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    1

    Intraoperative Use of Crystalloids

    M. Verhaegen

    Anesthesiology

    UZ KU Leuven

    Intraoperative IV Fluid Therapy:Historical Perspective (1)

    Fluid restriction

    Postoperative Salt Intolerance(Coller et al, Ann Surg 1944, 119: 533-541)

    No isotonic saline solution or Ringerssolution should be given during the day ofoperation and during the subsequent firsttwo postoperative days

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    2

    Intraoperative IV Fluid Therapy:Historical Perspective (2)

    Fluid restriction

    Trauma/surgery: large fluid deficits Acute Changes in Extracellular Fluid Associated

    with Major Surgical Procedures(Shires et al., Ann Surg 1961, 154: 803-810)

    Major surgery is associated with significant

    functional extracellular fluid volume deficits Replace with large volumes of balanced

    electrolyte solutions

    Intraoperative IV Fluid Therapy:Historical Perspective (3)

    Fluid restriction

    Trauma/surgery: large fluid deficits

    Crystalloid / colloid controversy More recent concepts of intraoperative

    crystalloid administration

    Problems associated with specificcomponents and/or their concentration

    Sodium, chloride, lactate

    Kinetic principles of fluid therapy

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    Body fluids: VolumeCompositionConcentration

    Microcirculatory organ perfusion

    O2-delivery

    Cellular function

    Organ function

    Body Fluid Compartments

    Total body water = 60 % of body weight (BW)

    2/3

    Intracellular water= 40 % of BW

    1/3

    Extracellularwater

    = 20 % of BW

    Plasma (4 % of BW)

    Extracellularwater

    = 20 % of BW

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    Body Fluid Compartments: Composition

    2716Protein (g/dl)

    2275Phosphorus (mEq/l)

    282410Bicarbonate (mEq/l)

    1101054Chloride (mEq/l)

    2250Magnesium (mEq/l)

    33

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    Starlings Equation

    Q = kA [ ( Pc - Pi ) + ( i - c ) ] (mEq / L)Q = fluid filtrationk = capillary filtration coefficient

    A = area of the capillary membranePc = capillary hydrostatic pressure

    Pi = interstitial hydrostatic pressure = reflection coefficient for albumini = interstitial colloid osmotic pressurec = capillary colloid osmotic pressure

    Osmolality (mOsm/kg)

    281.3282.6Total

    0.21.2Protein

    281.1281.4[Na+] (non-protein)

    ISFPlasma

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    5429.15454.2Total

    3.923.2Protein

    5425.25431.0[Na+] (non-protein)

    ISFPlasma

    25.1 mmHg

    Osmotic pressure (mmHg)

    Capillary

    Ar ter ial Veno us

    Interstitium

    Lymphatic

    drainage

    Pc =

    40 mmHgPc =

    10 mmHg

    c = 23 mmHg

    Pi = 2 mmHgi = 4 mmHgFiltration Absorption

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    Intraoperative Fluid Therapy

    Basal fluid requirements

    Correction of preoperative fluid deficits

    Fasting

    Disease-related fluid losses

    Intraoperative fluid losses

    Blood loss Redistribution: Third space fluid loss

    Other fluid losses

    Basal water losses parallel energy expendituresMaintenance fluids (hospitalized pts): 100 ml/100 kcal/d

    From Holliday MA and Segar WE, Pediatrics (1957), 19

    1000

    1500

    1700

    1900

    2100 2300

    2500

    Computed need foraverage hospital patients

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    501 ml/kg/h> 20

    202 ml/kg/h11 - 20

    404 ml/kg/h0 10

    70 kgVolumeWeight (kg)

    Total 110 ml/h

    4-2-1 rule

    IntraoperativeBasal Fluid Requirements

    Volume 4-2-1 rule

    Increased

    Composition Electrolytes

    Sodium: 1 mEq/kg/d

    Potassium: 0.7 mEq/kg/d

    Glucose?

    Replacement fluid D5W (+ electrolytes)

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    Intraoperative Glucose

    Indicated in type I diabetes mellitus

    2-3 g/kg/d

    Indicated if risk of hypoglycemia

    TPN

    Insulinoma

    Prolonged (> 24 h) fasting Avoid if risk of cerebral ischemia

    Hyperglycemia-induced cerebral acidosis

    Correction ofPreoperative Fluid Deficit

    Preoperative fasting fluid deficit

    Basal maint. fluids/h x npo period (h)

    1st

    hour: 50 % of deficit 2nd hour: 25 % of deficit

    3rd hour: 25 % of deficit

    Additional fluid deficits

    Disease-related fluid losses

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    10

    Elhakim et al., Acta Anaesth Scand (1998), 42

    Time

    VASfor nausea

    (mm)

    1 h 2 h 4 h 6 h 24 h 48 h 72 h0

    5

    10

    15

    20

    25

    30

    Crystalloid

    No crystalloid

    **

    *

    **

    * P>0.05

    Elhakim et al., Acta Anaesth Scand (1998), 42* P>0.05

    No crystalloidCrystalloid

    1048 - 72 h

    3024 - 48 h

    806 - 24 h

    004 - 6 h

    102 - 4 h

    220 - 2 h

    806 h 3 d

    34Day unit (6 h)

    Vomiting (n)

    *

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    Surgical Fluid Losses (1)

    Blood loss

    Redistribution and subsequent loss ofextracellular and intracellular fluid

    Replacement with crystalloids

    Volume crystalloid:blood

    3:1 to 5:1 (even 7:1) Composition

    NaCl 0.9 %

    Balanced electrolyte solution

    Cervera et al., Am J Surg (1975), 129

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    Surgical Fluid Losses (2)

    Redistribution: Third space fluid loss

    Sequestered extracellular fluid

    Volume related to surgical trauma Minor: 2 - 4 ml/kg/h

    Intermediate: 4 - 8 ml/kg/h

    Major: 8 - 15 ml/kg/h

    Replacement fluid NaCl 0.9 %

    Balanced electrolyte solution

    Roberts et al., Ann Surg (1985), 202

    187 113253 50Duration (min)

    10.6 1.912.3 7.0ECV postop (l)

    12.5 2.412.5 2.3ECV preop (l)

    530 921660 96Fluid (ml)

    D5WLactated Ringers

    * P

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    Intraoperative Crystalloid Therapy:Lack of Good Target Points (1)

    Cardiovascular parameters

    ECG

    Blood pressure

    Central venous pressure

    Pulmonary artery catheter

    Transesophageal echocardiography

    Perfusion directed therapy

    Fluid overload

    Intraoperative Crystalloid Therapy:Lack of Good Target Points (2)

    Cardiovascular parameters

    Perfusion directed therapy

    Global Lactate

    Regional: Gastrointestinal Gastrointestinal Pco2 tonometry

    Organ specific Kidney: urine output

    Fluid overload

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    Intraoperative Crystalloid Therapy:Lack of Good Target Points (3)

    Fluid overload

    Intraoperative absorption of irrigating fluidsduring endoscopic surgery

    Transurethral resection of the prostate

    Hysteroscopic surgery

    Absorption can be accurately monitored

    Fatal postoperative pulmonary edema inhealthy (?) persons

    Arieff, Chest 1999; 115 (5)

    Fatal Postoperative Pulmonary Edema:Pathogenesis and Literature Review(Arieff: Chest 1999, 115: 1371-1377)

    Fatal postoperative pulmonary edema

    13 patients (incidence of 0.02 %) 10 generally healthy

    3 serious associated medical conditions

    Age 38 21 y

    Within 3 postoperative days Range: 3 to 66 h, mean SD: 27 20 h

    No predictive variables

    No predictive warning signs Cardiorespiratory arrest first clinical sign in 8 pts

    Fluid overload as single cause Mean net fluid retention of 7.0 4.5 l first 27 h postop

    (24 % increase of total body water)

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    Intraoperative Crystalloid Therapy:Problems

    Serum osmolality

    Effects on brain water and ICP

    Hyperchloremic metabolic acidosis

    Lactate

    Adverse pharmacologic effects?

    Acute Effects of Changing Osmotic Pressurein the Cerebral Capillaries

    18654545640282.6292.6[Na+] 5 mEq/l

    2302301.2Protein

    4604602.4Protein x 2

    054545454282.6282.6[Na+],protein,

    non-protein

    (Pl.-IF)IFPlasmaIFPlasmaOsmoles

    Osm.Press.

    Osmot. pressure(mmHg)

    Osmolality(mOsm/kg)

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    I.V. Fluids: Osmolality

    308308Normal saline

    254273Lact. Ringers

    Osmolality

    (mOsm/kg)

    Osmolarity

    (mOsm/L)

    Williams et al., Anesth Analg 88 (1999)

    -0.04#

    0.04#

    7.38

    7.43

    7.38

    7.44

    7.42

    7.41

    Whole blood pH

    NS

    LR

    1 2*

    -1 2*

    141 2

    140 2

    141 2

    139 2

    140 2

    140 1

    Serum [Na+] (mEq/l)

    NS

    LR

    0 4*

    -4 3*

    290 5

    287 4

    289 5

    285 5

    288 5

    288 4

    Serum osmolal. (mOsm/kg)

    NS

    LR

    T2-T1T3T2T1

    * P

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    The Effect of the Reduction of Colloid Oncotic Pressure,

    with and without Reduction of Osmolality, on Post-Traumatic Cerebral Edema.(Drummond et al.: Anesthesiology 1998, 88)

    Blood Hetastarch Saline Half saline

    Percussed hemisphere

    Contralateral hemisphere81

    80

    79

    78Percentw

    aterbyweight

    *

    *

    *

    *

    * P < 0.05 vs corresponding hemisphere in blood and hetastarch group

    Drummond et al., Anesthesiology 88 (1998)

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    Hyperchloremic Metabolic Acidosis

    Dilutional acidosis

    Metabolic acidosis resulting from rapidadministration of fluids that contain near-physiologic concentrations of sodiumaccompanied by anions (usually chloride)other than bicarbonate or bicarbonate

    precursors, such as lactate.(D.S. Prough, Anesthesiology 2000)

    Dose-dependent

    Acidosis Associated with Perioperative Saline Administration.Dilution or Delusion?

    (Prough: Anesthesiology 2000, 93, editorial)

    20.422.925.2Liskaser

    18.418.623.5Scheingraber

    21.020.425.0McFarlane

    21.621.023.6Rehm

    25.025.127Waters

    ActualPredictedFirst author

    After infusionBeforeinfusion

    [HCO3-] (mEq/l)

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    Rapid Saline Infusion Produces Hyperchloremic Acidosis inPatients Undergoing Gynecological Surgery.(Scheingraber et al.: Anesthesiology 1999, 90)

    1 075 799717 459Urine output (ml)

    704 447962 332Estimated blood loss(ml)

    67 1871 14Volume after 120 min

    (ml/kg)

    138 20135 23Time of infusion (min)

    Lact. Ringers(n = 12)

    Saline

    (n = 12)

    Scheingraber et al., Anesthesiology 90 (1999)

    106104115104Chloride(mM)

    12.5 1.815.8 1.411.8 1.416.2 1.2Anion gap(mM)

    23.0 1.123.3 2.018.4 2.023.5 2.2Bicarbonate(mM)

    120 min0 min120 min0 min

    Lactated Ringer sSaline

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    Scheingraber et al., Anesthesiology 90 (1999)

    Lactated RingersNormal saline

    7.50

    7.45

    7.40

    7.35

    7.30

    7.25

    7.20

    0 30 60 90 120 min 0 30 60 90 120 min

    0 30 60 90 120 min0 30 60 90 120 min

    50

    46

    42

    38

    34

    30

    26

    4

    0

    -4

    -8

    -12

    3.0

    2.5

    2.0

    1.5

    1.0

    0.5

    0.0

    mmHg

    mmol/l

    mmol/l

    pH Carbon dioxide

    Base excess Lactate

    # # #

    ####*

    #*

    #* #*

    *

    *

    ** *

    ** *

    * P

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    Scheingraber et al., Anesthesiology 90 (1999)

    Change(mmol/l)from0

    tominute120

    Saline group Ringer group

    0

    -5

    -10

    BicHH

    BicHH

    SID

    SID

    Prot-Prot-

    BicS

    BicS

    0

    -5

    -10

    Bicarbonate calculationBicHH = Henderson-Hasselbach equationBicS = Stewart formula

    Stewarts Modelof Acid-Base balance

    Independent variables affecting [H+]

    pCO2

    Total concentration of weak acids Strong ion difference (SID)

    = [strong cations] [strong anions] Strong electrolytes dissociate completely

    when in water

    = [Na+] + [K+]+ [Mg2+]+[Ca2+] [Cl-] [XA]

    SID decrease = acidosis

    SID increase = alkalosis

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    Liskaser et al.: Role of Pump Prime in the Etiology andPathogenesis of Cardiopulmonary Bypass-AssociatedAcidosis (Anesthesiology 2000; 93) (1)

    CPB pump prime fluids

    Group I (n=11): 500 ml Haemaccel1000 ml Ringers Injection

    Group II (n=10): 1500 ml Plasmalyte 148

    Blood sampling

    t1 = immediately before CBP

    t2 = 2 min after CBP at full flows

    t3 = end of the case

    Liskaser et al., Anesthesiology 93 (2000)

    230Gluconate

    270Acetate

    3.00Mg2+

    06.8Ca2+

    54.4K+

    98151Cl-

    140146Na+

    Group II

    Plasmalyte 148(mEq/l)

    Group I

    Ringers Injection

    Haemaccel (mEq/l)

    Strong ion

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    Liskaser et al., Anesthesiology 93 (2000)

    8.208.70

    7.4015.00

    11.409.80

    III

    Anion gap(mEq/l)

    -0.65

    2.32

    -3.65

    -3.20

    0.95

    1.17

    I

    II

    Base excess(mM)

    23.65

    25.88

    20.35

    20.77

    25.20

    25.38

    I

    II

    Bicarbonate(mM)

    7.40

    7.44

    7.36

    7.39

    7.40

    7.40

    I

    II

    pH

    t3t2t1

    Median value of variable

    GroupMeasuredvariable

    Liskaser et al.: Role of Pump Prime in the Etiology andPathogenesis of Cardiopulmonary Bypass-AssociatedAcidosis (Anesthesiology 2000; 93) (2)

    Physicochemical analysis Strong ion difference apparent (SIDa)

    SIDa = [Na+]+[K+]+[Mg2+]+[Ca2+]-[Cl-]

    Strong ion difference effective (SIDe) Contribution of weak acids to the electrical

    charge equilibrium in plasma (Figgesmathematical model)

    Strong ion gap (SIG)

    SIG = SIDa SIDe lactate

    Normal 0 Positive = unmeasured anions

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    Liskaser et al., Anesthesiology 93 (2000)

    5.105.744.35SIG (mEq/l)

    32.1627.0935.94SIDe (mEq/l)

    36.8632.5340.42SIDa (mEq/l)

    -0.65-3.650.95Base excess(mM)

    Median value of variable

    3.174.793.36SIG-lactate(mEq/l)

    22.0018.0031.50Albumin (g/l)

    108.50113.00103.50Cl- (mM)

    t3t2t1Measuredvariable

    Group I: Haemaccel and Ringers Injection

    Liskaser et al., Anesthesiology 93 (2000)

    4.6412.854.02SIG (mEq/l)

    23.5017.0028.50Albumin (g/l)

    2.32-3.201.17Base excess

    (mM)39.2139.6139.43SIDa (mEq/l)

    2.2911.362.33SIG-lactate(mEq/l)

    Median value of variable

    34.4027.3935.55SIDe (mEq/l)

    103.00101.50104.00Cl- (mM)

    t3t2t1

    Measuredvariable

    Group II: Plasmalyte

    113.00

    32.53

    5.74

    4.79

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    Replacing 1 Liter of Blood Loss withCrystalloid (3:1)

    273 l of lactated Ringers

    1653 l of NaCl 0.9 %

    Excess chloride load

    (mmol)

    Crystalloid

    Hyperchloremic Metabolic Acidosis:Therapy

    Switch to balanced electrolyte solution

    Lactated Ringers

    Plasmalyte Hyperventilation

    pH > 7.2 and preferably > 7.3

    Furosemide

    (Fresh frozen plasma)

    Transfusion criteria

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    IV Fluid Solutions: Lactate

    Substrate for bicarbonate production

    Adverse effects? (animal studies)

    Increased apoptosis (GI tract, liver)

    Rate-dependent immune suppression

    (Panic disorder panic attack?) Neurobiological basis is unclear

    Plasma Volume Expansion (PVE):Static Concept

    Plasma volumePVE = Volume infused x

    Distribution vol.

    Distribution volume:

    D5W = total body water

    Lactated Ringers = extracellular vol.

    NaCl 0.9% = extracellular vol.

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    2 800

    2 800

    42 000

    14 OOO

    Distr. vol.(ml)

    1 000

    1 000

    1 000

    1 000

    PV(ml)

    -750250Alb. 25 %

    1000Alb. 5 %

    9 3003 70014 000D5W

    3 7004 700LR

    ICV(ml)

    IFV(ml)

    Vol. inf.(ml)

    Plasma volume x Distribution volumeVolume infused =

    Plasma volume

    Svensn et al., Anesthesiology (1997), 87

    S-albumin B-hemoglobin B-water

    TIME (min)Dilutionofpla

    smavolume

    0.25

    0.20

    0.15

    0.10

    0.05

    0

    Acetated Ringers

    0 60 120 180

    Dextran 70

    0 60 120 180

    0.20

    0.15

    0

    0.05

    0.10

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    One-compartment Volume of Fluid Space Model

    K i V V

    Kb

    Kr(V - V)

    V

    V = expandable space of volume

    V = target volume

    Ki = constant fluid infusion rate

    Kb = basal rate of fluid elimination(perspiration, basal diuresis)

    Controlled rate of fluid eliminationproportional by a constant Kr tothe relative deviation ofv fromV

    Svensn et al., Anesthesiology (1997), 87

    Two-compartment Volume of Fluid Space Model

    The net rate of fluid exchange between the 2 compartments isproportional to the difference in relative deviations from thetarget volumes by a constant Kt

    Ki V1V1

    KbKr(V1 - V1)

    V1

    Kt

    V2 V2

    Secondary fluid space

    Svensn et al., Anesthesiology (1997), 87

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    Plasma Volume Expansion (PVE):Kinetic Analysis

    Bolus of fluid

    Peak effects

    Rates of clearance

    Infusion of fluid necessary to maintainPVE at a certain level

    Effects of anesthesia, surgery andtrauma on fluid requirements

    Usefull during severe pathophysiologicdisturbances?

    0 20 40 60 80 100 120Time (min)

    0 20 40 60 80 100 120Time (min)

    0.2

    0.15

    0.10

    0.05

    0

    0.2

    0.15

    0.10

    0.05

    0

    Plasmadilu

    tion,(vV)/V

    Single bolus of Ringers40 ml/min for 40 min

    Bolus + continuous infusionof Ringers at 25 ml/min

    Hahn and Svensen, Br J Anaesth (1997), 79

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    Hahn and Svensen, Br J Anaesth (1997), 79

    V1 V2

    -900 ml-450 ml

    -0 ml

    -900 ml-450 ml

    -0 ml

    Dilution

    (Bloodhemoglobin)

    0.3

    0.2

    0.1

    0

    0.3

    0.2

    0.1

    0

    Central fluid space Peripheral fluid space

    0 50 100 150 0 50 100 150

    Time (min) Time (min)

    Drobin and Hahn, Anesthesiology (1999), 90

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    Volume Kinetics of Ringers Solution during Induction ofSpinal and General Anaesthesia.(Ewaldsson and Hahn: Br J Anaesth 2001, 87)

    20 ml/kg of Ringer acetate over 60 min (0.33 ml/kg/min)

    Spinal (n=10) or general (n=10) anesthesia

    20 min after start of infusion

    Ephedrine 5-10 mg IV ifSAP < 60 % of baseline

    Parameters

    Blood hemoglobin concentration

    Every 3 min during 60 min

    Urine output Additional patients (n=5)

    350 ml of Ringers over 2 min immediately after spinalfollowed by Ringers at 0.33 ml/kg/min

    Volume Kinetics of Ringers Solution during Induction ofSpinal and General Anaesthesia.(Ewaldsson and Hahn: Br J Anaesth 2001, 87)

    Results

    Infused fluid handled in similar way for spinal andgeneral anesthesia groups

    Most patients: two-volume model Small central volume compartment

    Reduced rate of equilibrium between thecompartments

    Infused fluid primarily in central blood volumeduring onset of anesthesia

    V1 increase by 125-150 ml in 5-10 min requires veryhigh infusion rate just after induction of anesthesia

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    Ewaldsson and Hahn, Br J Anaesth (2001), 87

    Spinal anesthesia

    Rapid infusion group

    0.33 ml/kg/min during 60 min

    0.33 ml/kg/min during 40 min350 ml over 2 min