بسم الله الرحمن الرحيم

1. بسم الله الرحمن الرحيم ”وربك الغفور ذو الرحمه لو يؤاخذهم بما كسبوا لعجل لهم العذاب“ ”ربنا اغفر لى ولوالدى وللمؤمنين يوم يقوم الحساب“ صدق الله العظيم

2. Fluid management& Electrolyte Disturbances: By Dr. WaelAlham Mohamedlecturer of Anesthesia & ICUSohag Faculty of Medicine

3. Fluid Management • Body fluid compartments (Average 70KG )

4. The Composition Of Fluid Compartments

5. Intracellular Fluid • *A membrane bound ATP-dependant pump exchange Na for K in a ratio 3:2 • *Cell membrane are relatively impermeable to Na and to lesser extent to K ,So K is the most important determinant of intracellular osmolality • *The impermeability of cell membrane to most proteins results in high intracellular protein concentration.

6. Interstitial Fluid • *Most interstitial water is in chemical association with proteoglycans forming gel * Interstitial Fluid pressure is negative (about -5mmHg),as the fluid volume increase the pressure rises and become positive, free fluid increase and appear clinically as edema • *The protein content is low (2g/L)

7. Intravascular Fluid **Most Its commonly referred to as plasma. electrolyte pass freely between plasma and interstitium resulting in nearly identical electrolyte composition. *Plasma proteins are the only osmotically active solute in fluid exchange between plasma and interstitium. *The interstitial compartment acts as an overflow reservoir for the intravascular compartment.

8. Electrolyte Content Of Body Fluids

9. Replacement Type Solutions : • Normal Saline (Na 154mEq/L,Cl 154mEq/L) • It’s the preferred solution in hypochloremic M alkalosis • Its used for diluting packed RBCs • If its given in large amount it cause hyper chlormic M Acidosis • 3%Normal Saline :each Na and Cl 512 mEq/L) • Its used for ttt of symptomatic hypo natremia & hypovolemic shock • 3-7.5% Saline solutions can be used in hypovolemic shock (Slowly through CV catheter as it may cause hemolysis

10. Composition Of Crystalloid Solution

11. Crystalloid Solutions A) Maintenance Type Solutions: Its hypotonic solutions used in absence of oral intake as fluid and electrolyte deficit can rapidly develop due to urine formation ,G I T secretions ,sweating and insensible loss from skin and respiratory tract. -Solutions such as D51/4N.S and D51/2N.S are commonly used because these loses are normally hypotonic (more water loss than Na loss)

12. Dextrose 5% • *It contain 50 gm/L of glucose ,its hypotonic (253 mosm/L) • *Its used to prevent ketosis and hypoglycemia due to fasting • -For replacement of pure water deficit • -as a maintenance fluid for patient on Na restriction • -Its content of water pass freely through BBB ,So volume overload from dextrose can lead to brain edema.

13. Maintenance fluid requirement

14. (2)Replacement Fluid Its used to replace : A) Pre existing deficit :according to the duration of the fast ,estimated by: Normal maintenance rate x Length of fast (For 70 kg man fasting 8 hours= 40+20+50 ml/h x 8 hours =880 ml The fluid used should be similar to the fluid lost e.g. hypotonic solution D5 ¼ NS or D5 ½NS

15. Replacement Fluid B) Abnormal fluid losses as: -Pre operative bleeding ,vomiting ,diuresis or diarrhea -Occult losses due to fluid sequestration by traumatized or infected tissues or ascites -Increased insensible losses due to hyper ventilation ,fever and sweating Ideally, all deficits should be replaced preoperatively in all patients by fluids similar to that lost

16. Surgical Fluid Losses • Blood Loss : • -Measurement in surgical suction container • -Blood on surgical sponges and laparotomy pads (fully soaked sponge 4x4 hold about 10 ml blood and a soaked pad holds 100-150 ml • -Serial hematocrite or hemoglobin concentrations reflect the ratio of blood cells to plasma (Rapid fluid shift and fluid replacement affect measurements

17. Replacing Blood Loss • Ideally, blood loss should be replaced with crystalloid or colloid solutions to maintain normovolemia until the danger of anemia outweigh the risks of transfusion. • -At that point ,further blood loss is replaced with RBCs to maintain Hb concent.or hematocrite at that level. • This point corresponds to 7-10 gm Hb/dl,or hematocrit of 21-30%.

18. Replacing Blood Loss • -We give lactated ringer 3-4 times the volume lost or colloid in a 1:1 ratio until transfusion point is reached, then blood is replaced unit for unit as its lost either with whole blood or reconstituted packed RBCs. • -One unit of RBCs will increase hemoglobin 1 g/L or hematocrite 2-3% in adult and 10 ml/kg of RBCs will increase hemoglobin 3g/L and hematocrite by 10%

19. Other Fluid Losses • Evaporative fluid losses are apparent with large wound and directly proportionate to surface area exposed and duration of surgery • Internal redistribution (third spacing): • Surgical dissections, inflamed, infected or traumatized tissue can sequester large amount of fluid in its interstitial space, across serosal surface (ascites), or into bowel lumen ,which become non functioning as it does not equilibrate with the rest of extracellular compartments.

20. Replacing Redistributive & Evaporative Losses • Procedures can be classified according the degree of tissue trauma :

21. Replacement Type Solutions • *Ringer lactate solution. Its the most physiologic solution ,and it has the least effect on extra cellular fluid. • *Normal Saline .Its the preferred solution for hypochloremic metabolic acidosis and for dilution packed RBCs prior to transfusion ,when its given in large amount ,it produce dilutional hyperchloremic acidosis, as plasma Hco3 decrease as Cl- concent. Increase. • *Hypertonic 3% saline is used for severe symptomatic hyponatremia&hypovolemic shock

22. Potassium BalanceDaily Requirements 1 meq/kg/day 1 meq of K+ per inch of banana If the average person weighs 70 kg then to fulfill your necessary daily requirements you need to eat a 6 feet banana

23. Disorders Of Potassium Balance • Intracellular K is 140 meq / L • Extra cellular K is 4 meq/ L (3.5-5.5 meq/L), reflecting the balance between K intake and excretion • Extra cellular K is regulated by : 1- Cell membrane Na-K-ATPase activity . 2-Serum K determine its urinary excretion

24. Inter Compartmental shift of K • 1- PH acidosis increase serum K Alkalosis decrease serum K ( Kchanges 0.6 meq/l per 0.1 unit change in arterial PH) 2- Circulating Insulin decrease serum K 3-Sympathetic stimulation alpha stim. increase serum K B2 stim. Decrease serum K

25. Inter Compartmental shift of K 4-Hypothermia dec. serum K due to cellular uptake , Re warming reverse this shift 5- Plasma osmolality e.g. hyperglycemia ,hyper natremia , mannitol administ. Increase serum K 6- Exercise inc serum K

26. Urinary Excretion • Increased serum K leads to increased aldosteron excretion from adrenal gland leading to excretion of K Also decrease serum K decrease its excretion • Increase renal tubular flow in distal nephrone increase K secretion

27. Hypokalemia

28. Definition Normal serum potassium 3.5-5.5 mEq/L HypOkalemia is a serum potassium less than3.5mEq/L

29. Causes Of Hypokalemia • I- Inter compartmental shift : B2 agonist Alkalosis Insulin Hypothermia (transient) • 2- K Depletion: Extra renal e g diarrhea nasogastric suction Renal e g Diuretics , Mg depletion prevent reabsorption of k in renal tubule • 3-Decreased K intake

30. Clinical manifestation Of Hypokalemia • I-CVS :ECG – P wave amplitude increase Prolonged P-R interval depressed S-T segment flattened or inverted T wave prominent U wave &QRS normal

31. CVS Effects • Dysrhythmia ,myocardial dysfunction ,myocardial fibrosis in chronic hypokalemia ,orthostatic hypotension Increased digitalis toxicity • Neuromuscular : Sk ms weakness ,Ileus ,ms cramp ,tetany

32. 3- Renal : • Nephrogenic D.I leads to polyurea • Alkalosis due to inc. HCO3 re absorption • Increase ammonia production leads to encephalopathy when liver function is impaired 4- Hormonal :decrease sec of aldosteron ,insulin ,GH . 5- Metabolic : encephalopathy when liver function is impaired

33. Management of Hypokalemia • Check urine output before correction . • Oral replacement is safest if there is no serous organ dysfunction (60-80 meq/day • I.V. replacement for serous cardiac manifestation ,ms weakness or severe hypokalemia with : ECG monitoring - avoid dextrose sol. – - peripheral vein 8meq/h ,central vein 10-20 meq/h

34. Causes ofHyperkalemia • 1- Inter compartmental shift e.g. acidosis ,B blockers, tissue breakdown ,hemolysis,… • 2-Decrease renal excretion e.g. renal failure ,dec mineral corticoid activity ,K sparing diuretics ,ACEI, NSAI • 3- Increased K intake e.g. old blood transfusion, salt substitute

35. Clinical manifestation Of Hyperkalemia • I- Skeletal ms weakness not seen until serum K> 7meq/L due : - sustained depolarization - inactivation of Na channel • 2- Cardiac (when serum K>7 meq/L)

36. ECG :Loss of P wave – prolonged P-R depressed S-T segment Tall peaked T wave –Wide QRS Short q-T may progress to V.F. ,a systole accentuated by by acidosis , hyponatremia ,hypocalcaemia

37. ECG ChangesDELYED DEPOLARISATION

38. ECG ChangesVentricular Tach/Torsades

39. ECG ChangesWidening of QRS Complex

40. Management of Hyperkalemia • Stop source of K intake ,drugs contribute to hyperkalemia Mineral corticoid replacement . 1- calcium to antagonize cardiac effects 3-5 ml CaCl 10% (acts immediately) or 5-10 ml Ca gluconate 10% 2- NaHCO3 in presence of M. acidosis ( It decrease serum K within 15 minutes ) 3- Glucose & Insulin 50 gm+10 u( dec serum K 1meq/h within one h

41. Management of Hyperkalemia • 4- Low dose epinephrine 0.5-2ug/min • 5- B2 agonist • 6- Lasix diuretics • 7-Potassium exchange resins as oral or rectal sodium polysterene sulphonate • 8-Dialysis : hemodialysis is more effective than peritoneal dialysis

42. TreatmentRemoval of Potassium From the Body Hemodialysis Peritoneal Dialysis

43. بسم الله الرحمن الرحيم تحيتهم فيها سلام و آخر دعوانا أن الحمد لله رب العالمين والصلاة والسلام على أشرف المرسلين سيدنا محمد وعلى اله وصحبه أجمعين اشكركم واستودعكم الله الذى لاتضيع ودائعه والسلام عليكم ورحمة الله وبركاته