Presentation on theme: "ELECTROLYTES AND SURGERY J.D. YELLE M.D.. BODY FLUID COMPARTMENTS Dependant on body size, weight, sex: – –constant for an individual total body water."— Presentation transcript:
BODY FLUID COMPARTMENTS Dependant on body size, weight, sex: – –constant for an individual total body water Dependents on lean body mass – – fat contains less water: means that obese person may have 20-30% less water lower % of TBW in females % of water from total body weight in adult male : 60% % of water from total body weight in adult female : 50% – –decreases in elderly: 52% males; 47% females – –highest proportion in newborns – –( first 2-3 years of age)maximum 75-80% – – at one year TBW 65% of body weight +/- 15%
Three Functional Compartments Intracellular water – –30-40% of body weight (40% X 70 kilogram = 28 liters) – –Water within cell and water in cell membrane Extracellular water – –20% of body weight (20% X 70 kilogram = 14.0 liters) -5%-7% Intravascular fluid (plasma) = 3.5 liters -15% Interstitial fluid =10.5 liters Fluid transport times I.V. 15-30 minutes equilibration time between plasma and ICF
Intracellular fluid Largest proportion is in skeletal muscle mass Potassium, magnesium are principal cations Phosphate, proteins are principal anions
Extracellular fluid Nonfunctioning component: connective tissue, bone, cartilage, cerebrospinal fluid, synovial fluid; this is 10% of interstitial volume Sodium is principal cation Chloride, bicarbonate principal anions SODIUM is the most osmotic active particle; – –most important determinant of ECF volume. Abnormalities of ECF volume regulation are due to net gain, loss of sodium and accompanying gain or loss of water.
Important Principles – –A. All metabolic processes are intracellular » »Solute provided to internal milieu of cell, i.e. ICF, via transport through ECF – –B. Extracellular » »(plasma ICF ) equilibration times are rapid, both for fluid and solute » »ECF ICF (equilibration times are slower and variable » »Glucose is rapid vs K + is slower
ECF VOLUME DEPLETION occurs when losses of both water and sodium occur most common fluid disorder in surgical patient composition of fluid loss will determine clinical picture – –...isonatremic losses will change the osmolality of ECF little therefore ICF volume will change minimally – –...hypotonic losses will cause loss from both ECF and ICF as water equilibrates across cell membrane, therefore larger volumes will be required to produce clinical signs than with loss of isotonic fluid.
Causes of ECF volume depletion GI losses: vomiting, diarrhea, naso-gastric suction, fistula drainage, Diuretics, renal or adrenal disease, Sequestration of fluid (ileus, burns, peritonitis) Signs and Symptoms Depend on volume and osmolality anorexia, nausea, vomiting, apathy, weakness, orthostatic light- headedness, syncope, weight loss, orthostatic hypotension, poor skin turgor, tachycardia, etc. Lab: Serum sodium not a good indicator; use urinary sodium, BUN/creat, rise in Hct, protein. Rx Replace water, electrolytes lost Assess: weight daily, further losses, serum electrolytes Central monitoring if severe
ECF EXCESS Often from renal sodium and water retention: CHF, nephrotic syndrome, hypoalbuminemia, renal failure, cirrhosis can be aggravated by administered salt Signs and Symptoms – –weight gain, edema (2-4 kg) retained, circulatory overload Rx – –underlying cause – –closely monitor to guide therapy, restrictions
SODIUM HYPONATREMIA 1) 1)altered relation of TBW to sodium 2) 2)altered distribution of body water due to osmotic effects 3) 3)pseudohyponatremia Assessment: – – clinical estimate of ECF volume status, – –measure plasma osmolality, – –Estimated plasma osmolality » »Osmolality (mOsm/kg) = » »2(Na(mEq/L) + K(mEq/L) + urea/2.8 + glucose/3 » »if measured is greater than 10 mOsm/kg over the estimated then there are osmotically active solutes (eg. mannitol) or pseudohyponatremia1)
1-Hyponatremia with decreased plasma osmolality » »symptomatic when serum sodium below 120-125 mEq/L; severity depends on degree of hyponatremia and rate of fall of level. Hyponatremia with ECF volume excess (renal failure, nephrotic syndrome, CHF, cirrhosis). – –Treat underlying disorder, water restriction, diuretics.
Hyponatremia with normal ECF – –SIADH: Malignant tumours, pulmonary and CNS disorders, stress – –Acute: (serum sodium less than 110-115) » »Rx - diuresis with furosemide, replace urine losses of Na and K, avoid rapid correction to greater than 130 mEq/L) – –Chronic: » »water restriction to 500-1000 ml daily,(rarely give small amounts 3% NaCl), Lithium carbonate, Demeclocycline (block ADH release) Severe Hypothyroidism: thyroxine replacement, water restriction Water Intoxication: hypotonic IV solutions, renal insufficiency. – –Treat as SIADH
Hyponatremia with decreased ECF – –Total body sodium is decreased out of proportion to water losses or sodium depletion treated with hypotonic fluid. – –Caused by » »extrarenal losses of sodium and water (vomiting, diarrhea, 3rd space). Urine sodium less than 20 mEq/L. » »renal (osmotic diuresis, salt-losing nephropathy, ATN, diuretics, hypoaldosteronism). Urine sodium greater than 20. Treat by volume reexpansion with isotonic saline and correct underlying disorder. In patients with closed head injury, mild hyponatremia may be fatal - this is the result of increased intracellular water as ECF osmolality is decreased.
2)Hyponatremia with normal plasma osmolality or pseudohyponatremia » »severe hyperlipidemia and hyperproteinemia Na + concentration and osmolality in plasma water are normal no specific therapy
3)Hyponatremia with increase plasma osmolality Accumulation of osmotically active particles in ECF (glucose, mannitol) Measured osmolality normal or elevated – –water shifts from ICF to ECF with Na dilution. Treat underlying disorder, usually hyperglycemia.
Low Sodium Syndromes Serum Na + Total body Na + ECF water Dehydration increasedecrease SIADH decreasesameincrease Water intox decreasesameincrease Na + Paradox decreasesame
HYPERNATREMIA Hypertonic ECF volume expansion or hypotonic fluid loss and ECF volume contraction replaced with inadequate amount of water or hypertonic solutions. Mental confusion, seizures, muscle irritability Sodium homeostasis is maintained normally by thirst and ADH (osmotic regulation) Water replacement/deficit: NormalBW - CurrentBW NBW = 0.6 X normal body weight CBW= Normal serum sodium X TBW/ Measured sodium Thus in a 60-kg woman with a Na+ of 168 the water deficit can be evaluate at: Water deficit= 0.6 x 60-((140X 60)/168 ) 14 L
POTASSIUM Total body potassium 30 mEq/kg or 3500 mEq Total EC K + ~ 2 % (70 kg man) = 140 mEq 98% in ICF conc. 150 mEq/L Typical diet 50-100 mEq daily, Daily needs 30-60 mEq / day – –K+ required for glucose transport and intracellular protein deposition – –Catabolism of ICF protein release K + into ECF » »1 gm prot 6 2 mEq K + ei. trauma, sepsis Sweat and stool excrete about 10 mEq daily, renal excretion regulates the balance Concentration changed by acid-base, increased ECF osmolality, insulin deficiency Fall in plasma pH - increase in serum potassium
Above Normal –Serum K+ raise proportionately Below normal –A decrease in serum K+ is not proportional
HYPOKALEMIA Serum K may not be affected until 200 mEq deficit occurs Causes: – –GI losses, urinary losses (diuretics, antibiotics, RTA etc.), – –inadequate intake (obligatory urinary losses), – –extra to intracellular shifts (acid-base changes, glucose or insulin) Signs and symptoms usually present at less than 2.5 mEq/L – –Neuromuscular: weakness, hyporeflexia, paresthesias, paralysis – –Cardiovascular: arrhythmias, increased dig sensitivity, ECG changes – –Nephropathy, glucose intolerance, – –GI abnormalities(constipation, paralytic ileus) metabolic alkalosis. Treatment:1- Correct underlying cause 2- Urine output is adequate 3- Oral, IV up to 10 mEq/hr 4- if needed more than 360 mEq/ 24 hr 6 may be given by dialysis
4 to 3 100-200 meq/l 3 to 2.5 100-200 meq/l per 0.25
HYPERKALEMIA Cause 1)decreased renal excretion; acute renal failure, Addison’s disease, etc. 2)redistribution of K + from ICF to ECF; due to acidosis, dig overdose, insulin deficiency and rapid rise in ECF osmolality 3)potassium load; supplements, blood transfusions, high-dose penicillin therapy; endogenous - tissue destruction 4)pseudohyperkalemia; blood sample clotting, haemolysis Signs and Symptoms – –when serum K greater than 6.5-7 mEq/L » » neuromuscular; weakness paresthesias, areflexia, muscular or respiratory paralysis cardiac: bradycardia, V fib, asystole, peaked T depressed ST, prolonged PR, absent P, Wide QRS, prolonged QT Therapy Always with renal failure or too rapid administration of K + - 10-20 cc 10% Calcium gluconate, Sodium bicarbonate - glucose and insulin ( 500 ml of 10% glucose with 15 U Insulin - cation-exchange resins (Kayexalate), dialysis
ACID/BASE PH is maintained within a narrow range by lungs, kidney, buffer systems – –Most important buffer is bicarbonate (significant concentration in ECF) Henderson-Hasselback Eqn. For bicarbonate/carbonic acid system; pH = pK + 1og BHCO 3 /H 2 O +CO 2 = 6.1 + ( log (27 mEq/L / 1.35mEq/L) = 20/1 = 1.3)=7.4 Add acid, bicarb will decrease, ventilation will increase to eliminate CO 2 with subsequent decrease in carbonic acid and 20/1 ratio will be reestablished. Addition of alkali has reverse effect. Resp. acidosis and alkalosis are ventilatory disturbances and compensation is renal with retention/excretion of acid salts/bicarb as required. Other buffers are phosphate, proteins, haemoglobin. – –Metabolism produces approx. 1 mEq/kg body weight daily in fixed acid – –Maximum acidification of urine by kidneys to pH of 4.5
METABOLIC ACIDOSIS Anion gap Accumulation of acid due to ingestion, endogenous production, or from loss of alkali Anion gap; AG = Na + - (C1 - + HCO 3 ) Normal = 12 +/- 4 mEq/L Increased anion gap – –renal failure, ketoacidosis, lactic acidosis, drug intoxication Normal anion gap – –loss of bicarb usually with accompanying hypokalemia; renal tubular acidosis, diarrhoea, carbonic anhydrase inhibitors – –addition of HC1 – –moderate renal insufficiency – –obstructive nephropathy – –hyporeninemic hypoaldosterone syndrome
Metabolic acidosis may develop in patient with normal kidneys whose capacity for handling chlorides is exceeded. This may occur with loss of alkaline GI fluids (biliary, pancreatic, small bowel secretions) with prolonged use of replacement fluid with inappropriate C1/bicarb ratio (eg. Normal saline). The pH change will not be corrected, and a balanced salt solution such as Ringer’s lactate is required. One of the most common causes is shock with accumulation of lactic acid. – –Vasopressors will compound problem. Infusions of bicarb. are generally futile. PH will return to normal as lactic acid is quickly metabolized. H 2 CO 3 + + H + º H 2 CO 3 º CO 2 + H 2 O : accumulation of CO 2 Dx: low pH, low bicarb, compensatory response is decreased CO 2 Treatment - depends on underlying aetiology Acute:Treat pH less than 7.2 – –Calculate Bicarb deficit – –HCO 3 deficit= Volume of distribution x deficit 70 Kg X.7( 10-6) » »Replace half the deficit in 3-4 hrs. Using 2-3 ampoules in 1L D5W » »can give 50-100 mEq over 30-60 minutes Chronic: chronic renal failure, use sodium bicarb tablets
METABOLIC ACIDOSIS Treatment - depends on underlying etiology Acute:Treat pH less than 7.2 – –Calculate Bicarb deficit – –HCO 3 deficit= Volume of distribution x deficit – –70 Kg X.7( 10-6) Replace half the deficit in 3-4 hrs. Using 2-3 ampules in 1L D5W – –can give 50-100 mEq over 30-60 minutes Chronic: chronic renal failure, use sodium bicarb tablets Lactic acidosis: treat cause,.
METABOLIC ALKALOSIS Hydrogen loss Gastrointestinal C Renal Diuretics Mineralocorticoid excess Hypercalcemia Penicillins Bartter’s syndrome C Bicarbonate retention Massive blood retention Administration of bicarbonate Milk and alkali Syndrome C Contraction alkalosis diuretics Loss of high chloride/low bicarbonate secretion C Hydrogen movement into cell Hypokalemia Refeeding
Hypochloremic hypokalemic metabolic alkalosis – –loss of fluid with high H + and C1 - conc. in relation to Na +. Loss of C1 - accelerates loss of Na + and bicarb in urine to partially compensate. Alkalosis causes excretion of K +. With progressive volume deficit K + and H + are excreted in urine to conserve Na + resulting in hypokalemia and uncompensated alkalosis. The initially alkaline urine becomes acid. Urine chloride greater than 20 mEq/L
Rx: Normal saline to restore volume, KC1 to correct hypokalemia Rx: underlying disorder, replace potassium deficit with KC1, spironolactone may be useful with mineralocorticoid excess Excess alkali administration - replace enough chloride so that kidney can absorb sodium with chloride and allow excretion of excess bicarb Severe metabolic alkalosis (pH above 7.6 and bicarb above 40-45 mEq/L may give isotonic HC1, also acetazolamide (carbonic anhydrase inhibitor 500 mg q8h)
RESPIRATORY ACIDOSIS Hypoventilation Decreased pH, elevated pCO, – –compensatory response is increase bicarb to distinguish acute from chronic Acute: – –HCO 3 - should rise by 1 meq/l for 10 mm of PCO 2 ƒ Chronic: – –HCO 3 - should rise by 4 meq/l for 10 mm of PCO 2 ƒ Rx: correct ventilation
RESPIRATORY ALKALOSIS Increased rate of pulmonary excretion of CO 2 Cause – –anxiety, sepsis, salicylates, hypoxemia, lung disease, excessive ventilation, CNS injury, etc. Decreased pCO 2, increased pH, compensation is decreased bicarb Mild resp. alkalosis occurs frequently without sign. – –Can be dangerous in patients with impaired cerebral blood flow where mild hypocapnia with cerebral vasoconstriction can cause significant damage. – –Other dangers: » »potassium depletion with risk of ventricular arrhythmias especially in digitalized patients or those with pre-existing hypokalemia; » »shift of oxygen dissociation curve to left with the result that Hgb cannot unload oxygen at tissue level.
FLUID ORDERS Pre-op – –Assess any volume or electrolyte deficits clinically and with lab data and correct. Intra-op – –Blood loss should be steadily replaced. Start at ? % of body fluid – –ECF replacement should begin with balanced salt solution. Post-op 1)deficit 2)maintenance requirements 3)anticipated losses
FLUID ORDERS Maintenance WATER – –Sensible losses; daily solute load has a minimal urinary volume for excretion. This is approx. 450 mOsm which at a urine concentration of 300 mOsm/L requires a urine volume of 1500 ml/day; feces - small (50-200 ml/day), can be ignored if not diarrhea. – –Insensible losses; from lungs and skin. Approx. 875 ml/day but range may be 500-1000 ml/day - can be up to 1500 ml/day -- these are hypotonic losses (can be replaced with D5W) Maintenance requirements are generally 2,000 - 2500 ml of fluid volume per day
FLUID ORDERS Electrolytes SODIUM – –normal daily salt intake 50-90 mEq (3-5 gm) – –excretion usually 40-200 mEq/day in urine – –maintenance requirements are met with 50-100 mEq/day POTASSIUM – –urinary excretion 40-200 mEq/day – –there is an obligatory potassium loss – –maintenance of 40-80 mEq/day will cover requirement
FLUID ORDERS Anticipated losses Ongoing ECF losses at operative site, 3rd space, interstitially GI losses (see “Volume and composition of GI secretions”) Usually isotonic or hypotonic and can be replaced vol. for vol. with isotonic solution and 40 mEq/L KC1 if renal function good.