8/22/2019 verhaegen
1/32
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
8/22/2019 verhaegen
2/32
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
8/22/2019 verhaegen
3/32
3
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
8/22/2019 verhaegen
4/32
4
Body Fluid Compartments: Composition
2716Protein (g/dl)
2275Phosphorus (mEq/l)
282410Bicarbonate (mEq/l)
1101054Chloride (mEq/l)
2250Magnesium (mEq/l)
33
8/22/2019 verhaegen
5/32
5
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
8/22/2019 verhaegen
6/32
6
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
8/22/2019 verhaegen
7/32
7
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
8/22/2019 verhaegen
8/32
8
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)
8/22/2019 verhaegen
9/32
9
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
8/22/2019 verhaegen
10/32
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)
*
8/22/2019 verhaegen
11/32
11
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
8/22/2019 verhaegen
12/32
12
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
8/22/2019 verhaegen
13/32
13
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
8/22/2019 verhaegen
14/32
14
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)
8/22/2019 verhaegen
15/32
15
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)
8/22/2019 verhaegen
16/32
16
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
8/22/2019 verhaegen
17/32
17
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)
8/22/2019 verhaegen
18/32
18
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)
8/22/2019 verhaegen
19/32
19
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
8/22/2019 verhaegen
20/32
20
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
8/22/2019 verhaegen
21/32
21
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
8/22/2019 verhaegen
22/32
22
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
8/22/2019 verhaegen
23/32
23
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
8/22/2019 verhaegen
24/32
24
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
8/22/2019 verhaegen
25/32
25
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
8/22/2019 verhaegen
26/32
26
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.
8/22/2019 verhaegen
27/32
27
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
8/22/2019 verhaegen
28/32
28
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
8/22/2019 verhaegen
29/32
29
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
8/22/2019 verhaegen
30/32
30
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
8/22/2019 verhaegen
31/32
31
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
8/22/2019 verhaegen
32/32
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