CURRENT CONCEPTS in peri-operative FLUID MANAGEMENT Prof. Mehdi Hasan Mumtaz.
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Transcript of CURRENT CONCEPTS in peri-operative FLUID MANAGEMENT Prof. Mehdi Hasan Mumtaz.
![Page 1: CURRENT CONCEPTS in peri-operative FLUID MANAGEMENT Prof. Mehdi Hasan Mumtaz.](https://reader035.fdocuments.us/reader035/viewer/2022062713/56649ce55503460f949b3213/html5/thumbnails/1.jpg)
CURRENT CONCEPTSin peri-operative
FLUID MANAGEMENT
Prof. Mehdi Hasan Mumtaz
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IMPORTANT ASPECTS
The kinetics of water compartments.
Recent developments colloid solutions.
Components of crystalloids.
Planning fluid therapy.
Specific therapies.
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THE KINETICS OF PVE
%total body
weight
Volume (L/70kg body
weight)
Total body water
Intracellular volume
Extracellular volume
Intersitial fluid volume
Plasma volume
60
40
20
16
4
42
28
14
11
3
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THE KINETICS OF PVE
INTRACELLULAR INTERSTITIAL VASCULAR
CAPILLARY
CELL
EG
OSMILALITY
Na+
COP
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THE KINETICS OF PVE
Starlings Equiblirium
Q=Ka[(Pc – Pi) + O-(IIi- IIc)]
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THE KINETICS OF PVE
Plasma Volume Expansion Equation
PV
PVE = Volume Infuse X ----------
VD
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THE KINETICS OF PVE
IVS ISS ICS
IL 5% Dextros
5/42 X 1000 =120ml
14/42 x 1000
=333ml
23/42 X 1000
=547ml
IL NaCl 0.9%
5/19 X 1000 =263ml
14/19X1000
=737ml
IL Colloid containing solution
5/5 X 1000 =1000ml
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PVEINTERACTION BETWEEN
Kinetic Effects ofAnalysis - Surgery & Trauma
- Anesthesia
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CURRENT PERIOPERATIVE FLUID MANAGEMENT
“AVOID HYPOVOLAEMIA”
But no tools are available to permit
Precise matching of fluid
Administration to fluid needs
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REFERENCE
Arieff Al. Fatal postoperative pulmonary edema: Pathogenesis
and literature review.
Chest 1999;115:1371-7.
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1
Restoration of Immune Function X -----------------
Time Factor
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HYPERINFUSION/HYPOINFUSION
Because:1. We cannot accurately evaluate blood volume.
2. We cannot accurately evaluate tissue perfusion.
3. We cannot accurately identify fluid overload.
4. We cannot accurately identify hypovolaemia.
5. We cannot accurately define the correct rate of fluid resuscitation.
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HYPOPERFUSION?
RENAL FAILURE
HEPATIC FAILURE
SEPSIS
ACHIEVE TARGET LEVEL DO2
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OXYGEN DELIVERY
DO2=Q x CaO2 x 10
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DO2 PRINCIPLES TO BE KEPT IN MIND
Crystalliods/colloid Q Hb.
Blood transfusion Hb Q.
Catechlamines tissue perfusion.
Lactate & PH1 superior to non-selectively DO2.
Why not VO2 .What about O2 utilization.
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COLLOID DEVELOPMENTCOLLOID/CRYSTALLOID CONTROVERSY
Schierhouta & Robers favour crystalloids
Cochrane collaboration favour colloids
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WHY CRYSTALLOIDS?
For Low cost. Better renal function preservation. Rapid redistribution if over-infusion.
Against. Large volumes required. Pulmonary oedema. Dilute serum proteins.
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WHY COLLOIDS?
For Small volume required. Prolonged retention.
Against. Low GFR. Interference with coagulation. More prolonged hydrostatic pulmonary
oedema.
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SOLUTION
More prolonged expansion of IV volume with colloids in situation of major fluid loss (extensive surgery).
Lower cost of crystalloids for most routine cases.
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WHICH COLLOIDS?
HES FORMULATION?
“high branched derivative of amylopection obtained from corn
starch”
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Characterised by: Average mol. Wt. Degree of substitution. Substitution sites.
HES 200,000/0.5/4.6
M. W. T
Substitution ratio
Half of anlydrousglucose
Sites have hyroxyethyl group
Times as many C2 as C6 sites
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HES 130,000/0.4/11.2 few clotting changes
HES 200,000/0.5/4.6
HES 70,000/0.5/3.2
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SPECIFIC COMPONENTS OF IV CRYSTALLOIDS
Sodium.
Lactate.
Chloride.
Potassium.
Bicarbonate.
Glucose.
Water.
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COMPONENTS
Sodium Serum osmilality
Lactate Precursor for HCO3
pharmacologic effects
Chloride Normal replacement
hyperchloraemic metabolic
acidosis
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COMPONENTS - Sodium
Reference:
Zornow MH, Todd MM, Moore SS. The acute cerebral effects of changes in
plasma osmolality and oncotic pressure.
Anesthesiology 1987;67:946-41.
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COMPONENTS – Sodium
Osmilality
(mOsm kg-1)
Osmotic pressure (mmHg)
Osmotic pressure
difference (mmHg)
osmoles plasma IF Plasma IF (Plasma-IF)
[Na+]protein non-protein
282.6 282.6 5454 5454 0
[Na+]acutely 5.0mEq/L
292.6 282.6 5640 5454 186
Protein 1.2 0 23 0 23
Protein X2 2.4 0 46 0 46
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REFERENCE
Drumond JC, Patel PM, Cole DJ, Kelly PJ. The effect of the reduction of
colloid oncotic pressure, with and without reduction of osmolailty, on
post-traumatic cerebral edema. Anesthesiology 1998;88:993-1002.
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REFERENCE
Fisher B, Thomas D, Peterson B. Hypertonic saline lowers raised intracranial pressure in children after head trauma. J Neurosurg.
Anesthesiology 1992;4:4-10.
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COMPONENTS – Lactate
PRECURSOR FOR BICARBONATE.
APOPTOSIS IN GIT & LIVER.
IMMUNE SUPRESSION.
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COMPONENTS – ChlorideReference: Liskaser Fj, Bellomo R, Hayhoe M, et
al. the role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass associated acidosis. Anestheology 2000;93:1170-3
Waters JH, Bernstein CA. Dilutional acidosis following hetastarch or albumin in healthy volunteers. Anesthesiology 2000-93:1184-7.
Hyperchloraemic metabolic acidosis
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COMPONENTS – ChlorideReference: Prough DS, Bidani A. Hyperchloremic
metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline. Anesthesiology 1999;90:1247-9
Prough DS, Acidosis associated with peri-operative saline administration: dilution or delusion?. Anesthesiology 2000;93:1167-9
Fluid containing no bicarbonate
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COMPONENTS – Chloride
Reference: Sevensen C, Hahn RG. Volume kinetics
of ringer solution, dextran 70, and hypertonic saline in male volunteers. Anesthesiology 1997;87:204-12
Acidosis is resolves more quickly if solution contains bicarbonates
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CRYSTALLOIDS SOLUTIONSPlasma* 0.9%
salineRinger’s lactate
Normosol
mEq/L
Na 141 154 130 140
CL 103 154 109 98
K 4-5 - 4 5
Ca/Mg 5/2 - 3/0 0/3
Buffer Bicarbonate (26)
- Lactate (28)
Acetate (27)
Gluconate (23)
pH 7.4 5.7 6.7 7.4
Osmolality (mosm/kg)
289 308 273 295
* Plasma values from Brenner BM, Rector FC Jr. eds. The kidney. Philadelphia: W. B. Saunders. 1981:95.
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ISOTONIC SALINE
Contain 9GNacl/L.
‘Normal’ saline – misnomer.
Slightly hypertonic to plasma.
PH-acid (5.7).
May produce hyperchloralmic metabolic acidosis.
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RINGERS’ LACTATE
Balanced solution.Iso/hypotonic to plasma.Lactate as buffer.Risks: K+ - determental in renal, adrenal
insufficiency. Ca++ - promotes ‘no reflow’. Incompatibility with drugs.
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DEXTROSE SOLUTIONS
Source of calories.
50G contributes 278 moSm.
Temporary osmotic load.
Addition of 50G to saline raise osmolaity twice.
Fuel for lactic acid in ischamemic organs.
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CRYSTALLOID SOLUTIONSPRODUCED BY DEXTROSE
Solution mOsm/L
0.9% saline 308
5% Dextrose in 0.9% saline 586
Ringer’s lactate 273
5% Dextrose in Ringer’s lactate 527
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COLLOID SOLUTIONS
25% Albumin
5%
Albumin
6%
Hetastarch
Dextran
40
COP (mmHg) 70 20 30 40
Unit size 50ml 250 or
500ml
500ml 250ml
*Potency 4:1 1.3:1 1.3:1 2:1
Bleeding - 0.001 0.010 0.010
#Unit cost $19.22/50ml $19.22/500ml $43.50/500ml $20.00/500ml
*Potency expressed as increase in vascular volume (mls) per ml of infused colloid.•# Manufacturer’s cost at our hospital as of March 1, 1989.
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FLUID DURING OPERATION CONTROVERSIAL?
Benefit No renal failure
Drawback Blood coaguability
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PHYSIOLOGICAL RESPONSE
toStress – Surgery
Stress - Anaesthesia
ADH
Aldosterone
Renin
Retention of H2O+Na+
Loss of K+
2-4 days
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MANAGEMENT GUIDE LIENS
Intr-operative: Hartman’s solution
orRingolact solution
Blood to maintain HB>10g/dl
Exceptions
- Septicaemia
- Lung trauma
-PAWP
15ml/kg/hr
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POSTOPERATIVE PERIOD
1. (24-48 hrs)5% Dextrose/water = 30ml/kg/day+30mmol K+/L. Replace specific losses. Maintain urine output > 0.5ml/kg/hr.
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POSTOPERATIVE PERIOD
2. After 48 hrs. Add sodium.
4% D/W 0.18% saline 30ml/kg/day.or
5% D/W 7ml/kg/day.+
Normal saline 23ml/kg/day. Assess serum K+ level. Consider parenteral nutrition.
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ECLAMPSIA &FLUID RESUSCITATION
Blood Pressure.
Colloid Osmotic Pressure
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FLUID THERAPY
INTRACELLULAR INTERSTITIAL VASCULAR
CAPILLARY
CELL
EG
OSMILALITY
Na+
COP
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CLINICAL/BIOCHEMICAL VARIABLES DURING FLUID THERAPY
Flow/ Pressure Variables. PCWP/CVP. CO/BP. SVR/Peripheral Temp.
O2 Transport Variables. DO2.
VO2.
Serum Lactate.
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CONCLUSION
Fluid therapy should be taken seriously.
Selection of solution.
Patients suffering from critical conditions. Heart. Renal. Pulmonary. Pre-eclampsia/ Eclampsia