Periop Fluid Therapy & Blood
Transcript of 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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Transfusion Reactions
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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Transfusion Reactions
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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Transfusion Reactions
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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Transfusion Reactions
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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Transfusion Reactions
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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Transfusion Reactions
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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Massive Blood Transfusion
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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Massive Blood Transfusion
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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Massive Blood Transfusion
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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Massive Blood Transfusion
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