.5 times

the control, i.e. > 17 seconds.
Dosage

10–15 ml/kg FFP to achieve minimum of 30%

coagulation factor concentration

5–8 ml/kg of FFP for warfarin therapy reversal

Frozen Plasma need not be of the same Rhtype
Side Effects
• Risk of transmission of hepatitis B and C, HIV
• Sensitization to foreign proteins may occur.
Contraindications
Not to be used
• For augmentation of plasma volume
• For augmenting albumin concentration
• Avoid administrating PRBCs and FFP to same patient as
it increases risk of infections
In such cases give whole blood if required.
 Cryoprecipitate
Manufacture
• Prepared as cold insoluble precipitate by thawing FFP at 4
C and removing supernatant

• 1 unit of cryoprecipitate will have volume of 10 and 20 ml

only.
Contents
• Principally factor VIII, XIII (80 IU of VIII and 40–60IU of
XIII)
• VWF 80 IU
• 100–250 mg of fibrinogen, fibronectin

Shelf Life
1 year frozen
Indications
Treatment of hemophilia A, has been replaced now by F VIII concentrates
Treatment of fibrinogen deficiency:
–Congenital deficiency
 Acquired deficiency:
-- DIC
-- Massive blood transfusion when fibrinogen levels < 80–100 mg/dl
-- Cryoprecipitate preferred to fibrinogen preparation due to high hepatitis rates

• von Willebrand disease

• Factor XIII replacement in:
–– Sepsis
–– Trauma
–– Burns

.
• Coagulum pyelotomy:
Coagulum formed by addition of thrombin and calcium
to cryoprecipitate
Used to trap calculi in renal pelvis to facilitate
pyelotomy removal
Dosage
1 dose or 10 U or 1 U/5 kgs increases fibrinogen by
50 mg/dl

ABO compatible units preferred but it is not very

important as concentration of antibodies in
cryoprecipitate is very low
Cryoprecipitate need not be group specific
• Should be administered through a filter as rapidly
as possible at at least 200 ml/hour
Infusion should be completed within 6 hours of
thawing.
 MASSIVE BLOOD TRANSFUSION

Replacement of 1 circulating blood volume (around 10–12

units of PRBCS) within 24 hrs
Loss of 50% of circulating blood volume within 3 hrs
Loss of 10% of circulating blood volume within 10 mins
Transfusion of 10 units of blood within 6 hrs
Transfusion of 4 units of blood within 1 hour with
continuing blood loss
Transfusion of 1 unit of blood within 5 minutes.
Method of Administration
Constant pressure infusion device
Do not prime the system with fluids containing Ca2+ like
Lactated Ringers

For faster rates of transfusion:

– Increase height of fluid above patient
– Manual compression of bag
– Using syringe and three way tap to aspirate and push
volume.
Warming of Stored Blood
Warming plates which have an upper (43 C) and lower
limits (33 C) is safest.
Transfusion goals
restore circulating blood volume
arrest bleeding
maintain Hb after minium acceptable level as per
cardiopulmonary reserve
HEMOSTATIC GOALS
Platelets >50000
fibrinogen >100
pt aptt <1.5 times the control
Complications
Coagulopathy
Occurs due to the following reasons:
Reduced synthesis and release of clotting factors (hepatic ischemia)
Dilution of endogenous clotting factors with colloids/RL
Thrombocytopenia and DIC
Chelation of calcium by citrate (least important)
Hypothermia.
Clotting factor deficiency occurs before thrombocytopenia
Concentration of II, V and VIII are reduced in stored blood
Transfusion guidelines:
–– If platelet count < 50000/μl, platelet transfusion
–– If INR > 1.5, transfuse FFP
–– If fibrinogen < 100 mg/dl, transfuse cryoprecipitate.
Citrate Toxicity
• Not caused by citrate ion per se, but because citrate
binds to Ca2+
• Each unit of blood contains 3 gms of citrate
Increased chances of citrate toxicity possible when:
–– Pediatric patients
–– Cardiac disease and low cardiac output states
–– Hypotension and hypovolemia
–– Hepatic disease
–– Liver transplantation
–– Hyperventilation
–– Alkalosis
–– Hypothermia
–– Hyperkalemia
Factors precipitating citrate toxicity:
–– Rate of blood transfusion more important than total
volume of blood transfused
Hypocalcemia occurs only when:

-- Rates of transfusion > 1 ml/kg/min

–– Rate of citrate metabolism reduces by 50% when body

temperature reduces from 37°C to 31 C.
Clinical features:
–– Reduced myocardial function
–– Hypotension, narrow pulse press, increased
diastolic pressure and CVP
–– Increased QTc, widened QRS and flattened
T-waves.
• Treatment:
–– 1 gm calcium gluconate (10%) given IV for every
5 units blood/FPP
–– 13.4% calcium chloride contains 0.192 mmol/ml
of Ca2+
–– 10% calcium gluconate contains only 0.22
mmol/ml of Ca2+
–– CaCl2 is not used much even though it contains
more Ca2+ as it very irritant to veins.
Hyperkalemia
Serum K+ is as high as 19–30 mEq/l in stored blood after
21 days
because RBCs exchange K+ ions to uptake H+ ions
generated by metabolism

Precipitating factors:
– Large amounts of blood must be given for hyper K+ to
occur
– Rate of blood infusion > 120 ml/min
– Premature infants are especially susceptible
• Transfuse only fresh (< 8 days old) plasma reduced or
washed PRBCs if rapid transfusion is required > 10–15
ml/kg/2 hours Hypokalemia occurs 24 hrs after
transfusion as the
transfused cells correct their electrolyte composition and
K+ enters cells.

Thus, metabolic acidosis and hyper K+ occur first

but net result is hypokalemia and alkalosis.
Hypernatremia
• Serum Na+ of whole blood and FFP > normal blood levels
due to sodium citrate

• Hypernatremia occurs when large volume of plasma is

given to patients with liver disease, cardiac and renal
disease

Na+ increases to 150–160 mm/l after 3 weeks of

storage of plasma.
Acid Base Abnormalities
• Causes of acidosis of bank blood:
– pH of storage media like CPDA is very low (5.5)
When blood is added, its pH reduces to 7.0

–– Accumulation of lactic acid and pyruvate by

RBC metabolism reduces pH further to 6.9 after
21 days storage

–– PCO2 increases to 150–220 mm Hg as the

plastic container does not provide air escape
mechanisms for CO2.
• On blood transfusion, the citrate present in stored blood
is metabolized in liver
This generates large amounts of bicarbonate which
neutralize metabolic acidosis initially

Thus, prophylactic sodium bicarbonate administration is not

recommended

Thus, initially, metabolic acidosis and hyperkalemia occur

while later alkalosis and hypokalemia occur.
Hypothermia
One unit of PRBCs transfused even at 40 C will reduce
core temperature of 70 kg patient by 0.25 C

• Blood warming device must be used for any

transfusion requiring > 2 U blood
• If < 30 􀂃C ventricular irritability and cardiac arrest
occurs
harmful effects of hypothermia:
– Shifts ODC curve to left
– Reduces metabolism of citrate
– Increased incidence of arrhythmias
– Impairs hemostasis
– Increases oxygen consumption
– Increased postoperative infection
– Shivering increases O2 consumption by 400%.
Tissue Oxygenation
• Depletion of 2, 3-DPG shifts ODC curve to left
tissue oxygen delivery is reduced
• Transfusion of 2,3-DPG depleted blood while
increasing Hb, results in less efficient oxygen
delivery
• After transfusion, 2,3-DPG returns to normal in 12–24
hrs.
Hyperbilirubinemia
paradoxical conjugated hyper bilirubinemia occurs
Increased load of conjugated bilirubin from destroyed
RBCs

conjugated hyperbilirubinemia
TRANSFUSION-RELATED
ACUTE LUNG INJURY
Non cardiogenic form of pulmonary edema occurring
after blood product administration

• New acute lung injury occurring within 6 hrs of a

completed transfusion with ratio of PaO2/FiO2<
300 mm Hg or O2 saturation as measured by pulse
oximetry of less than 90% when the patient is
breathing room air: NHBLI definition.
Incidence
1 : 5000 units transfused
Associated with transfusion of all products:
– Whole blood
– PRBCs
– FFP, platelets, cryoprecipitate
Pathogenesis
Antigranulocyte Antibody Theory
• Donor blood contains antibodies against recipient WBC
antigen
• Antigen-antibody binding occurs causing cellular
activation
• The activated neutrophils lodge in pulmonary
capillaries
• Reactive oxygen metabolites released which cause
pulmonary endothelial leakage.
Granulocyte Priming Theory
• Biologically active substances (such as lipids and
cytokines) are present within the transfusing blood

• Biological Response modifiers or BRM

• These can prune the activity of granulocytes in pulmonary
vasculature
causes increased vascular permeability
Two Event Hypothesis
TRALI occurs due to a combination of both theories
The first event is caused by the recipients underlying
clinical conditions like:
– Surgery
– Infection
– Inflammation.

This primes circulating neutrophils and sequesters

them in pulmonary circulation
The second event involves transfusion of
antileukocyteantibodies or BRMs in stored blood
component

These in turn activate the primed neutrophils

causing endothelial damage and capillary leak.
Other Possible Mechanisms
Direct injury to pulmonary endothelium

Immune complex formation with complement

Activation

BRM like ILs causing direct injury

Clinical Features
Acute onset dyspnea, severe hypoxemia
Fever, chills, rigors
Noncardiogenic pulmonary edema
Fluid in ET tube within 1–2 hrs after transfusion but
in full force within 6 hrs
If undiluted edema fluid obtained from ETT, edema
fluid protein: plasma protein ratio > 0.6 suggests
TRALI
Chest X-ray shows bilateral chest infiltrates
Risk Factors
• Multiparous donors:
– Percentage of antileukocyte antibodies after 1st
pregnancy is 9%
– Percentage of antileukocyte antibodies after 2nd
pregnancy is 18%
– Percentage of antileukocyte antibodies after 3rd
pregnancy is 23%.
• Underlying clinical conditions: Two hit hypothesis
–– Trauma
–– Surgery
– Sepsis
– Systemic Inflammatory Response Syndrome(SIRS)

• Massive transfusion: strong association between

exposure to multiple transfusions and development
of TRALI.
Differential Diagnosis
Transfusion associated circulatory overload(TACO):
– Raised JVP
– Increased systolic BP at the time dyspnea develops
– Widened pulmonary vascular pedicle on chest X-ray

Hemolytic transfusion reaction

Anaphylaxis
Diagnostic Criteria
AECC Conference Recommendations
No pre-existing acute lung injury before transfusion
Onset of lung dysfunction within 6 hrs of transfusion

Acute lung injury as evidenced by:

– Acute onset of signs and symptoms
– Hypoxemia:
- PaO2/FiO2< 300 or
- Room air SpO2< 90% or
– Bilateral infiltrates on chest X-ray without cardiomegaly
No clinical evidence of left atrial HTN
(Pulmonary Artery Occlusion Pressure (PAOP)
< 18 mm Hg)
Treatment
• Immediately stop blood transfusion
• Mainly supportive hemodynamic and ventilatory support

• Supplemental O2 if mild manifestations

• Mechanical ventilation with low tidal volume and plateau
pressures if moderate-severe manifestations

• Diuretics have no role in TRALI can be tried if TRALI

cannot be differentiated from TACO
• IV corticosteroids have been tried to reduce complement
mediated granulocyte activation
 JEHOVAH’S WITNESS
Christian movement with following beliefs:

Prohibits consumption of blood

Belief prevents them from accepting blood and its
components

Belief that blood which is removed from body is unclean

and should be disposed

Believe procedures with removal and storage of

their own blood is unacceptable.
Legal Issues
Consent
Procurement of informed consent before any medical intervention

Patient interviewed in the presence of independent witness while obtaining

consent.

Children
• Full and frank discussion between anesthetist,surgeon and parents
• Children under 16 yrs can give consent themselves

• If consent for transfusion is refused:

– An application is made to high court
– Application for specific issue order which allows transfusion without removing
parent authority.
In emergencies, blood should be given.
Emergencies
Perform blood transfusion if Jehovahs witness status
unknown

If relatives suggest patients may not accept blood

transfusion, documentation of same to be done

 If refusal of transfusion consent is retracted, make a

witnessed entry in patients notes.
Preoperative Preparation
• Optimize Hb%, treat anemia
• Optimize nutritional feeding
To increase RBC production: iron, folate, Vitamin
B12, Erythropoeitin
– To promote clotting: Vitamin K.

Prophylactic embolization:
– Pelvic tumors
– Vascular tumor like metastasis
– Aneurysmal bone cyst.
 Prescribe for cell salvage apparatus.
Recent advances:
– Intraoperative blood salvage
– Acute normovolemic hemodilution (ANH)
– Acute hypervolemic hemodilution (AHH)
– Use of blood substitutes

Drugs to enhance hemostasis:

– Factor VII a
–Tranexemic acid: 10 mg/kg IV up to 30 mg/kg/day
– Aprotinin
– Ethamsylate
– Desmopression.

• Adequate topical hemostatasis:

– Argon lazer beam cautery (diathermy)
– Spray coagulation
– Use of arterial tourniquet

– Hemostats:
-- Collagen and cellulose pads
-- Fibrin glue
PERIOPERATIVE BLOOD CONSERVATION
STRATEGY
Types
 Preoperative Autologous Blood Donation
 Intraoperative blood salvage
 Postoperative blood salvage
 Acute normovolemic hemodilution.
PREOPERATIVE AUTOLOGOUS DONATION1,2,3,14
Introduction
 Procedure in which patients own blood is collected,
through repeated phlebotomies over a span of 4–5 weeks
to be transfused during the surgery.

Patient Selection
AABS Recommendations
elective surgery can be scheduled several weeks in future
Surgical procedure for which blood is usually cross
matched
Hb > 11 g% or HCT > 33%
•May donate up to 10.5 ml/kg
no weight/age bar
No medical contraindication for donation of blood.

Advantages
 Low K+ compared to stored blood
 Relatively normal pH, normothermic
 Functionally superior cells
 High levels of 2,3-DPG.
INDICATIONS
• Major vascular surgery
• Liver transplantation
• Prostatectomy
• Major orthopedic surgeries: Spine, THR, TKR, etc.
Contraindications
 Active bacterial infection
 History of indwelling urinary catheter/device penetrating
skin
Cardiac disease:
– Significant AS
– Cyanotic heart disease
– Uncontrolled HTN
– Frequent unstable angina
– History of MI/CVA within 6 months of the planned
donation.
Crossover Usage
 If the amount of blood collected preoperatively exceeds the actual usage
subsequently, the remaining
blood may be used for homologous transfusion to other patients

 No longer permitted by AABB as autologous donors are not voluntary donors.

Techniques
• Optimal donating period begins 4-6 weeks before surgery in order to:
– Allow sufficient number of units to be collected
– Also to enable more complete RBC regeneration before surgery.

Blood donated at weekly intervals

depending on the physical status of the patient
 Upto a maximum of 4 units of blood can be collected or 10.5 ml/kg
Last blood donation not be collected later than 72 hrs before surgery to allow for
restoration of intravascular volume
• Patient receives supplemental iron 2 mg/kg/day ×
3 weeks in the form of:
–– Ferrous sulphate 325 mg PO TID
–– Ferrous gluconate 325 mg five times a day.

Erythropoietin given to anemic patients (HCF< 39%)

scheduled for noncardiac, nonvascular surgery can cause up
to 50% RBC volume expansion
• Collected blood has shelf life of 35–42 days
• Collected blood is stored till patients are discharged/till unit
become outdated.
PREOPERATIVE AUTOLOGOUS BLOOD
TRANSFUSION
 Patient Selection
AABS RECOMMENDATIONS
Patients in whom elective surgery can be scheduled
several weeks in future
Surgical procedure for which blood is usually cross
matched
Hb > 11 g% or HCT > 33%
May donate up to 10.5 ml/kg excluding samples for
testing
No weight/age bar
No medical contraindication for donation of blood.
ADVANTAGES
Low K+ compared to stored blood
Relatively normal pH, normothermic
Functionally superior cells
High levels of 2,3-DPG.
DISADVANTAGES
Expensive
Blood may have to be discarded if not transfused
Can administer wrong unit of blood to patients.
 PREOPERATIVE AUTOLOGOUS BLOOD
TRANSFUSION
INTRODUCTION
Procedure in which patients own blood is collected,
through repeated phlebotomies over a span of 4 5
weeks to be transfused during the surgery.
INDICATIONS
Cardiac surgery
Major vascular surgery
Liver transplantation
Prostatectomy
Major orthopedic surgeries: Spine, THR, TKR, etc
CONTRAINDICATIONS
Active bacterial infection
History of indwelling urinary catheter/device penetrating skin
Cardiac disease:
 Significant AS
 Cyanotic heart disease
 Uncontrolled HTN
 Frequent unstable angina
 Significant LMCA narrowing
 History of MI/CVA within 6 months of the planned donation.
Active seizure disorder
Hb < 11 gm%
Hemorrhagic shock.
COMPLICATIONS
Risk of contracting infection during phlebotomy
Vasovagal attack during blood donation
Human errors in transfusing blood like transfusing wrong
unit of blood
Iatrogenic anemia, MI/cerebral hypoxia.
TECHNIQUES
Blood is collected at the nearest blood collection facility
Optimal donating period begins 4-6 weeks before surgery in order to:
Allow sufficient number of units to be collected
Also to enable more complete RBC regeneration before surgery.
Blood donated at weekly intervals or once in 3 days depending on the physical
status of the patient
Upto a maximum of 4 units of blood can be collected or 10.5 ml/kg
Last blood donation not be collected later than 72 hrs before surgery to allow
for restoration of intravascular volume
Patient receives supplemental iron 2 mg/kg/day × 3 weeks in the form of:
Ferrous sulphate 325 mg PO TID
Ferrous gluconate 325 mg five times a day.
Iron supplementation increases RBC expansion from 14 to 19%
Blood drawn last is usually given first in PABD
Erythropoietin given to anemic patients (HCF < 39%) scheduled for noncardiac,
nonvascular surgery can cause up to 50% RBC volume expansion
Collected blood has shelf life of 35–42 days
Collected blood is stored till patients are discharged/ till unit become outdated.
INTRAOPERATIVE BLOOD SALVAGE
INTRODUCTION

Collection and reinfusion of blood lost during surgery.

INDICATIONS

Cardiac surgery, aortic reconstruction surgery

Orthopedic surgery:
 Spine instrumentation
 Joint arthroplasty.
Liver transplant
Splenectomy
Trauma patients
Ruptured ectopic pregnancy.
CONTRAINDICATIONS

 Sickle cell disease

 Contaminated surgical field with:
 Malignant cells: Risk of metastasis
 Bowel contents
 Amniotic fluid: Risk of amniotic fluid embolism
 Presence of pro-coagulant material like topical collagen in surgical
field.
CHARACTERISTICS OF SALVAGED BLOOD

Free Hb levels of 200–500 mg% is common

2,3-DPG levels are high
FDP and complement activation is present
Platelets and coagulation factors are deficient
Salvaged blood is more alkaline.
METHODS OF COLLECTION

Semicontinuous flow devices

Canister collection
Single use reservoir.
COMPLICATIONS

Hemolysis
Renal failure due to free Hb
Air embolism, amniotic fluid embolism
Reinfusion of debris from surgical field:
 Fat, air
 Platelets, lymphocytes, free Hb, RBC stroma
 Heparin, bacteria
 Debris like PMMA/bone cement.
Dilutional coagulopathy as all clotting factors and platelets are
removed by washing.
TECHNIQUE
Cell salvage device used to salvage blood from operative field
Recommended maximum vacuum setting is not more than 150 mmHg
Suction should be done from within the blood pool and not at the
blood-air interface.
Anticoagulate the salvaged blood
RBCs separated by centrifugation
They are washed with saline and filtered through 40 μm filters
Washed RBCs suspended in saline in aliquots of 125/225 cc with
hematocrit of 45–65
Blood can be stored:
 At room temperature for up to 4 hrs
 At 1–6 °C for 24 hrs provided storage at 1–6°C is begun within 4 hrs of ending
collection.
Storage at room temperature for recovered blood: 4 hrs
(washed/unwashed)
Storage at room temperature for ANH blood: 8 hrs.
POSTOPERATIVE BLOOD SALVAGE
INTRODUCTION
Postoperative recovery of defibrinogenated blood from mediastinal
chest tubes and wound drains after TKR or THR with immediate
reinfusion of unwashed blood.
INDICATIONS
Cardiac surgery:
 Reinfusion of blood from mediastinal tubes
 This may affect lab tests like creatinine kinase
 Increased CK may be present even though no preoperative MI has
occurred
 Blood collected from heart lung machine can be transfused back
after processing.
Orthopedic surgery: TKR/THR/spinal fusion instrumentation
Post-traumatic salvage:
 Following chest/abdominal trauma
 Blood from hemothorax/hemoperitoneum.
TECHNIQUE
Blood salvaged postoperatively is collected from
mediastinal/chest/joint drains and transfused back
without washing
Being defibrinogenated, it does not require
anticoagulation prior to transfusion
Up to 1400 ml of unprocessed blood can be reinfused as
it has high concentration of cytokines
If transfusion of blood has not begun within 6 hrs of
initiating collection, the blood must be discarded
Shelf life of 6 hrs.
COMPLICATIONS
Theoretical risk of reinfusion of:
 Free Hb, RBC stroma
 Marrow fat, tissue debris
 Toxic irritants/methacrylate debris
 FDPs and complement.
Risk of bacterial contamination if storage time > 6 hrs
Mild coagulopathy develops as:
 Platelets are deranged: Prolonged bleeding time
 No clotting factors are present: Prolonged PT, aPTT
Renal insufficiency if large amounts of free Hb present
Air embolism
Complement activation causing:
Noncardiogenic pulmonary edema
Upper airway edema.
ACUTE NORMOVOLEMIC
HEMODILUTION
INTRODUCTION
Entails withdrawal of patients blood early in the
intraoperative period with simultaneous administration
of crystalloid or colloids to maintain normovolemia
When replacement of ANH collected in part by synthetic
oxygen carriers, it is called Augmented Hemodilution
Blood is collected on the day of surgery rather than over
several weeks as in PABD
Also in PABD, no crystalloids are given to increase the
blood volume.
USEFULNESS
Reduces amount of allogenic blood transfusion to 1-2
units/patient
Provides fresh supply of coagulation factors and platelets
Improved tissue perfusion with hemodilution as blood
viscosity is reduced
Patients loses blood of low HCT intraoperatively
Withdrawn blood is reinfused at the end of surgery. Less
Hb is lost in blood
Blood component sequestration:
 Blood is collected intraoperatively
 It is subjected to various procedures like apheresis and
centrifugation
 Individual blood components are separated.
ACUTE HYPERVOLEMIC HEMODILUTION:
Involves rapid infusion of fluid to achieve hemodilution
without prior withdrawal of blood
Associated changes:
 Decrease in PCV and SVRI by around 30%
 Increase in CI and LVEDP
 Increase in PAP and PCWP which normalize on stoppage of surgery
 Slight increase in MAP and decrease in HR,
 Low chance of pulmonary edema.
PATIENT SELECTION CRITERIA
For surgeries where likelihood of transfusion exceeds
10%
Preoperative Hb level is atleast 12 g%
Absence of clinically significant coronary pulmonary,
renal/liver disease
Absence of severe HTN
Absence of infection and risk of bacteremia.
CONTRAINDICATIONS
ABSOLUTE
Severe anemia with HCT < 24%
Hemorrhagic shock
Myocardial pump failure
Hemostatic disorders
Limited ability to increase cardiac output like AS,nLV
dysfunction
Respiratory failure
End stage renal disease
Severe sepsis.
CONTRAINDICATIONS
RELATIVE
Less severe anemia
Severe respiratory distress
CCF/LV dysfunction
History of stroke
CAD/carotid artery disease
ESRD.
COMPENSATORY MECHANISMS IN ANH
Blood:
Reduced blood viscosity
Reduced RBC aggregation
Shift of ODC to right
Reduced oxygen carrying capacity (below 30%).

Oxygen utilization: Increased blood flow to tissues with

increased O2 extraction
COMPENSATORY MECHANISMS IN ANH
Cardiac:
Increased cardiac output
Coronary vasodilatation

Cerebral: Increased cerebral blood flow: hyperventilation avoided

GIT:
Increased HbF
Increased O2 extraction in liver
Centrilobular hepatic necrosis

Renal: Renal vasoconstriction causing decrease in fraction of CO

to kidneys
Pregnancy: ANH done with caution as reduction in material HCT
reduces placental perfusion.
TECHNIQUE
Informed consent
Timing: Prior to induction of anesthesia with
awake patient is better
Blood collection:
Site of collection:
Peripheral line not preferred as tube resistance and
sludging occurs
Arterial line not used as we cannot monitor IBP during
procedure
Central venous line is best and IJV/subclavian vein used.
 Calculation of volume to be collected:

Calculates estimated blood volume (EBV)

EBV = 70 ml/kg in females and 75 ml/kg in males
Baseline HCT noted
Target HCT:
7g/dl in healthy patients
10g if CVS/RS/CNS disease
Calculate average HCT = (Baseline HCT + Target HCT) / 2
Volume of blood collectable
= (Baseline HCT – Target HCT) / Average HCT × EBV
ANTICOAGULATION OF SPECIMEN:
CPD anticoagulant added to blood collection bag
This is then attached to a port in the IV line.
SAMPLE COLLECTION:
450 ml of blood is collected per bag
Collect whole blood and mix blood in bag with CPD
Bag is agitated using an agitator/by manually kneading the bag every minute.
ASANGUINOUS FLUID ADMINISTRATION:
3 ml crystalloid replaced for every 1 ml blood collected
1 ml colloid replaced for every 1 ml blood collected
Ensure that blood collection and fluid infusion do not mix if 3 port CV line is
used.
STORAGE:
Can be stored at room temperature for up to 8 hrs
After 6 hrs refrigerate at 0 􀂃C
Intermittent agitation done to ensure that sludging does not
occur.
REINFUSION OF WHOLE BLOOD:
Given according to surgical condition
Any remaining blood given in operating theater or refrigerated
Diuretic given if risk of hypervolemia
Last collected blood infused first as when whole blood is
collected with ANH, each subsequent unit becomes more dilute
MONITORING DURING ANH:
Heart rate, BP
Capnography
ECG
Pulse oximetry
If more advanced cases, with large volume of blood
sequestered:
CVP/PAP
Cardiac output
Transesophageal Echocardiography.
COMPLICATIONS
Iatrogenic anemia may not be safe
MI/cerebral hypoxia possible if severe hemodilution
Bleeding diathesis during surgery due to:
Dilutional thrombocytopenia
Hypofibrinogenemia as coagulation factors are being sequestered.
Volume overload.
Risk of anaphylaxis and HIV transmission present
Also topical use of fibrin sprays, bone wax/ surgical/platelet
gel.
THANKS