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Body Fluids & Fluid Management in Surgical Patients

Raed Al-Taher, MD r.altaher@ju.edu.jo. Body Fluids & Fluid Management in Surgical Patients. tiny.cc/ raedlectures. Dear attendees, please: Confirm your attendance using your mobile phones through this link.. t iny.cc/ raedlectures. INTRODUCTION.

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Body Fluids & Fluid Management in Surgical Patients

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  1. Raed Al-Taher, MD r.altaher@ju.edu.jo Body Fluids & Fluid Management in Surgical Patients tiny.cc/raedlectures Dear attendees, please: • Confirm your attendance using your mobile phones through this link.. tiny.cc/raedlectures

  2. INTRODUCTION Changes in both fluid volume and electrolyte composition occur: • preoperatively • intraoperatively • postoperatively • in response to trauma • In response to sepsis We need to suspect and monitor these changes.. And manage them.

  3. BODY FLUIDS

  4. Total Body Water (TBW) • Males: ≈60% of total body weight.

  5. Total Body Water (TBW) • Females: ≈50% of total body weight. ( adipose tissue |  muscle mass) • Lean tissues (as muscle and solid organs) have higher water content than fat and bone.

  6. Obese individuals:  10-20% Malnourished individuals:  10% Newborns: ≈80% (the highest) ( to ≈65% by 1 year of age)

  7. Fluid Compartments Plasma + ISF = Extracellular Fluid mostly in skeletal muscle mass

  8. How to measure Fluid Compartments? • ECF: • Using indicator dilution methods. • Distribution volumes of NaBr and radioactive sulfate. • ICF: • Determined indirectly • ICF = TBW - ECF

  9. Composition of Fluid Compartments • ECF compartment: • balanced between.. • Sodium (Na+) (principal cation) • Chloride (Cl-) and bicarbonate (HCO3-) (principal anions) • ICF compartment: • composed primarily of.. • Potassium (K+ ) and magnesium (Mg2+) (cations) • Phosphate (PO43-) and sulfate (SO42-) (anions) • Organic acids & proteins (organic anions)

  10. Composition of Fluid Compartments The concentration gradient between compartments is maintained by.. ATP–driven Na+-K+ pumps (within the cell membranes)

  11. Composition of Fluid Compartments Plasma and ISF differ only slightly in ionic composition Gibbs-Donnan equilibrium Proteins  osmolality of plasma

  12. Composition of Fluid Compartments • Sodium (Na+) • confined to the ECF compartment • remains associated with water (due to its osmotic and electrical properties) • Sodium-containing fluids • distribute throughout the ECF • add to the volume of both the intravascular and interstitial spaces • expands the interstitial space by ≈3 times as much as the plasma

  13. Osmotic Pressure • Physiologic activity of electrolytes in solution depends on: • number of particles per unit volume (mmol/L) • number of electric charges per unit volume (mEq/L) • number of osmotically active ions per unit volume (mOsm/L) • Equivalent = atomic weight (g)/valence • Univalent ions (as Na+): 1 mEq is the same as 1 mmol. • Divalent ions (as Mg2+): 1 mmol equals 2 mEq. • Number of milliequivalents of cations must be balanced by the same number of milliequivalents of anions. • Movement of water across a cell membrane depends primarily on osmosis. • To achieve osmotic equilibrium, water moves across a semipermeable membrane to equalize the concentration on both sides. • Osmotic pressure (in mOsm): refers to the actual number of osmotically active particles. • For example, 1 mmol of sodium chloride contributes to 2 mOsm (one from sodium and one from chloride).

  14. Osmotic Pressure Principal determinants of osmolality are the concentrations of sodium, glucose, and urea (BUN): Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8) Osmolality of the ICF and ECF is maintained between 290 and 310 mOsm in each compartment. Because cell membranes are permeable to water, any change in osmotic pressure in one compartment is accompanied by a redistribution of water until the effective osmotic pressure between compartments is equal. For example, if the ECF concentration of sodium increases, there will be a net movement of water from the intracellular to the extracellular compartment (and vice versa). For practical clinical purposes, most significant gains and losses of body fluid are directly from the extracellular compartment.

  15. BODY FLUID CHANGES

  16. Normal Exchange of Fluid and Electrolytes • Healthy person consumes an average of 2000 mL of water per day. • Daily water losses include: • 800 to 1200 mL in urine • 250 mL in stool • 600 mL in insensible losses (skin 75% | lungs 25% |  by fever, hypermetabolism, and hyperventilation)

  17. Normal Exchange of Fluid and Electrolytes • Sensible water losses: • as sweating or pathologic loss of GI fluids • vary widely • include the loss of electrolytes as well as water • Sweat is hypotonic  sweating usually results in only a small sodium loss • GI losses are isotonic to slightly hypotonic  contribute little to net gain or loss of free water  appropriately replaced by isotonic salt solutions

  18. Classification of Body Fluid Changes disturbances in volume disturbances in concentration disturbances in composition

  19. Disturbances in Fluid Balance Isotonic gain or loss of salt solution results in extracellular volume changes, with little impact on intracellular fluid volume. If free water is added or lost from the ECF, water will pass between the ECF and intracellular fluid until solute concentration or osmolarity is equalized between the compartments.

  20. Disturbances in Fluid Balance Volume deficit: • Extracellular volume deficit is the most common fluid disorder in surgical patients • Acute volume deficit: • associated with cardiovascular and CNS signs • Chronic volume deficit: • display tissue signs ( skin turgor | sunken eyes) • cardiovascular and CNS signs

  21. Disturbances in Fluid Balance • Lab. Ex: •  BUN (due to  GFR and hemoconcentration) • Urine osmolality > serum osmolality •  Urine sodium (<20 mEq/L) • Serum sodium: • does not necessarily reflect volume status • may be high, normal, or low

  22. Disturbances in Fluid Balance • Common causes of volume deficit in surgical patients: • Loss of GI fluids (most common) • Nasogastric suction • Vomiting • Diarrhea • Enterocutaneous fistula • Sequestration of fluids secondary to: • Soft tissue injuries • Burns • Intra-abdominal processes (as peritonitis, obstruction, or prolonged surgery)

  23. Disturbances in Fluid Balance Volume excess: • Extracellular volume excess: • Iatrogenic • Secondary (renal dysfunction, CHF, or cirrhosis) • Symptoms: • Fit patients: edema and hyperdynamic circulation (well tolerated) • Elderly and patients with cardiac disease: may develop CHF and pulmonary edema

  24. Volume Control • Volume changes are sensed by both osmoreceptors and baroreceptors. • Osmoreceptors: • Specialized sensors that detect even small changes in fluid osmolality • Drive changes in thirst and diuresis through the kidneys • Ex.: when plasma osmolality is increased, thirst is stimulated and water consumption increases [Hypothalamus is also stimulated to secrete vasopressin , which increases water reabsorption in the kidneys] • Baroreceptors: • Specialized pressure sensors located in the aortic arch and carotid sinuses • Respond to changes in pressure and circulating volume • Their responses are both: • Neural (sympathetic and parasympathetic pathways) • Hormonal (renin-angiotensin, aldosterone, atrial natriuretic peptide, and renal prostaglandins)

  25. Concentration Changes Changes in serum sodium concentration are inversely proportional to TBW.  TBW :  serum Na+ concentration  TBW :  serum Na+ concentration

  26. Hyponatremia • A low serum sodium level (due to sodium depletion or dilution) • There is an excess of extracellular water relative to sodium. • Extracellular volume can be high, normal, or low. • Dilutional hyponatremia: • From excess extracellular water • Associated with a high extracellular volume status • Excessive oral water intake • Iatrogenic IV excess free water administration • ADH secretion in postoperative patients ( reabsorption of free water from the kidneys) – self limiting • Drugs (cause water retention): as antipsychotics, TCAs, and ACE inhibitors

  27. Hyponatremia • Depletional hyponatremia (concomitant ECF volume deficit is common): • Decreased Na+ intake: • Consumption of a low-sodium diet • Use of enteral feeds low in sodium • Increased loss of sodium-containing fluids • GI losses (vomiting, prolonged NG suctioning, or diarrhea) • Renal losses (diuretic use or primary renal disease) • Hyperosmolar hyponatremia • Untreated hyperglycemia (corrected sodium concentration should be calculated) • Mannitol administration Every 100 mg/dL plasma glucose above normal ----------------------- Plasma sodium decrease by 1.6 mEq/L

  28. Hyponatremia • Pseudohyponatremia: • Due to extreme elevations in plasma lipids and proteins • There is no true decrease in extracellular sodium relative to water

  29. Hypernatremia • Results from: • Loss of free water • Gain of sodium in excess of water • Can be associated with an increased, normal, or decreased extracellular volume: • Hypervolemic hypernatremia: • Urine sodium concentration is typically >20 mEq/L • Urine osmolarity is >300 mOsm/L • Hypovolemic hypernatremia: • Urine sodium concentration is <20 mEq/L • Urine osmolarity is <300 to 400 mOsm/L

  30. Mx of Hypernatremia Treatment of hypernatremia usually consists of treatment of the associated water deficit. In hypovolemic patients, volume should be restored with normal saline before the concentration abnormality is addressed. Once adequate volume has been achieved, the water deficit is replaced using a hypotonic fluid such as 5% dextrose, 5% dextrose in ¼ normal saline, or enterally administered water.

  31. Mx of Hypernatremia The amount of water required to correct hypernatremia is: Slower correction should be undertaken (rapid correction can lead to cerebral edema and herniation) Hypernatremia is less common than hyponatremia (but has a worse prognosis)

  32. Mx of Hyponatremia Can be treated by free water restriction and, if severe, the administration of sodium. Rapid correction of hyponatremia can lead to pontine myelinolysis, with seizures, weakness, paresis, akinetic movements, and unresponsiveness, and may result in permanent brain damage and death.

  33. Potassium Abnormalities Average dietary intake of potassium is ≈ 50 to 100 mEq/d (excreted primarily in the urine) Extracellular potassium is maintained within a narrow range (principally by renal excretion) Only 2% of the total body potassium is located within the extracellular compartment (critical to cardiac and neuromuscular function) Minor changes can have major effects on cardiac activity

  34. Hyperkalemia • Serum potassium concentration above the normal range of 3.5 to 5.0 mEq/L • Causes: • Excessive potassium intake (oral or IV) • Increased release of potassium from cells: • Red cell lysis after transfusion • Hemolysis • Rhabdomyolysis • Crush injuries • Acidosis • Rapid rise in extracellular osmolality from hyperglycemia or IV mannitol • Impaired potassium excretion by the kidneys (acute and chronic renal insufficiency) • Drugs: • Potassium-sparing diuretics (spironolactone) • ACE inhibitors • NSAIDs • Small shifts of intracellular potassium out of the intracellular fluid compartment can lead to a significant rise in extracellular potassium.

  35. Hypokalemia • Much more common than hyperkalemia in the surgical patient. • Causes: • Inadequate potassium intake • Excessive renal potassium excretion (due to Mg2+ depletion) • Potassium loss in pathologic GI secretions (diarrhea, fistulas, vomiting, or high NG output) • Intracellular shifts from metabolic alkalosis or insulin therapy • The change in potassium associated with alkalosis: Potassium decreases by 0.3 mEq/L for every 0.1 increase in pH above normal • Drugs that induce magnesium depletion cause renal potassium wastage (such as amphotericin, aminoglycosides, cisplatin, and ifosfamide)  potassium repletion is difficult unless hypomagnesemia is first corrected.

  36. Hypokalemia Drugs that induce magnesium depletion cause renal potassium wastage. Such as amphotericin, aminoglycosides, cisplatin, and ifosfamide. Potassium repletion is difficult unless hypomagnesemia is first corrected.

  37. ECG changes • Hyperkalemia: • High peaked T waves (early) • Widened QRS complex • Flattened P wave • Prolonged PR interval (first-degree block) • Sine wave formation • Ventricular fibrillation • Hypokalemia: • U waves • T-wave flattening • ST-segment changes • Arrhythmias (with digitalis therapy)

  38. Mx of Hyperkalemia • Exogenous sources of potassium should be stopped • Kayexalate(cation-exchange resin): binds potassium in exchange for sodium • Shifting potassium intracellularly: • glucose (& insulin) infusion • bicarbonate infusion • nebulized albuterol (10 to 20 mg) • Calcium chloride or calcium gluconate (5–10 mL of 10% solution | when ECG changes are present | to counteract the myocardial effects of hyperkalemia) [All of the aforementioned measures are temporary, lasting from 1 to ≈4 hours] • Dialysis(in severe hyperkalemia when conservative measures fail)

  39. Mx of Hypokalemia Oral repletion: for mild, asymptomatic hypokalemia Caution should be exercised when oliguria or impaired renal function is coexistent

  40. Calcium Abnormalities • The vast majority of the body’s calcium is contained within the bone matrix (<1% found in the ECF) • Serum calcium (three forms): • Protein bound (40%) • Complexed to phosphate and other anions (10%) • Free ionized (50%)  responsible for neuromuscular stability and can be measured directly • Changes in albumin concentration will affect total serum calcium measurement: • Adjust total serum calcium down by 0.8 mg/dL for every 1 g/dL decrease in albumin. • Changes in pH will affect the ionized calcium concentration: • Acidosis -  protein binding -  ionized fraction of calcium.

  41. Calcium Abnormalities • Daily calcium intake is 1 to 3 g/day. • Mostly excreted via the bowel • Little by urinary excretion • Total body calcium balance is under complex hormonal control.

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