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Fluid and electrolyte in surgical patients
This document discusses fluid and electrolyte balance, with an emphasis on surgical patients. It covers topics like total body water, fluid compartments, electrolyte composition and balance, osmotic pressure, factors that can disturb fluid and electrolyte balance like volume deficits or excesses, and management of specific issues like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, and hypocalcemia. Key points emphasized include fluid shifts between compartments, renal regulation of electrolytes, and symptoms and treatment of various electrolyte abnormalities.
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Fluid and electrolyte in surgical patients
- 1. Fluid and Electrolyte WithEmphasis On The Surgical Patient KALEAB TESFAYE MOGES
- 2. Body fluids • Waterconsists of 60% of total body weight, in healthy young male adult • Relationship of total body weight and total body water is a reflection of body fat • Lean tissue have higher water content • Muscle • Solid organs • Low water content in bone and fat • Young, lean, male => high water content • Deuterium => used for to measure TBW by dilution • Female TBW is ~ 50% b/c ↑adipose tissue and ↓muscle mass • TBW is additionally corrected by • ↓ 10-20% in obese • ↑ 10% in malnutrition • The highest TBW is in the new born=> 80%, decreases to 65% @ 1 year and remains constant
- 3. Fluid compartment • TBW= intracellular fluid + Interstitial fluid + plasma • Largest compartment is the intracellular fluid ~2/3rd (40%) of the TBWt., and the largest proportion is in skeletal muscle mass • ECF is 20% of TBWt. • Plasma 5% of TBWt. • Interstitial fluid 15%
- 4. Composition of fluidcompartments • ECF is balanced b/n • Na (the principal cation) • Cl • HCO3 • ICF is composed of • K • Mg • PO4 • SO4 • Proteins • Concentration gradient is maintained by Na/K ATPase pump • Plasma and interstitial fluid differ only in slight ionic composition, b/c of higher protein content in the plasma when compared with interstitium • Ions and protein diffusion is restricted but water diffuses freely, thus volume increment in water increases the volume of all compartments • Na is confined to the ECF and is strongly associated with water, thus administration of a Na containing fluid increases the volume of plasma and interstitial fluid(expanded 3X↑) (The principal cations) (The principal anions) (The principal anions)
- 5. Osmotic pressure • Activityof an electrolyte in a solution depend on 3 things • Number of particle/volume (mmol/L) • Number of electric charges/volume (mEq/L) • Number of ions/volume (mOsm/L) • An equivalent of an ion is calculated as, Eq = atomic weight (g)/valence • Valance is the outer shell electron of an atom • For univalent ions • Na+1 , 1mEq is equal to 1mmol • For divalent ions • Mg2+ , 1mmol is equal to 2 mEq • Movement of water depends on osmosis, water moves to achieve osmotic equilibrium on each side, and movement is determined by concentration on each side of the membrane • Osmotic pressure is measured in mOsm, which is the actual number of osmotically active particles
- 6. • Principal determinantsof osmolality are • Glucose • Na • BUN • Serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8) • Intracellular osmolality = 290mOsm and extracellular osmolality = 310mOsm • Any change in osmolality is accompanied by redistribution of water until equilibrium is achieved Osmotic pressure
- 7. Normal exchange offluids and electrolytes • Average healthy adults gets water on avg. 2000ml/d • 75% from drinking • 25% extracted from solid food • Water loss per day • 800-1200ml/d urine • 250ml/d stool • 600ml/d insensible losses • Skin 75% • Lung 25% • Insensible loss is increased by • Fever • Hypermetabolic state • Hyperventilation • Regardless of oral intake, the kidney produces 500-800ml of urine per day to excrete metabolic products • Renal Na excretion can be as low as 1mEq/d and as high as 5000mEq/d based on intake, serum concentration and plasma volume • Sweat is isotonic and has minimal Na • GIT loss is hypotonic
- 8. Classification of bodyfluid changes • 3 categories 1. Change in volume 2. Change in concentration 3. Change in composition • Though each is a separate entity can occur simultaneously • 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 • Unlike with sodium, the concentration of most other ions in the ECF can be altered without significant change, producing only a compositional change
- 9. Disturbance in fluidbalance • Extracellular volume deficit is the most common fluid disorder in surgical patients • Most common source of loss is GI • Vomiting, NG-Tube suction, enerocutanious fistula • Other causes are • Sequestration secondary to burns, peritonitis, obstruction, prolonged surgery • Acute deficit is associated with cardiovascular and CNS signs • Chronic deficit is manifested as tissue signs (decreased skin turgor, sunken eyes) as well as CVS and CNS signs • Lab • If deficit is sever enough, hemoconcentration and raised BUN b/c of decreased GFR • Urine osmolality > serum osmolality • Low urine Na < 20mEq/L • Serum sodium may be ↑,↓ or N (does not reflect volume status)
- 11. • Extracellular excessvolume can be due to • Renal cause • Iatrogenic • CHF • Cirrhosis • Both interstitial and plasma volumes are increased • Symptoms are mainly CVS and pulmonary • It may be well tolerated in healthy patients • In elderly, cardiac patients may rapidly progress in to CHF and pulmonary edema with small excess volume Disturbance in fluid balance
- 12. Volume control • Changesin volumes are sensed by • Osmoreceptors • Detect change in fluid osmolality and affect thirst and diuresis • If plasma osmolality ↑ => thirst + ↑ ADH => correction of osmolality • Baroreceptors • Detect change in pressure and volume • Alter sodium excretion and free water reabsorption Change in concentration • Changes in serum sodium concentration are inversely proportional to TBW. Therefore, thus changes in TBW are reflected by abnormalities in serum Na levels.
- 13. Hyponatremia • Can occurwith • Normal ECF • Low ECF • High ECF • Most cases are due to • Dilution • Secondary to excessive ECF • High ECF from • PO intake • IV • Increased ADH, specially immediate post op patients, usually self limiting • Drugs causing water retention, Tricyclic antidepressants, ACE inhibitors (elderly are more susceptible) • P/E are usually normal and lab shows hemodilution • Depletion • Can be due to • Increased loss • Diuretics or primary renal diseases • Decreased intake • Low Na diet, enteral feeding, GI loss (vomiting, NG-T suction, diarrhea)
- 14. • Hyperglycemia andmannitol can lead to hyponatremia • b/c glucose has extracellular osmotic force causing shift of water towards ECF => dilution • For every 100mg/dL ↑ in serum glucose Na ↓ by 1.6mEq/L • High levels of plasma lipids and protein can lead to pseudohyponatremia • On evaluation • 1st exclude hyperosmolar states • Mannitol, hyperglycemia, pseudohyponatremia • Depletion Vs Dilution • Urine Na <20mEq/L => depletion • Urine Na >20mEq/L • Dilutional is usually with hypervolemia • SIADH is usually associated with normovolumia • With normal RFT symptoms don’t occur till <120mEq/L Hyponatremia
- 15. Management • Most canbe managed with free water restriction if mild, sodium administration if sever • If neurological symptoms occur • 3% NS should be given • Correction rate should not exceed >1mEq/L per hour until serum Na 130mEq/L or resolution of neurologic symptoms • If asymptomatic • Correction rate should not be >0.5mEq/L per hour (12mEq/day) • If chronic • Less than 0.5mEq/L • Rapid correction will lead to pontine myelinolysis • Seizure, focal deficit, akinetic movement and unresponsiveness • Can progress to permanent brain damage and death • Serial MRI to confirm Hyponatremia
- 16. Hypernatremia • Secondary to •Loss of free water • ↑Na gain • It can occur with • Normal ECF • Causes • Diabetes insipidus • Diuretics • Non renal water loss (GI, skin) • Low ECF • High ECF • causes • Administration of sodium containing fluids • Hyperaldosteronism • Cushing’s syndrome • Congenital adrenal hyperplasia • Urine sodium>20mEq/L and urine osmolality > 300mOsm/L
- 17. Hypernatremia • Symptomatic hypernatremiaoccurs in • Impaired thirst • Water restriction • Symptoms are rare until >160mEq/L, but once present related to significant morbidity and mortality • CNS is the most affected, b/c of hyperosmolar nature of the disease water shifts out of the cell => leading to cellular dehydration=> traction on cerebral vessels and lead to subarachnoid hemorrhage • Classic sign of hypovolemic hypernatremia • Tachycardia + orthostasis + hypotension (what makes it a classic feature?)
- 18. Hypernatremia management • Mainlymanagement of water deficit with NS • Once volume is restored then replace the rest with hypotonic solutions • 5% dextrose • 5% dextrose in 1/4th NS • PO water • Formula to calculate water requirement to correct hypernatremia • Rate of correction should not be above • 1 mEq/L/hr. or 12mEq/L/Day (for acute) • 0.7 mEq/L/hr. (for chronic) • If chronic hypernatremia is rapidly corrected • Cerebral edema and herniation • Carful when hydrating with 5% dextrose in water b/c of rapid correction
- 19. Potassium • Average intake50-100mEq/d • Extracellular K is strictly monitored within a narrow range, mainly by renal excretion of potassium • Renal potassium excretion can range from 10-700mEq/d • Only 2% of total body potassium is extracellular • Intra cellular and extracellular potassium distribution is influenced by • Surgical stress • Acidosis • Tissue catabolism
- 20. Hyperkalemia • >5.5 mEq/L,sever > 6 mEq/L • Causes • Increased intake • Oral or IV or post transfusion (RBC lysis) • Increased K release from cells • Hemolysis, rhabdomyolysis, crush injury • Hyperglycemia, mannitol can cause shift of potassium to the ECF • Impaired excretion • AKI • Potassium sparing diuretics • Miscellaneous medications associated with hyperkalemia • NSAIDs, spironolactone, ACEI • b/c 98% of total body potassium is intracellular, small shift to plasma will lead to significant rise in level.
- 21. • Symptoms aremainly • GI • N and V, intestinal colic and diarrhea • Cardiac • ECG changes :- peaked T wave (early sign), wide QRS, flat P wave, prolonged PR interval (1st degree block) , ventricular fibrillation • Neuromuscular • Range from mild weakness to ascending paralysis and respiratory failure Hyperkalemia
- 22. • 3 components 1.Potassium removal • Kayexalate => potassium binding resin in exchange for Na, PO or IV • Thiazide diuretics • Dialysis 2. Potassium shift • Dextrose and insulin • 10 units of regular insulin in 500 mL of 10% dextrose, given over 60 minutes or • 10 units of regular insulin, followed immediately by 50 mL of 50% dextrose • To prevent hypoglycemia Pt. can be put on maintenance 10% dextrose • This lowers serum potassium by 0.5 – 1.2 mEq/L • Selective Beta agonists (Albuterol) • Given as 10 to 20 mg in 4 mL of saline by nebulization over 10 minutes • This lowers serum potassium by 0.5 – 1.2 mEq/L • Albuterol and insulin => will have additive effect and lower serum potassium 1.2 – 1.5 mEq/L • Sodium bicarbonate • ↑ pH => Hydrogen shift extracellularly and potassium shift intracellularly, has limited efficacy and not used alone 3. Cardiac protection (should be the 1st stape) • calcium gluconate is 1000 mg (10 mL of a 10 percent solution) infused over two to three minutes, • Remove potential exogenous source should be removed Hyperkalemia management
- 23. Hypokalemia • More commonthan hyperkalemia in surgical patients • Mild 3.0 – 3.4mEq/L , sever <2.5 mEq/L • Caused by • Inadequate intake • Increased loss • GI loss => diarrhea, vomiting, fistula, NG-T suction • Intracellular shift • Associated with alkalosis • For every 0.1↑ in pH => there is a 0.3 mEq/L↓ in potassium • Miscellanies drugs • Amphotericin, aminoglycosides • Symptoms are • GI • Ileus, constipation • Skeletal muscle • Weakness, ↓DTR • Cardiac • ECG changes => U waves, flat T waves ST segment changes and arrhythmia
- 24. • Management ispotassium replacement • Severe hypokalemia • IV infusion 40-60 meq of elemental potassium, in 1000ml Normal saline, 6-8 hours. • Use non dextrose containing fluids • Maximum concentration of potassium is 60meq in one liter of fluid • Maximum rate of infusion (in the presence of perfuser machine) is 10meq/hour PLUS Potassium chloride, 600mg P.O, (8 mEq of potassium) 2-3tabs, 3-4 times/day. • Mild to moderate hypokalemia • Potassium chloride, 600mg P.O, (8 meq of potassium) 2-3tabs, 3-4 times/day Hypokalemia
- 25. Calcium • 99% foundin the bone matrix, <1% found in the ECF • Daily intake 1-3g, most is excreted by the bowel and small amount in the urine • Serum calcium is distributed in the ECF in 3 forms • Ionized 50% • The only fraction that is responsible for neuromuscular action and measurable directly • Protein bound 40% • Complexed with phosphate and other ions 10% • Relationship of calcium (total) and albumin • For every 1g/dL ↓in serum albumin => there is a 0.8mg/dL ↓ in serum calcium • Relationship of pH and ionized calcium • Acidosis will ↓ protein binding => ↑ ionized calcium
- 26. Hypercalcemia • Total >10.5mEq/L • Ionized > 4.8 mg/dL • Causes • Hyperparathyroidism • Hypercalcemia of malignancy • Osteolytic metastasis • Paraneoplastic syndrome • Symptoms • Neurological • Musculoskeletal • GI • Renal • Cardiovascular • ECG => short QT, prolonged PR, prolonged QRS flat T-wave, AV block
- 27. • Management requiredwhen • Symptomatic, which usually occurs @ serum level > 12mg/dL • Critical level > 15mg/dL => may rapidly deteriorate => death • Management is mainly hydration Hypercalcemia
- 28. Hypocalcemia • Total <8.5 mEq/L • Ionized < 4.2 mg/dL • Causes • Pancreatitis • Massive soft tissue infections • Renal failure • Pancreatic and small bowel fistula • Hypoparathyroidism • Toxic shock syndrome • Magnesium abnormalities • Tumor lysis syndrome => hyperphosphatemia • Osteoblastic metastasis • Massive blood transfusion => citrate binding of calcium • Hyperproteinemia • Unlikely to be secondary to decreased intake b/c of massive storage in the bone able to maintain normal level for prolonged periods
- 29. • Asymptomatic hypocalcemiacan be secondary to hyperproteinemia • Symptoms can develop with normal calcium level • Alkalosis => decreases the ionized calcium • Symptoms do not occur until ionized < 2.5mg/dL • Symptoms • Paranesthesia of the face, extremities • Muscle crams • Carpopedal spasm • Stridor • Tetany • Seizure • Signs • ↑ DTR • Chvostek’s sign (spasm resulting from tapping over the facial nerve) • Trousseau’s sign (spasm resulting from pressure applied to the nerves and vessels of the upper extremity with a blood pressure cuff) • ECG • Prolonged QT, T-wave inversion, heart block and ventricular fibrillation Hypocalcemia
- 30. Management of hypocalcemia •IV calcium • Indications • Acutely symptomatic • Serum calcium ≤7.5 mg/dL • Dose • 1 to 2 g of calcium gluconate (equivalent to 90 to 180 mg elemental calcium), in 50 mL of 5 % dextrose can be infused over 10 to 20 minutes • Should be given slowly b/c risk of cardiac dysfunction (systolic arrest) • This dose increase serum calcium for 2-3 hours, thus should be followed by maintenance • Gluconate is preferable b/c less likely to cause tissue necrosis • Maintenance • 11 g of calcium gluconate (equivalent to 990 mg elemental calcium) to NS or 5 % DW to provide a final volume of 1000 ml. This solution is administered at an initial infusion rate of 50 mL/hour
- 31. • PO calcium •For pt with mild hypocalcemia • asymptomatic • Serum 7.5-8 mg/dl • 1.5-2 g of elemental calcium • Hypocalcemia will be refractory unless coexisting hypomagnesemia is not corrected first • Also consider changes in pH and potassium • Calcium supplementation is not routinely done with massive transfusion
- 32. Magnesium • 4th mostabundant mineral in the body, Avg. dietary intake20mEq/d, excreted in urine and feces • Physiologically important b/c it is essential for function of many enzymes • Kidney can conserve magnesium excretion, <1mEq/day, and it is the primary responsible organ for magnesium homeostasis • Primarily intracellular • 50% (2000 mEq) of total Mg is found in bone • The other 50% is found as • 1/3rd is found bound to albumin (affected in hyperproteinemia) • When treating hypomagnesemia, replacement should be given until upper limit of normal
- 33. Hypermagnesemia • Rare • Causesinclude • Sever renal insufficiency • Magnesium containing drugs • Anti-acids • Laxatives • Excess intake • TPN • Massive trauma • Thermal injury • Acidosis • Clinical • GI • N and V • Neuromuscular • Weakness, lethargy and ↓DTR • Cardiac • Decreased cardiac conduction => hypotension and arrest • ECG => similar signs as to hyperkalemia
- 34. • Remove exogenoussource • Correct volume deficit • Correct acidosis • Is acutely symptomatic => calcium chloride 5-10ml to antagonize CVS effects • If elevated serum level or symptom persist => dialysis is indicated Hypermagnesemia management
- 35. Hypomagnesemia • Can becaused by • Poor intake • Starvation • Alcoholism • Prolonged IV fluid therapy • TPN with inadequate Mg supplementation • Renal excretion • Alcohol abuse • Diuretics • Amphotericin B • 1° aldostronism • Pathologic loss • Diarrhea • Malabsorption • Acute pancreatitis • Magnesium depletion is characterized by • Neuromuscular and CNS hyperactivity
- 36. • Symptoms aresimilar to hypocalcemia • ↑DTR, Chvostek’s sign, Trousseau’s sign • ECG => prolonged QT, prolonged PR, ST segment depression, flat/inverted P wave, Torsades de pointes and arrhythmia • When hypomagnesemia is present with hypokalemia/hypocalcemia, hypomagnesemia should be treated first and aggressively Hypomagnesemia
- 37. Hypomagnesemia • Asymptomatic/mild =>oral • Sever deficit <1mEq/L or symptomatic • 1-2g magnesium sulfate IV over 15min. With ECG monitoring, can be given within 2 min, if Thorsades de pointes is present • Simultaneous administration of calcium gluconate will counter act the ADRs of rapid magnesium sulfate administration as well as correct hypocalcemia which is often present
- 39. Acid-Base balance Normal Acid-Basehemostasis • Systemic pH is maintained b/n 7.35-7.45 • This is maintained by extracellular and intracellular buffers and reparatory and renal regulation • The control of arterial CO2 tension (Paco2) by the CNS and respiratory system and the control of plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali • Henderson- Hasselbalch equation • Metabolic and reparatory components regulating pH • Under most circumstances, CO2 production and excretion are matched, and the usual steady- state Paco2 is maintained at 40 mmHg • ↓CO2 excretion => hypercapnia • ↑CO2 excretion => hypocapnia • But levels will continue to be regulated neural respiratory centers • Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production • Increases or decreases in Paco2 represent • Abnormalities in neural respiratory control • compensatory changes in response to a primary alteration in the plasma HCO3
- 40. Renal tubular acidosis •Clinical syndrome characterized by • Metabolic acidosis from defect in renal tubular hydrogen secretion/bicarbonate absorption • b/c bicarbonate is freely filtered at the glomeruli and to balance this the proximal tubule must resorbe or regenerate the bicarbonate • Type I (Distal) • Most common form of RTA (70%) and associated with stone formation • dysfunction of the α-type intercalated cells, which secrete protons into the urine via an apical Hydrogen ATPase • Symptoms of nephrolithiasis lead to initial Dx • Characterized by inability to acidify the urine with systemic acidosis, failure to decrease urine pH below 5.5 • Present as nephrolithiasis in an adult • FTT, vomiting and diarrhea in children • Most common stone is calcium phosphate b/c of Hypercalciuria, hypocitraurea and increased urine pH • Profound hypocitraturia, perhaps the most important factor in stone formation, due to impaired citrate excretion as a result of metabolic acidosis • The classic findings include hypokalemic, hyper-chloremicnon metabolic acidosis along with nephrolithiasis, nephrocalcinosis, and elevated urine pH (>6.0).
- 41. • Type II(Proximal) • Characterized by defect in