CURRENT CONCEPTSin 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

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

THE KINETICS OF PVE

INTRACELLULAR INTERSTITIAL VASCULAR

CAPILLARY

CELL

EG

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

PVEINTERACTION BETWEEN

Kinetic Effects ofAnalysis - 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. 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.

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 non-selectively DO2.

Why not VO2 .What about O2 utilization.

COLLOID DEVELOPMENTCOLLOID/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

Substitution ratio

Half of anlydrousglucose

Sites have hyroxyethyl group

Times as many C2 as C6 sites

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)

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

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 – 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

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

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 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.

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 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

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.

FLUID DURING OPERATION CONTROVERSIAL?

Benefit No renal failure

Drawback Blood coaguability

PHYSIOLOGICAL RESPONSE

toStress – Surgery

Stress - Anaesthesia

ADH

Aldosterone

Renin

Retention of H2O+Na+

Loss of K+

2-4 days

MANAGEMENT GUIDE LIENS

Intr-operative: Hartman’s solution

orRingolact 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

CELL

EG

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