periop fluid therapy & blood

7/29/2019 Periop Fluid Therapy & Blood

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Perioperative fluid therapy

and

complications of blood

and blood byproducts

Amir B. Channa FFARCSKing Khalid Univ. Hosp.

Riyadh


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IV Fluid Therapy & Complication ofBlood Transfusion

Importance of Water

Major homeostatic mechanisms operating

through kidneys & lungs, manitain:Volume

Tonocity

Specific ionic composition &

H+ ion concentration


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Distribution of Water

Plasma 3L

Interstitial fluid11L

Intracellular fluid28L

66% ICF

33% ECF

Total body water

70 kg male TBW 42 L Channa AB


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Comparison of Whole Blood & Packed RedBlood cells

Value

Volume(mL)

Erythrocyte mass(mL)

Hematocrit(%)

Albumin (g)

Globulin (g)

Total protein (g)

Plasma sodium (mEq)

Plasma potassium (mEq)

Plasma acid (citric-lactic)

(mEq)

Donor/recipient ratio

Whole Blood

517

200

40

12.5

6.25

48.8

45

15

80

1 unit/patient

Packed RBCs

300

200

70

4

2

36

15

4

25

1 unit every 4-6 patients


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Questions

1. Physiological changes during surgery &

anaesthesia lead to shifts in fluid balance i.e..Stress response with secretion of epi or norepi,

cortisol, ADH

2. CNB spinal & epidural do chemical or

pharmacological sympathectomy which fluids will

you use, patients may be elderly and on DIG,

Diuretics, or anti-hypertensive

3. Volatile agents BLUNT the normal physiological

response to hypovolemia & stress in addition to it

they affect myocardium, venous return blood

pressure & release of ADH


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Questions

4. You may have to use vasopressors viz ephidrine,

phenylephrine or other inotropic agents. How will

you titrate IV fluids & vasopressors

5. Mechanical ventilators affects preload decreases

ANH & increase ADH therefore increase water &

salt and if blood loss then what?

6. PCO2 & its vasopressor response

7. PEEP, CPAP & CVP interactions


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Clinical scenarios

Periop. fluid balance

Bowel resection

Liver failure

Heart failure

Cerebral edema Cerebral edema + hypernatremia

ARF

ARDS

Acutely burned patient Pregnant patient with pre-eclampsia


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Goals of Intraop. fluid Administration Maintain good tissue perfusion &

Adequate oxygen delivery

Normal electrolyte concentration

Normoglycemia & pH


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Total fluid requirement address the

following issues Deficit replacement

Compensatory intra-vascular vol.

Expansion

Maintenance fluids

Restoration of losses

Substitution for fluid redistribution (third

space fluids)


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Overview

Clear understanding of water & electrolytephysiology

Major disturbance of fluid & electrolytebalance that may alter

CVS Neurologic &

Neuromuscular

Sick alv. cap. membrane

Cell membrane & Intracellular functions

Volume & composition, H2O, ionic pumps, enzymatic &messenger signalling functions

Drug dynamics & kinetics


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Distribution

Extra cellular fluid (int. + IV) Interstitial fluid

Very little in the form of free fluid

Associated with proteoglycan forming gel

-ve pressure (-5 mmHg) If interstitial fluid volume increases +ve pressure

rises

Free fluid in gel increases

EdemaVery little plasma proteins cross capillary clefts

(protein=2gm/dl)

Returned to vascular compartment as lymph


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Distribution

Intravascular fluid

Plasma

Small electrolyte cross freely to form interstitialcompartments

Identical electrolyte composition

Tight intracellular junctions do not allow albumin

to go to interstitial comp.


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Definitions

Colloids Substances unable to pass through

semi permeable membrane

It is a suspension of particle rather than a solution Remains confined to intra-vascular compartment

(at least initially)

Do not correct water and electrolyte deficiencies

Imbibe (suck) fluid from int. comp. Plasma volume expansion

Haemodilution

Lower hematocrit


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Definitions

Colloids(cont) Increase flow in the microcirculation &

Prevent DVT

O2 delivery / unit time

E.g. albumin, PPF, hetastarch, dextran, gelfusine,haemacel, hypotonic saline, perfluoro carbons,

flusol DA


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Definitions

Crystalloids

True solution

No particulate matterAccelerate coagulation

DVT (4 X the fluid restricted group - Janvarin)


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Colloid/Crystalloid Controversy(in shock & hemorrhage)

Arguments in favor ofCOLLOID

Most logical choice for intravascular expansion Since greater portion remains in IVC & for longer time

( t/2 3-6 hours)

Less volume required to restore

Colloids enter int. space & increase int. osmotic pressureexacerbating edema

Thus initial resuscitation is rapid Less peripheral/pul. edema if used within minutes

Costly

Risk of anaphylaxis

Coagulopathy

Poor clot quality

BP

CVPPA WP


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Colloid/Crystalloid Controversy

(in shock & hemorrhage)

Arguments in favor ofCRYSTALLOID Expands IVC adequately but 2-4 times of colloid

Replaces the extravascular losses

It leaves IVC faster ( t/2 20-30 minutes)

Replenishes interstitial compartment Thus small increase in plasma volume

They do not produce interstitial compartment edema

Cheap

Increase GFR Increases coagulation

Periphral edema is not problem

No risk of allergic reaction


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Dynamics of IV Fluids

Water solution Intracellularly

All hypotonic solns e.g. 5% dextrose called as

maintenance type of fluids

Electrolyte solution

Interstitial compartment

Isotonic

Called replacement of fluids


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Dynamics of IV Fluids

Colloids

IV compartment

For losses of palsma blood etc.

Since most of intraop. Losses

Isotonic therefore replacement type of fluids RL

solution (hartmanns soln)

Normal (or abnormal) saline

Dilutional hyperchloremic acidosis


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Difficulties in assessing fluidresuscitation

Infusion of Colloid/Crystalloid is guided by: CVS end points viz BP, CVP, which have

No relation with interstitial fluid or ECF etc.

Lung water increase markedly before gas

exchange is impaired

Certain clinical conditions e.g sepsis, CHF, ARDS,contused lung have different

Pathophysiology

Dynamics of crystalloid & colloid e.g.-CV disease

-impaired gas exchange

-increased vascular permeability

-edema interfering with oxygenation and healing andreturn of blood functions

USA- prefer crystalloids

UK- prefer colloids


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Signs of fluid loss (hypovolemia)

SignMucous membrane

Sensorium

Orthostatic changes

in heart rate

in blood pressure

Urinary flow rate

Pulse rate

Blood pressure

5%Dry

Normal

None

Mildly decreased

Normal or increased

Normal

10%Very dry

Lethargic

Present

Decreased

Increased >100bpm

Mildly increased with

respiratory variation

15%Parched

Obtunded

Marked

>15mmHg increase

>10mmHg decreased

Markedly decreased

Markedly Increased>120bpm

Decreased

Fluid loss (Expressed as Percentage of Body Weight)

Mentation, capillary refill time > 5sec


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Physical examination

Laboratory evaluation

as surrogate of IV volume &

adequacy of tissue perfusion

Hemodynamic measurements

CVP

PAP

PAWP etc


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Albumin

Single polypeptide 585 amino acids

Synthesized in endoplasmic reticulum ofhepatocytes

9-12 gm/day Can increase 2-3 times if needed or stimulated

COP

ECF pressure in liver

Insulin Thyroxine &

Cortisol

5% removed / hour


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Albumin

Clinical properties

Binding & transport

Strongve charge binds

Ca++ 40 % Ca

Thyroxin

Bilirubin

Amino acids

Warfarin

NSAIDs

Digoxin

Maintains COP 80%


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Albumin

Clinical properties

Free radical scavenging Platelet inhibition &

Anti thrombotic effects

Affects vascular permeability by binding-

subendothellium of capillary


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Serum Albumin Decreases

Dilutional effect crystalloid or colloid

Redistribution due to altered capillarypermeability e.g. sepsis (5X increase)

Decreased synthesis (sepsis) Increased loss from kidneys &

IL-6 mediated inhibiton- in SIRs, sepsis

Correlation between albumin & COP POOR Therefore edemaassociated with hypo

albuminemia may be due to lymphaticobstruction


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? Should Albumin be used inCritical Patients

60% albumin leaves IVC in 4 hours

Potentially worsening Edema

Hypoalbuminemia not indication for

albnumin therapy

Stokwell

GreenhalghCocharne study


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Expansion of IV Compartment

1000ml of5% dextroseexpands plasma by

1000 x 4/6 = 67ml

1000 ml ofcrystalloidexpands plasma by

1000 x 4/20 = 167 200 ml

1000 ml ofcolloidsexpands plasma by

1000 x 4/4 = 1000ml


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Periop. Fluid Therapy

Pre-existing deficits

Normal maintenance requirements

Abnormal losses

Pre-existing losses

Fasting (100-110 ml x no. of HR)

Perop. Bleeding, fistulae

Vomitting Diarrhea

Diuresis ketosis

Occult losses -


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Pre-existing losses

Fasting (100-110 ml x no. of HR) Perop. Bleeding, fistulae

Vomitting

Diarrhea Diuresis ketosis

Occult losses inflammatory traumatic edema

Sequestration in third comp. Increased insensible losses (0.5 ml/kg/hr)

Fever (add 12% for 1oC)

Hypoventilation

Sweating


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Redistribution of Evaporative Losses

Degree of TissueTrauma

Minimal (e.g. hemiorraphy)

Moderate (e.g. cholecystectomy)

Severe (e.g. bowel resection)

Additional FluidRequirement

0-2 mL/kg/hr

2-4 mL/kg/hr

4-8 mL/kg/hr


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Surgical Losses

BloodAlways underestimated by surgeon

Occult losses: occult bleeding into wound

Under surgical drapes

Swabs: 4x4 = 10ml

Laps: = 100-150ml Obligatory losses of fluids

Evaporation

Redistribution third space


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Surgical Losses

Traumatized Inflammed

Infected tissues

Burns Extensive injuries

Peritonitis

Surgical dissections

Serosal surfacesAscites

Pleural effusions

Pericardial effusion etc

Bowel lumen


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Replacing Blood Losses

Crystalloid

orColloid

Maintain normovolemia till the

danger of anemia out weighs

the risk of transfusionie. 7-8 Gm/dl

(or HCTof 21-24%)

Colloid the ratio of 1:1

Crystalloid the ratio of 2:4

Or mixture if both


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Average Blood Volumes

Age

Neonates

Premature

Full term

Infants

Adults

Men

Women

Blood volume

95mL/kg

85mL/kg

80mL/kg

75mL/kg

65mL/kg


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Average Blood Volumes

Patients with normal HCT should only betransfused after 10-20% loss of blood volume

One unit of blood pack cells Increases Hb by 1Gm/dl

Or HCT by 2-3%

10 ml pack cells/kg

Increases Hb by 3gm/dl

Or HCT by 10%


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Changes in Blood During Storage

RBC become Spherical

Cell wall thickened

Easy rupture Hemolysis

0.5-1%/day

10-20% may be destroyed with in 24 hrs

WBC become Looses their phagocytic & bactericidal properties

with in 4-6 hrs

But maintain antigenic properties


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Changes in Blood During Storage

Plateletes Non functional with in 48 hours at 4oC

Otherwise 5-7 days

Factors V & VII V decreased 50% by 21 days

VII decreased 75% in 24 days

ATP & 2,3 DPG

K

Ca++

NH3 O2 O2 dissociation curve shifted to left

Lactic/Pyruvic acids


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Blood & Blood By products

Whole blood Packed red blood cells (PCV)

Leuko depleted blood

Fresh frozen plasma Platelets

Factors

Freeze dried factor VII can transmitinfection

Cryoprecipitate (VIII) antihemophilic

Christmas (IX) concentrate


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Blood & Blood By products

Granulocyte transfusions

Frozen RBC

Albumin

5%

20%

25%

Plasma protein fraction

Immunoglobulins


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Blood Components

Component

Whole blood

Concentrated red cells

Red cells with additive(SAGM)

FFP(random donor)

Cryoprecipitate

Platelets(adult theraputic dose)

Volume

450+45ml

280+60ml

350+70ml

150-300ml

15-25ml

200-300ml

Comments

HCT 0.35-0.45

HCT 0.55-0.75

HCT 0.50-0.70

>140 mg fibrinogen/unit

>240x109 platelets


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Blood Preservative (Additives)

Heparin medium 24-48 hrs

EDTA medium

ACD medium 3 weeks

CPD medium 4 weeks

CPDA medium 5-6 weeks

SAGM (UK) 4 weeks

At 4oC (6

o)


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Products

Whole blood

500 ml per bag with a HCT of 0.40

No functioning platelets after 2-3 days:2,3DPG by 2 weeks

Normal concentrations of albumin & clottingfactors, except factors V & VIII, which are

reduced to 10-20% of normal

Not sterilized, so there is a risk oftransmitted pathogens


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Products

Red cell concentrate (packed cells)

250 ml per bag with HCT of 0.60 No functioning platelets; 2,3-DPG levels

maintained for 14 days

Storage is 35 days with SAGM; 42 days with

A-CPD


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Products

Platelet concentrates Single donor

Usually as a pool of 5-6 single unit

donations; 4 units of platelets contain 1 unitFFP

Small numbers of red cells & leukocytes

Infection risk as for whole blood, but

increased by multiple donors Use ABO-compatible platelets. Maximum

storage is 5 days at 4oC

1 unit will increase 10x109/l/m2 BSA


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Products

Fresh frozen plasma (FFP) Prepared from plasma from single

donation;150ml per bag at 3oC

Shelf life 1 year Contains all clotting factors, albumin &

gammaglobulin

Use immediately after thawing. Usually give

at least 4 units Must be ABO-compatible & Rh(D)-negative if

recipient is a Rh(D) fertile female

Risk of anaphylactic reactions


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Products

Cryoprecipitate Prepared from freshly prepared plasma

frozenat70oC

Precipitates from FFP when slowly thawed;supplied as 6-8 units

High in factor VIII, fibrinogen, vonWillerband factor & fibrinonectin

Indicated for DIC and von Willerbandsdisease

Shelf life 1 year


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Products

Human albumin solution

Prepared by fractioning of multiple units of

plasma giving 96% albumin & 4% globulin.Available as 4.5 or 20% (hypotonic)

solution. Each 20g of albumin requires

20000 blood donations. Pasteurized at 60%for 10 h to kill all microorganisms including

viruses


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Products

Plasma protein factor (PPF) Prepared in a similar manner to albumin but

contains more globulin (83% albumin, 17%globulin)

Factor VIII concentrate Freeze-dried protein as 250 units Sterilized to inactivate viruses

Factor IX concentrate Freeze-dried protein as 250 units Sterilized to inactivate viruses

Also contains factors II & X


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Products

Immunoglobulin products

Fractionation of plasma to produce pool

with >90% IgG No risk of viral transmission

Used for immune thrombocytopenia andimmunodeficiency states


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Transfusion Reactions

Acute Heamolysis due to antibodies directed

against red cells

Fever donor leukocytes attack host redcells

Anaphylaxis due to antibodies directedagainst recipient IgA

Transfusion-related acute lung injurydue to donor antibodies directed againstleukocytes. Clinically identical to ARDSresolves in 48 hrs


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Acute

Hyperkalemia5-10 mmol K+ in a unit ofblood stored for 4-5 weeks. Effects ofadditional K+ are exacerbated by acidosisand hypothermia. Hyperkalemia is usuallytransient

Citrate toxicity citrate is added as apreservative to bind excess calcium andprevent clotting. Metabolized to bicarbonate.Excess causes metabolic alkalosis


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Acute

Acid-base disturbance citrate frompreservative and lactate from red cells

Hypocalcemia citrate anticoagulant bindsionized calcium; BP, pulse pressure. GiveCaCl2 only if there are symptoms / signs (not

Ca2+

gluconate, which must be metabolizedto release free Ca2+)


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Acute Febrile reaction due to bacterial

contamination

Microemboli aggregates of all cellularcomponents, increase with age of blood.Cause complement activation, hemolysis andthrombocytopenia. Removed by 170umfilter; +/- 40um screen and depth filters

Hypothermia left shift of dissociationcurve, platelet & clotting dysfunction

Air embolus

Fluid overload


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Delayed Hemolytic transfusion reactionfrom

red cell antibodies

Graft-versus-host diseaseAlloimmunization(reaction to minor

foreign antigens) 10% of all transfusionreactions:

Red cell antibodies including anti-Rh(D)

Leukocyte antibodies

Platelet antibodies


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Delayed Viral infection

hepatitis B(1:20000 units)

hepatitisC(1:1000 units)

HIV (1:400000 units)

cytomegalovirus

parovirus (causes aplastic anemia in sicklecell patients)

Other infections Syphillus

Malaria

trypanosomiasis


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Delayed

Tumor recurrenceincreased risk

Sensitization resulting in antibodyformation and subsequent difficulties withcross-matching

Iron overload occurs with repeated

transfusions - haemochromatosis


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Massive Blood Transfusion

Defined as the acute administration of morethan 1.5 times the patients blood volume, or

replacement of the patients total blood volumewithin 24h

Transfusion of 10 units of blood within 6 hrs

Transfusion of 5 units of blood within 1 hrs


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Blood groups for urgent transfusion are: O Rh(D) negitive if patient not cross matched

Uncross-matched blood (type-specific) if patientsblood group is known

Blood transfusion may be avoided by: Reducing blood loss hypotensive anesthesia,

antifibrinolytic agents

Tolerating a lower HCT

Transfusing autologus blood prior donation, use ofcell saver

Artificaial blood

erythropoietin


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Cell saver

Returned blood is warm, with normal levels of 2,3-DPG: contraindicated with sepsis, contamination

with intestinal contents or tumor cells Artificial blood

Perfluorocarbons oxygen sol. 20 x plasma

Recombinant Hb (rHb1.1)

Purified Hb


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Complications:

Impaired O2 delivery to tissues

Impaired coagulation (FFP+platelets only if lab

suggests) Hypothermia

Hypocalcemia (if rapid transfusion)

Hyperkalemia

Metabolic acidosis followed by alkalosis

Fluid over load

TRALI


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Filters

Particularly due to micro emboli

Post transfusion pul. insufficiency Ordinary blood set filters 200m

Paul 70m

Utlipore 40m

Bently 70-80m

O di i ti f O i


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O2dissociation curve for O2carryingmolecules

O2 content

(ml/dl)

10 20 30 40 50 60

PO2

(kPA)

Perflurocarbons

Hb solution

Blood

5

10

15

20

Mechanism of T ansf sion ind ced


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Mechanism of Transfusion-inducedImmunomodulation

Overload of reticuloendothelial system with iron

salts causing most of the changes

Prostaglandin E2 production by monocytes is

increased, which down regulates macrophages

calls II antigen expression, inhibits interleukin-2

production

Inhibition of interleukin-2 by TH lymphocytes willdecrease B-cell stimulation and antibody

production

Mechanism of Transfusion induced


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Mechanism of Transfusion-inducedImmunomodulation

Clonal depletion theory remove or

incapacitiate cells that would reject graft

Decrease suppressor T-lymphocyte production Anti-idiotypic productionT-cell receptors or

antibodies generated against blood transfusion

form new antigens that compete for bindinglocations on initial antibodies

D l t d I F ti


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Down regulated Immune FunctionsFollowing Allogenic Blood Transfusions

Reduced response in mixed lymphocyte culture

Decreased cytokine production

Decreased response to mitogens (substance thatstimulates mitosis and lymphocyte

transformation) or soluble antigens in vivoor in

vitro Increased suppresser-cell number or function

Decreased natural killer-cell activity

D l t d I F ti


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Down regulated Immune FunctionsFollowing Allogenic Blood Transfusions

Decreased monocyte function

Decreased cell-mediated cytotoxicity against

certain target cells Enhanced production of soluble mediators and

anti-idiotypic antibodies suppressive or mixed

lymphocyte response

periop fluid therapy & blood

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