CURRENT CONCEPTS in peri-operative FLUID MANAGEMENT

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CURRENT CONCEPTS
in peri-operative
FLUID MANAGEMENT
Prof. Mehdi Hasan Mumtaz
IMPORTANT ASPECTS
The kinetics of water compartments.
Recent developments colloid
solutions.
Components of crystalloids.
Planning fluid therapy.
Specific therapies.
THE KINETICS OF
PVE
Total body water
Intracellular volume
Extracellular volume
Intersitial fluid volume
Plasma volume
%total
body
weight
Volume
(L/70kg body
weight)
60
40
20
16
4
42
28
14
11
3
THE KINETICS OF PVE
INTRACELLULAR
INTERSTITIAL
VASCULAR
CAPILLARY
EG
CELL
OSMILALITY
Na+
COP
THE KINETICS OF PVE
Starlings Equiblirium
Q=Ka[(Pc – Pi) + O-(IIi- IIc)]
THE KINETICS OF PVE
Plasma Volume Expansion Equation
PV
PVE = Volume Infuse X ---------VD
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
PVE
INTERACTION BETWEEN
Kinetic
Analysis
Effects of
- Surgery & Trauma
- Anesthesia
CURRENT PERIOPERATIVE
FLUID MANAGEMENT
“AVOID HYPOVOLAEMIA”
But no tools are available to permit
Precise matching of fluid
Administration to fluid needs
REFERENCE
Arieff Al. Fatal postoperative
pulmonary edema: Pathogenesis
and literature review.
Chest 1999;115:1371-7.
1
Restoration of Immune Function X ----------------Time Factor
HYPERINFUSION/
HYPOINFUSION
Because:
1.
2.
3.
4.
5.
We cannot accurately evaluate blood volume.
We cannot accurately evaluate tissue
perfusion.
We cannot accurately identify fluid overload.
We cannot accurately identify hypovolaemia.
We cannot accurately define the correct rate of
fluid resuscitation.
HYPOPERFUSION?
RENAL FAILURE
HEPATIC FAILURE
SEPSIS
ACHIEVE TARGET LEVEL DO2
OXYGEN DELIVERY
DO2=Q x CaO2 x 10
DO2 PRINCIPLES TO BE
KEPT IN MIND
Crystalliods/colloid Q  Hb.
Blood transfusion Hb  Q.
Catechlamines tissue perfusion.
Lactate & PH1 superior to nonselectively DO2.
Why not VO2 .
What about O2 utilization.
COLLOID DEVELOPMENT
COLLOID/CRYSTALLOID CONTROVERSY
Schierhouta & Robers  favour crystalloids
Cochrane collaboration  favour colloids
WHY CRYSTALLOIDS?
For



Low cost.
Better renal function preservation.
Rapid redistribution if over-infusion.
Against.



Large volumes required.
Pulmonary oedema.
Dilute serum proteins.
WHY COLLOIDS?
For


Small volume required.
Prolonged retention.
Against.



Low GFR.
Interference with coagulation.
More prolonged hydrostatic pulmonary
oedema.
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.
WHICH COLLOIDS?
HES FORMULATION?
“high branched derivative of
amylopection obtained from corn
starch”
Characterised by:



Average mol. Wt.
Degree of substitution.
Substitution sites.
HES 200,000/0.5/4.6
M. W. T
Times as many C2 as C6
sites
Substitution ratio
Half of anlydrousglucose
Sites have hyroxyethyl
group
HES
130,000/0.4/11.2 few clotting changes
HES
200,000/0.5/4.6
HES
70,000/0.5/3.2
SPECIFIC COMPONENTS
OF IV CRYSTALLOIDS
Sodium.
Lactate.
Chloride.
Potassium.
Bicarbonate.
Glucose.
Water.
COMPONENTS
Sodium
Serum osmilality
Lactate
Precursor for HCO3
pharmacologic effects
Chloride
Normal replacement
hyperchloraemic metabolic
acidosis
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.
COMPONENTS – Sodium
Osmilality
(mOsm kg-1)
osmoles
Osmotic pressure Osmotic pressure
(mmHg)
difference
(mmHg)
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
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.
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.
COMPONENTS – Lactate
PRECURSOR FOR BICARBONATE.
APOPTOSIS IN GIT & LIVER.
IMMUNE SUPRESSION.
COMPONENTS – Chloride
Reference:


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
COMPONENTS – Chloride
Reference:


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
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
CRYSTALLOIDS SOLUTIONS
Plasma*
0.9%
saline
Ringer’s
lactate
Normosol
Na
141
154
130
140
CL
103
154
109
98
K
4-5
-
4
5
Ca/Mg
5/2
-
3/0
0/3
Buffer
Bicarbon
ate (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.
mEq/L
ISOTONIC SALINE
Contain 9GNacl/L.
‘Normal’ saline – misnomer.
Slightly hypertonic to plasma.
PH-acid (5.7).
May produce hyperchloralmic
metabolic acidosis.
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.
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.
CRYSTALLOID SOLUTIONS
PRODUCED 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
COLLOID SOLUTIONS
25%
Albumin
5%
Albumin
6%
Hetastarch
Dextran
40
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
COP (mmHg)
#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.
FLUID DURING OPERATION
CONTROVERSIAL?
Benefit
Drawback
No renal failure
Blood coaguability
PHYSIOLOGICAL
RESPONSE
to
Stress – Surgery
Stress - Anaesthesia
ADH
Aldosterone
Renin
Retention of H2O
+Na+
Loss of K+
2-4 days
MANAGEMENT GUIDE
LIENS
Intr-operative:


Hartman’s solution
or
Ringolact solution
Blood to maintain HB>10g/dl
Exceptions
- Septicaemia
- Lung trauma
-PAWP
15ml/kg/hr
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.
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.
ECLAMPSIA &
FLUID RESUSCITATION
Blood Pressure.
Colloid Osmotic Pressure
FLUID THERAPY
INTRACELLULAR
INTERSTITIAL
VASCULAR
CAPILLARY
EG
CELL
OSMILALITY
Na+
COP
CLINICAL/BIOCHEMICAL VARIABLES
DURING FLUID THERAPY
Flow/ Pressure Variables.



PCWP/CVP.
CO/BP.
SVR/Peripheral Temp.
O2 Transport Variables.


DO2.
VO2.
Serum Lactate.
CONCLUSION
Fluid therapy should be taken seriously.
Selection of solution.
Patients suffering from critical
conditions.




Heart.
Renal.
Pulmonary.
Pre-eclampsia/ Eclampsia
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