Fluid and electrolyte management in surgical patients.


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Fluid and electrolyte management has to be aggressive. It is pivitol in speedy recovery in GI surgery. Changes should be anticipated and treated promptly. A detailed knowledge of this is essential for optimum management especially in the ICU.

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Fluid and electrolyte management in surgical patients.

  1. 1. <ul><li>FLUID AND ELECTROLYTE MANAGEMENT IN SURGICAL PATIENTS </li></ul><ul><li>BY </li></ul><ul><li>DR. KETAN VAGHOLKAR </li></ul><ul><li>M.S. (BOM)., D.N.B., M.R.C.S., F.A.C.S. </li></ul><ul><li>PROFESSOR OF SURGERY </li></ul><ul><li>& </li></ul><ul><li>CONSULTANT GENERAL SURGEON </li></ul><ul><li>Fellow in Hepatobiliary & Pancreatic Surgery at the Department of Visceral & Transplantation Surgery, Inselpital, University of Bern, Switzerland. </li></ul><ul><li>Elected as a Member of the Society for Surgery of the Alimentary Tract (SSAT), U.S.A. </li></ul><ul><li>Member of the European Digestive Society, (Switzerland) </li></ul><ul><li>Member of the National Academy of Medical Sciences (India) </li></ul><ul><li>Member of the Association of Surgeons of India. </li></ul><ul><li>Member of the Association of Colon & Rectal Surgeons of India. </li></ul><ul><li>Member of the Indian Chapter of IHPBA. </li></ul>
  2. 2. ANATOMY OF BODY FLUID COMPARTMENTS 1) TOTAL BODY WATER : Water constitutes 60% of total body weight as measured by deuterium oxide or tritiated water. Males 60%, Females 50% normal variation + 15%. Highest proportion of total body water is in newborn infants with maximum of 75 to 80%. At Yr. 65%. 2) VOLUME OF TOTAL BODY WATER IS - 40 Lts. ICF - 25 Lts. (40%) ECF (Plasma & - 15 Lts. (20%) Interstitial fluid) 3) IONIC COMPOSITION OF ICF AND ECF ICF : Cations Anions K+,Mg+ Phosphate & Proteins. ECF : Cations Anions Na+ Cl, HCO3 4) OSMOLARITY of body fluid is 290 to 300 mOSm / Lt.
  3. 3. ANATOMY OF BODY FLUID COMPARTMENTS Cell wall acts as a semipermeable membrane. As water is freely permeable, it maintains osmotic equilibrium despite the changes in ICF and ECF. Protein-1 Protein-16 Organic Acids-5 Organic Acids-5 Protein-40 Mg-2 Mq3 HCO 3 -10 Na-10 SO 4 & -3 PO 4 Ca-3 SO 4 & -3 PO 4 Ca-5 Mg.-40 HCO 3 -30 K-4 HCO 3 -27 K-4 HPO4 & -150 SO 4 K-150 Cl-144 Na-144 Cl-103 Na-142 Anions Cations Anions Cations Anions Cations 200 mEq/L 200 mEq/L 153 mEq/L 153 mEq/L 154 mEq/L 154 mEq/L INTRACELLULAR INTERSTITIAL PLASMA
  4. 4. <ul><li>CLASSIFICATION OF BODY FLUID CHANGES </li></ul><ul><li>VOLUME </li></ul><ul><li>Change in volume involves a distributional change. </li></ul><ul><li>CONCENTRATION </li></ul><ul><li>Concentration change involves change in the concentration of ions viz. Na. </li></ul><ul><li>COMPOSITION </li></ul><ul><li>Composition change involves change in the acid base balance. </li></ul>
  5. 5. VOLUME CHANGES None None Marked decrease in temp. Mild decreased in temp. METABOLIC Anasarca Rales, vomiting, diarrhea Pitting Edema, rales Atonic muscles, Sunken eyes Decreased Skin turgor, dry tongue TISSUE SIGNS Pulmonary Edema Increased CVP Increased CO. Loud HS Murmers, Gallops, Increased P2. Hypotension, Distant H.S., Cold extremities, Absent peripheral pulses Orthostatic Hypotension, Tachycardia, Collapsed Veins, Collapsed Pulse. CVS At operation Edema of the bowel, omentum and mesentry Nausea, ileus, vomiting and distention Decreased food consumption GIT --- --- Decreased Tenden reflex Stupor Coma Sleepiness Apathy Slow response CNS Severe Moderate Severe Moderate Excess Deficit
  6. 6. MANAGEMENT STRATEGY IN VOLUME CHANGES * Restriction of further water and salt intake * Diuretic therapy for more severe overload with myocardial inotropic support as necessary. * In cases with severe renal impairment, removal of excessive volume by haemodialysis or peritoneal dialysis. * Estimate of the deficit * An account of the maintenance requirement * The replacement of continuing excessive losses. * Modifications reflecting the effects of associated stress, surgery, age, size, cardiac and renal functions VOLUME EXCESS VOLUME DEFICIT
  7. 7. CONCENTRATION CHANGES Severe Moderate Severe Moderate None None Metabolic Oliguria Oliguria to anuria Renal Decreased Saliva, tears, dry and sticky, mucous membranes, swollen & red tongue, flushed skin. Increased salivation, lacrimation, watery diarrhoea, finger printing of Skin (Increased ICF) Tissue Signs Tachycardia Hypotension Decreased Pulse Secondary to Increased ICP Changes in BP CVS Increased ICP (Decompensated Phase) Increased ICP (Compensated Phase) Maniacal behaviour Weakness Loss of reflexes Increased tendon relfexes Delirium Restlessness Convulsions Twitching muscles CNS Hypernatremia (Water Deficit) Hyponatremia (Water intoxication)
  8. 8. <ul><li>MANAGEMENT STRATEGY IN CONCENTRATION CHANGES </li></ul><ul><li>HYPONATREMIA </li></ul><ul><li>Estimation of sodium deficit by the formula. </li></ul><ul><li>Na deficit = (145-x) x 60/100 x body wt. (mEq/L) </li></ul><ul><li>Half correction of the estimated sodium deficit as calculated from the above formula. </li></ul><ul><li>HYPERNATREMIA </li></ul><ul><li>Estimation of sodium excess by the formula </li></ul><ul><li>Na excess = (x-145) x 60/100 x body wt = y </li></ul><ul><li>Volume of 5% Dext. Solution to be infused = y / 154 </li></ul>
  9. 9. COMPOSITION CHANGES HENDERSON HASSELBACH EQUATION i.e. 6.1 + 1.34 = 7.4 pH of the human body ranges between 7.36 to 7.44 TYPES OF COMPOSITION CHANGES * Respiratory Acidosis * Respiratory Alkalosis * Metabolic Acidosis * Metabolic Alkalosis
  10. 10. COMPOSITION CHANGES This is by the restoration of normal alveolar ventilation : Treatment Renal Retention of HCO 3 . Excretion of acid salts. Increase NH3 formation. Cl Shift into cells. : Compensation Increased denominator Ratio <20 : 1 : Depression of Resp. center CNS injury Pulmonary Disease : Causes CO 2 retention (decreased alveolar ventilation) : Defect RESPIRATORY ACIDOSIS
  11. 11. COMPOSITION CHANGES Correction of the underlying cause, including the alleviation of pain, emotional distress and hypoxia. Rebreathing and increasing airway dead space are both used where appropriate. : Treatment Renal Excretion of HCO 3 . Retention of acid salts. Decreased NH3. : Compensation Decreased denominator Ratio >20 : 1 : Hyperventilation Pain Assisted Ventilation : Causes Increased loss of CO 2 (increased alveolar ventilation) : Defect RESPIRATORY ALKALOSIS
  12. 12. COMPOSITION CHANGES Removal of the underlying cause / Reestablishment of volume and adequate perfusion rapidly reverses lactice acidosis. Sodium bicarbonate infusion should be used cautiously. Large doses may be needed to restore cardiac function (2-3 mmol/kg) following cardiac arrest with acute and severe acidosis. Replacement is calculated from the equation. (24-plasma [HCO3-]) x estimated ECF. : Treatment Pulmonary Increased rate and depth of breathing Renal (Slow) : Compensation Decreased Numerator Ratio < 20 : 1 : Diabetes Azotemia Diarrhoea & small bowel fistula. : Causes Retention of fixed acids Loss of base HCO 3 : Defect METABOLIC ACIDOSIS
  13. 13. COMPOSITION CHANGES Volume repletion with saline and K+ repletion with KCI are usually adequate to correct the alkalosis. Oral NH 4 Cl or 0.1 molar HCI acid infusion are rarely, if ever indicated. : Treatment Pulmonary (rapid) Decreased rate and depth of breathing. Renal (Slow) : Compensation Increased Numerator Ratio > 20 : 1 : Pyloric Obstruction. Excess intake of HCO 3 . Diuretics. : Causes Loss of fixed acids. Gain of base HCO 3 K depletion. : Defect METABOLIC ALKALOSIS
  14. 14. BUFFERING MECHANISMS FOR COMPOSITION CHANGES Acute (Uncompensated) Chronic (Partially Compensated)   N   Met. Alkalosis   N   Met. Acidosis N     Resp. Alkalosis N     Resp. Acidosis Plasma HCO3 (Metabolic Component) pCO 2 (Resp. Component) Ph    Met. Alkalosis    Met. Acidosis     Resp. Alkalosis     Resp. Acidosis Plasma HCO3 (Metabolic Component) pCO 2 (Resp. Component) Ph
  15. 15. MIXED ACID-BASE DISTURBANCES * These are difficult to diagnose. * These tend to cancel each other out and result in minimal pH change. E.G. Metabolic acidosis in combination with respiratory alkalosis may occur with speticaemia. Metabolic acidosis with a respiratory acidosis is a frequent event in the emergency situation of cardio respiratory arrest. Standard HCO 3 : Conc. Of bicarbonate in plasma, when whole blood with fully oxygenated hemoglobin has been equilibrated with CO 2 at a PCO 2 of 40mm. Of Hg. At a temp of 38 0 C. SBC : 24.5 mEq/L Base excess directly expresses the amount in mEq of fixed base (fixed acid) added to each liter of blood. +ve value – base excess -ve value – excess acid (base deficit) Base Deficit or excess (mEq) = + (BE) x 0.30 x body wt.
  16. 16. VOLUME & IONIC COMPOSITION OF VARIOUS GASTRO INTESTINAL SECRETIONS 35 100 5 145 (50-800) Bile 115 75 5 140 (100-800) Pancreas - 40 30 60 - Colon 30 104 5 140 3000 Ileum - 80 5 140 No active secretion (100-2000) Duodenum - 130 10 60 1500 Stomach 30 10 26 10 1500 Saliva HCO 3 mEq/L CI mEq/L K mEq/L Na mEq/L Vol. (cc)
  17. 17. ALTERATIONS IN POTASSIUM HYPERKALEMIA : CLINICAL FEATURES : CVS (ECG) : Peaked T waves Widened QRS Complexes. Depressed ST-T segments. Disappearance of T waves. Heart Block. Diastollic cardiac arrest. GIT : Nausea, Vomiting, Colic, Diarrhoea. Rx (TREATMENT) : Stop exogenous K administration Rx underlying cause Reverse cardio toxic effects. 1) 1 gm of 10% cal gluconate with ECG monitoring. 2) Glucose insulin drip. 45 mEq NahCO 3 in 1000 cc. of D 10 W+20 Cl. 3) Rapid alkalinization of ECF by lactate/HCO 3 . 4) Cation exchange resins. 5) Peritoneal dialysis / hemo dialysis.
  18. 18. <ul><li>ALTERATIONS IN POTASSIUM </li></ul><ul><li>HYPOKALEMIA : </li></ul><ul><li>CAUSES : 1) Increased Renal Excretion. </li></ul><ul><li>2) Administration of K free fluids. </li></ul><ul><li>3) Parental nutrition without K. </li></ul><ul><li>4) Fistulas. </li></ul><ul><li>CLINICAL FEATURES : Facial Paralysis </li></ul><ul><li>Decreased tendon reflexes. </li></ul><ul><li>Paralytic ileus. </li></ul><ul><li>ECG : Alteration of T Waves. </li></ul><ul><li>TREATMENT : </li></ul><ul><li>Replacement of estimated deficits. This is accomplished more slowly for mild deficits with oral supplements and K+ rich foods or by intravenous therapy if the deficit is more severe. Monitoring with an ECG and serum K+ measurements are recommended if K+ is given more rapidly. (max. 40 mEq/Lit. but not exceeding 40 mEq/hour.). </li></ul><ul><li>Correction of alkalosis although, when this is mild, the simple provision of K+ and rehydration is usually sufficient also to correct the alkalosis. </li></ul><ul><li>Correction of other predisposing factors, including modification of diuretic therapy and treatment of the causes of catabolism and excessive fluid losses. </li></ul><ul><li>Consider prevention by adequate K+ supplements in patients at risk. </li></ul>
  19. 19. ALTERATIONS IN CALCIUM Calcium (Ca) : (Ionised 45%) responsible for NM stability. Acidosis – Increased ionized fraction. Alkalosis – Decreased ionized fraction. HYPOCALCEMIA : (<8 mg %) CAUSES : Acute pancreatitis Soft tissue infections ARF / CRF Intestinal Fistulas Hypoparathymation. CLINICAL FEATURES : Carpopedalspasm Chvostek’s Sign Trousseau’s Sign TREATMENT : To Rx the underlying Cause 1) Oral or IV infusion of calcium gluconate / lactate slowly under ECG monitoring. 2) For blood induced hypocalcemia : 2 cc of CaCl2 / 500 cc of blood if the rate of transfusion is 100 cc/m.
  20. 20. ALTERATIONS IN CALCIUM HYPERCALCEMIA : (> 15 mg %) CAUSES : Malignancy Sarcoidosis Milk Aklali syndrome Hyper Vitaminosis D Hyperparathyroidism. CLINICAL FEATURES : Fatigue Somnolent Lassitude Stupor Weakness Coma TREATMENT : Fluid replacement Diuretics (lasix) Oral / IV inorganic phosphates to inhibit true resorption (Contraindicated in CRF patients) IV NaSulphate (CRF pts) Steroids / Mithramycin.
  21. 21. THANK YOU