ELECTROLYTES AND SURGERY

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ELECTROLYTESAND SURGERY

• J.D. YELLE M.D.

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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
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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

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Intracellular fluid

• Largest proportion is in skeletal muscle mass
• Potassium, magnesium are principal cations
• Phosphate, proteins are principal anions

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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.

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• 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

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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.

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Causes of ECF volume depletionGI losses
vomiting, diarrhea, naso-gastric suction, fistula
drainage, Diuretics, renal or adrenal
disease,Sequestration of fluid (ileus, burns,
peritonitis)Signs and SymptomsDepend 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.RxReplace water, electrolytes
lostAssess weight daily, further losses, serum
electrolytesCentral monitoring if severe
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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

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SODIUM

• HYPONATREMIA
• altered relation of TBW to sodium
• altered distribution of body water due to osmotic
  effects
• 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)

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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.

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• 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

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• 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.

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2)Hyponatremia with normal plasma osmolality

• or pseudohyponatremia
• severe hyperlipidemia and hyperproteinemia
• Na concentration and osmolality in plasma water
  are normal
• no specific therapy

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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.

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Low Sodium Syndromes
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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

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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

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• Above Normal
• Serum K raise proportionately
• Below normal
• A decrease in serum K is not proportional

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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 hr6
• may be given by dialysis

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4 to 3 100-200 meq/l 3 to 2.5 100-200 meq/l
per 0.25
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HYPERKALEMIA

• Cause
• 1)decreased renal excretion acute renal
  failure, Addisons 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

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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 BHCO3/H2O CO2
• 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 CO2 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

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METABOLIC ACIDOSISAnion gap

• Accumulation of acid due to ingestion, endogenous
  production, or from loss of alkali
• Anion gap AG Na - (C1- HCO3) 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

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• 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 Ringers
  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.
• H2CO3 H º H2CO3 º CO2 H2O accumulation
  of CO2
• Dx low pH, low bicarb, compensatory response is
  decreased CO2
• Treatment - depends on underlying aetiology
• Acute Treat pH less than 7.2
• Calculate Bicarb deficit
• HCO3 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

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METABOLIC ACIDOSIS

• Treatment - depends on underlying etiology
• Acute Treat pH less than 7.2
• Calculate Bicarb deficit
• HCO3 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,.

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METABOLIC ALKALOSIS

• Hydrogen loss
• Gastrointestinal
• C Renal
• Diuretics
• Mineralocorticoid excess
• Hypercalcemia
• Penicillins
• Bartters 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

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• 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

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• 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)

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RESPIRATORY ACIDOSIS

• Hypoventilation
• Decreased pH, elevated pCO,
• compensatory response is increase bicarb to
  distinguish acute from chronic
• Acute
• HCO3- should rise by 1 meq/l for 10 mm of PCO2
• Chronic
• HCO3- should rise by 4 meq/l for 10 mm of
  PCO2
• Rx correct ventilation

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RESPIRATORY ALKALOSIS

• Increased rate of pulmonary excretion of CO2
• Cause
• anxiety, sepsis, salicylates, hypoxemia, lung
  disease, excessive ventilation, CNS injury, etc.
• Decreased pCO2, 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.

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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

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FLUID ORDERSMaintenance

• 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

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FLUID ORDERSElectrolytes

• 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

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FLUID ORDERSAnticipated 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.

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DEHYDRATION

• Mild dehydration loss of 4 body weight
• Hematocrit, protein,
• Dry skin
• Urine osmolality 500-700 mOsm/l SG
  1.020-1.025
• Serum osmolality W or
• Moderate dehydration 6 Above and dry tongue
• Dry axilla, groins
• Urine osmolality 700-900 mOsm/l SG 1.025- 1.030
• Severe dehydration 8 , Above
• Soft globe, weakness, hypotention, lethargy,
  ileus
• Urine osmolality 900-1240 mOsm/l SG 1.030-1.036
• Shock gt 8

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