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CURRENT CONCEPTS in peri-operative FLUID MANAGEMENT

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. THE KINETICS OF PVE.

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CURRENT CONCEPTS in peri-operative FLUID MANAGEMENT

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  1. CURRENT CONCEPTSin peri-operativeFLUID MANAGEMENT Prof. Mehdi Hasan Mumtaz

  2. IMPORTANT ASPECTS • The kinetics of water compartments. • Recent developments colloid solutions. • Components of crystalloids. • Planning fluid therapy. • Specific therapies.

  3. THE KINETICS OF PVE

  4. THE KINETICS OF PVE INTRACELLULAR INTERSTITIAL VASCULAR CAPILLARY EG CELL OSMILALITY Na+ COP

  5. THE KINETICS OF PVE Starlings Equiblirium Q=Ka[(Pc – Pi) + O-(IIi- IIc)]

  6. THE KINETICS OF PVE Plasma Volume Expansion Equation PV PVE = Volume Infuse X ---------- VD

  7. THE KINETICS OF PVE

  8. PVEINTERACTION BETWEEN Kinetic Effects of Analysis - Surgery & Trauma - Anesthesia

  9. CURRENT PERIOPERATIVE FLUID MANAGEMENT “AVOID HYPOVOLAEMIA” But no tools are available to permit Precise matching of fluid Administration to fluid needs

  10. REFERENCE Arieff Al. Fatal postoperative pulmonary edema: Pathogenesis and literature review. Chest 1999;115:1371-7.

  11. 1 Restoration of Immune Function X ----------------- Time Factor

  12. HYPERINFUSION/HYPOINFUSION Because: • 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.

  13. HYPOPERFUSION? RENAL FAILURE HEPATIC FAILURE SEPSIS ACHIEVE TARGET LEVEL DO2

  14. OXYGEN DELIVERY DO2=Q x CaO2 x 10

  15. 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.

  16. COLLOID DEVELOPMENTCOLLOID/CRYSTALLOID CONTROVERSY Schierhouta & Robers  favour crystalloids Cochrane collaboration  favour colloids

  17. WHY CRYSTALLOIDS? • For • Low cost. • Better renal function preservation. • Rapid redistribution if over-infusion. • Against. • Large volumes required. • Pulmonary oedema. • Dilute serum proteins.

  18. WHY COLLOIDS? • For • Small volume required. • Prolonged retention. • Against. • Low GFR. • Interference with coagulation. • More prolonged hydrostatic pulmonary oedema.

  19. 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.

  20. WHICH COLLOIDS? HES FORMULATION? “high branched derivative of amylopection obtained from corn starch”

  21. 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

  22. HES 130,000/0.4/11.2few clotting changes • HES 200,000/0.5/4.6 • HES 70,000/0.5/3.2

  23. SPECIFIC COMPONENTS OF IV CRYSTALLOIDS • Sodium. • Lactate. • Chloride. • Potassium. • Bicarbonate. • Glucose. • Water.

  24. COMPONENTS • Sodium Serum osmilality • Lactate Precursor for HCO3 pharmacologic effects • Chloride Normal replacement hyperchloraemic metabolic acidosis

  25. 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.

  26. COMPONENTS – Sodium

  27. 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.

  28. 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.

  29. COMPONENTS – Lactate • PRECURSOR FOR BICARBONATE. • APOPTOSIS IN GIT & LIVER. • IMMUNE SUPRESSION.

  30. 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

  31. 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

  32. 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

  33. CRYSTALLOIDS SOLUTIONS

  34. ISOTONIC SALINE • Contain 9GNacl/L. • ‘Normal’ saline – misnomer. • Slightly hypertonic to plasma. • PH-acid (5.7). • May produce hyperchloralmic metabolic acidosis.

  35. 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.

  36. 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.

  37. CRYSTALLOID SOLUTIONSPRODUCED BY DEXTROSE

  38. COLLOID SOLUTIONS

  39. FLUID DURING OPERATION CONTROVERSIAL? Benefit No renal failure Drawback Blood coaguability

  40. PHYSIOLOGICAL RESPONSEtoStress – SurgeryStress - Anaesthesia

  41. MANAGEMENT GUIDE LIENS • Intr-operative: • Hartman’s solutionorRingolact solution • Blood to maintain HB>10g/dl • Exceptions - Septicaemia - Lung trauma -PAWP 15ml/kg/hr

  42. POSTOPERATIVE PERIOD • (24-48 hrs)5% Dextrose/water = 30ml/kg/day+30mmol K+/L. • Replace specific losses. • Maintain urine output > 0.5ml/kg/hr.

  43. POSTOPERATIVE PERIOD 2. After 48 hrs. • Add sodium.4% D/W 0.18% saline 30ml/kg/day. or5% D/W 7ml/kg/day. +Normal saline 23ml/kg/day. • Assess serum K+ level. • Consider parenteral nutrition.

  44. ECLAMPSIA &FLUID RESUSCITATION Blood Pressure. Colloid Osmotic Pressure

  45. FLUID THERAPY INTRACELLULAR INTERSTITIAL VASCULAR CAPILLARY EG CELL OSMILALITY Na+ COP

  46. CLINICAL/BIOCHEMICAL VARIABLES DURING FLUID THERAPY • Flow/ Pressure Variables. • PCWP/CVP. • CO/BP. • SVR/Peripheral Temp. • O2 Transport Variables. • DO2. • VO2. • Serum Lactate.

  47. 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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