Understanding electrolytes distribution and detection of electrolyte imbalance are important in perioperative electrolyte management.

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ANESTHESIA DEPARTMENT
Electrolyte Disorder Management, 2021
Prepared By: Kanbiro Gedeno
kanbgedeno45@gmail.com

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Introduction:
 Fluids and electrolytes are present in a number of ‘compartments’ in the body, according to their
chemical composition.
 Homeostatic mechanisms are adequate for the maintenance of electrolyte balance.
 Sodium is the most prevalent cation in the extracellular fluid (ECF) 140mmol/L, but has a typical
intracellular concentration of around 10mmol/L. In contrast, potassium is the most prevalent cation in
the intracellular fluid 150mmol/L.
 The cell membrane acts as the barrier between the potassium-rich intracellular fluid and the sodium-rich
extracellular fluid.
 Excitable cells can change their permeability to allow the influx and efflux of ions that constitute an
action potential. At rest, the large concentration gradients are maintained by the action of Na+ / K+ -
ATPase, a transmembrane protein which pumps out 3 Na+ for each 2 K+ it pumps in.
Sodium (Na):
 Major ECF Cation and regulates volume of body fluids balance.
 Needed for nerve impulse & muscle fiber transmission (Na/K pump).
 Regulated by kidneys/ hormones.
 Hormones increasing sodium reabsorption:
 RAAS=> Aldosterone: Juxtaglomerular apparatus NaCl content sensing
 ADH: Hypothalamic osmoreception
 Hormones increasing sodium excretion:
 Atrial natriuretic peptide (ANP): Atrial volume sensing
 Na+ intake is typically far in excess of minimum daily requirements: 2 to 3 mEq/kg/day at birth and
decrease to 1 to 1.5 mEq/kg/day in adulthood
 Kidney strives to achieve Na+ balance: Na+ excretion equal to Na+ ingestion.
 The kidney respond for different kinds of water and Na imbalance with different mechanisms:
 Free water challenge – diuresis
 Na load – Natriuresis
 Hyponatremia (< 135mEq/L)=> Water shifts from ECF into cells.
 Mild: 125-134mEq/L
 Moderate: 120-124mEq/L
 Sever: <120mEq/L

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 Causes of Hyponatremia:
 Assessment of serum osmolality, TBW status, and urinary Na+ concentration is vital for the accurate
diagnosis of the underlying cause of hyponatremia
 Hyponatremia can occur in patients who are: Hypotonic, Normotonic, Hypertonic
 Consider the volume status of the patient.
 Clinical Manifestations:
 Speed of onset is much more important for manifestation of symptoms than the absolute Na+
concentration.
 Nausea and vomiting, Headache,
 Muscular weakness
 CNS symptoms: serum Na+< 120meq/l
 Confusion, restlessness, dizziness, visual disturbance, Psychosis, Lethargy, Seizures, Coma,
 ECG change: occurs when Na+< 115meq/l
 Widen QRS complex, elevation of S-T segment
 Respiratory depression
 Mortality is high if untreated
 Management of hyponatremia:
 Speed of onset determines speed of correction.
 The dose of sodium required to correct a deficit may be calculated using the following formula:
o Na deficit = TBW X (desired Na – present Na)
 The optimal rate of correction to be 0.6 to 2 mmol/L/hr. until the sodium concentration is 125 mEq/L;
correction then proceeds at a slower rate
o Management of symptomatic hyponatraemia:
A. Acute hyponatraemia <48hr
 Maximum increase 2 mmol/L/hour until symptoms resolve OR
 Hypertonic saline (3%) administered at a rate of 1 to 2 mL/kg/hr for 3 to 4 hours, to increase plasma
(Na+) by 1 to 2 mEq/L/hr, through a large vein.
 If fluid excess give furosemide.
 Rapid correction can cause: central pontine myelinosis, subdural hemorrhage and cardiac failure.
 Treat the cause and consult an endocrinologist.
 Monitor Na+ levels and re-evaluate clinically.
B. Chronic hyponatraemia>48hr:
 Maximum increase 0.5 mmol/L/hour (10 mmol/day).

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 Use 0.9% normal saline, and if SIADH fluid restrict.
o Management of asymptomatic hyponatraemia:
 Treat the cause.
 Fluid restrict to 1L per day.
 Hypernatremia (>145 mmol/L): An increase in extracellular Na+.
 Low, normal, or high total-body sodium content, and water shifts from cells to ECF.
 Mild: 145 – 150 mmol/L
 Moderate: 151 - 160 mmol/L
 Severe: > 160 mmol/L
 Causes of Hypernatremia :
 Excessive loss of water, inadequate intake of water, lack of ADH, excessive intake of sodium (e.g:
solutions containing a high sodium concentration: sodium bicarbonate or hypertonic saline).
 Clinical Manifestations:
 CNS: lethargy or mental status changes, which can proceed to coma and convulsions
 Thirst, shock, peripheral edema, myoclonus, ascites, muscular tremor, muscular rigidity, hyperactive
reflexes, pleural effusion, and expanded intravascular fluid volume.
o Acute and severe hypernatremia:
 The osmotic shift of water from the cells can lead to shrinkage of the brain with tearing of the
meningeal vessels and intracranial hemorrhage.
o Slowly developing hypernatremia: is usually well tolerated because of the brain's ability to regulate its
volume
 Management of Hypernatremia
 The speed of correction depends on the rate of development of hypernatremia and associated
symptoms.
 Restore normal osmolality and volume: Removal of excess sodium by the administration of diuretics
and hypotonic crystalloid solutions.
 Sodium depletion (hypovolemia):
 Hypovolemia correction (0.9% saline)
 Hypernatremia correction (hypotonic fluids)
 Sodium overload (hypervolemia)
 Enhance sodium removal (loop diuretics, dialysis)
 Replace water deficit (hypotonic fluids)

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 Normal total body sodium (euvolemia)
 Replace water deficit (hypotonic fluids), and if there, control diabetes insipidus.
 Water deficit calculation for hypernatremia only for water loss:
o Normal TBW X Normal Na = Present TBW X Present Na
o Water deficit = Normal TBW – Present TBW
The goal rate of correction: 0.7 mmol/L/hr, and correct slowly over at least 48 hours, and the plasma (Na+)
should not be reduced by more than 1 to 2 mEq/L/hr, to prevent cerebral oedema, convulsions and central
pontine myelinolysis.
Potassium (k):
 Potassium is the most abundant Cation in the ICF and nearly 98% of total-body K is intracellular.
 Aids in muscle contraction, nerve & electrical impulse conduction, regulates enzyme activity, regulates
IC H20 content, and assists in acid-base balance.
 Daily requirements of term infant are 2 to 3 mEq/kg/day and adults 1 to 1.5 mEq/kg/day.
 Regulated by kidneys/ hormones, and inversely proportional to Na.
o In the short-term (minutes), potassium balance is influenced by:
 Potassium entry in to the cell is facilitated by:-
 Insulin and cathecolamine which can stimulate Na+/k+ ATPase, B-adrenergic agonists, metabolic-
alkalosis
 potassium exit is facilitated by:- A-adrenergic agonists and M-acidosis
o Long-term regulation of potassium excretion and balance primarily involves:
 Kidney and Aldosterone
 In response to increases in EC K levels: aldosterone is secreted from the zona glomerulosa of the adrenal
gland, acts on cortical collecting ducts to increase K secretion into the tubular fluid and increase K
excretion.
 A Normal K level is importance in the regulation of resting membrane potential of cells=> in the
resting state, cell membrane conductance is higher for potassium than for sodium.
 Alterations in EC K conc. alter the resting membrane potential, which may cause the cell to be
unresponsive or over-responsive to sodium shifts into the cell.
 Regulation transmembrane potassium gradient:
 The most important transcellular enzyme involved in potassium regulation is Na+/K+ -ATPase.
 β2-Adrenergic drugs increase the activity of Na+/K+-ATPase by binding to cell surface receptors.

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 Insulin causes more sodium to enter the cell through a Na+/H+- antiporter, which decreases
intracellular proton concentration.
 To maintain electric neutrality, any increase in sodium must occur via exchange for potassium,
decreasing extracellular potassium.
 Potassium transport is affected by pH, the body uses potassium to decrease excess EC H+ by moving
potassium out of cells and H+ into cells
 Hypokalemia ( < 3.5mEq/L):
 Mild: 3.0 – 3.5 mmol/L
 Moderate: 2.5 – 3.0 mmol/L
 Severe:< 2.5 mmol/L
 May occur because of: an absolute deficiency or redistribution into the intracellular space.
 Life threatening-all body systems affected.
 A reduction in serum K of 1mEq/L indicates a net loss of 100 to 200 mEq of K in a normal adult.
 Hypokalemia in the range of 2 to 2.5 mEq/L is likely to cause clinical manifestation.
 Surgical stress may reduce the serum potassium concentration by 0.5 mEq/L = counter balanced in
SUX induced increment 0.5 mEq/L.
 The administration of exogenous catecholamines, such as terbutaline and epinephrine also decreases
potassium levels.
 Clinical Manifestations:
 CVS:
 Cardiac dysrrythms and ECG changes: prolonged PR interval, flat or inverted T-wave, ST segment
depression, U wave elevation, atrial fibrillation and premature ventricular systoles.
 NM: Skeletal muscle weakness(hypoventilation), paralysis, tetanic
 Renal: polyuria(defect in renal concentrating ability)
 Decreased insulin, growth hormone and aldosterone secretion
 Management:
 The treatment of hypokalemia consists of potassium repletion, correction of alkalemia, and removal of
offending drugs
 If perioperative therapy is indicated, intravenous potassium chloride should be used.
 Potassium(K) deficit calculation formula:-
o K deficit (mmol) = Weight x 0.4 x (K normal lower limit – K measured).
 The rate of potassium administration is typically limited to approximately 0.5 mEq/kg/hr.

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 The typical replacement rate is 10 to 20 mEq/hr for a normal adult with constant monitoring of the
electrocardiogram.
 Safe administration of potassium is enhanced by:
 The use of continuous electrocardiogram monitoring, bedside potassium measurement, and delivery
with an infusion pump
o Mild and moderate >2meq/l
 Oral replacement safest < 200 mmol per day= typically KCl tablets (Sando-K) 2 tabs QID = 96
mmol K+.
 IV infusion of KCL<10meq/hr.
o Severe <2meq/l: associated with ECG changes and intense neuromuscular weakness, and oral
replacement not possible
 Infusion of KCL up to 20meq/hr of 40meq/l with continuous ECG monitoring.
 If treating cardiac manifestations aim for serum K+ > 4.0 mmol/L
 Correction of underlying cause, checks other electrolytes, and excludes Cushing’s and Conn’s
syndromes.
 Hyperkalemia (>5.5 mEq/L):
 Mild: 5.5 – 6.0 mmol/L
 Moderate: 6.1 – 7.0 mmol/L
 Severe: >7mmol/L
 Causes of Hyperkalemia
 In response to drugs that diminish renal potassium excretion.
 Any condition or drug resulting in adrenal inhibition or decreasing aldosterone levels can cause
potassium retention.
 Angiotensin II antagonists, angiotensin-converting enzyme inhibitors, spironolactone, Mannitol
 After sudden transcellular shifts of potassium from the intracellular fluid to the ECF.
 Potentially lethal hyperkalemia during anesthesia may occur with reperfusion of a large vascular bed
after a period of ischemia (usually >4 hours)=> Ischemia results in significant acidosis in the
affected area, which causes an outflow of intracellular potassium.
 Hyperkalemia also should be considered in the conditions with lysis of the cellular components of
blood.
 Succinylcholine, Triamterene
 The most common cause of chronic hyperkalemia occurring with anesthesia is renal failure.
 Clinical Manifestations
 Alterations in cardiac conduction increase automaticity and enhance repolarization.

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 Cardiac dysrhythmias
 ECG changes:
 5.5 to 6.5 mEq/L: Tall, peaked T waves, ST depression
 6.5 to 7.5 mEq/L: Prolonged PR interval
 Greater than 7.5 mEq/L: Widened QRS
 Greater than 9.0 mEq/L: Sine wave pattern, bradycardia, ventricular tachycardia, increased risk for
cardiac arrest are potentiated by hypocalcaemia, hyponatraemia & acidosis.
 CNS: skeletal muscle weakness, paralysis, parasthesia, confusion
 Management:
 Acute hyperkalemia is more poorly tolerated than chronic hyperkalemia.
 A patient undergoing anesthesia with even moderately elevated potassium concentration (>5.5 mEq/L)
should have continuous ECG monitoring
 If serum K+ > 6.5 mmol/L or ECG changes:
 Treat incidence of serious cardiac compromise is significant, eliminate the cause and monitor ECG
and serum K+.
 Management components:
 Physiologic antagonists: (calcium)=> Stabilizes the myocardium
 5-10mL of 10% Ca gluconate in 10 min OR 3-5 mL of 10% Ca Cl
 Agents to shift potassium into cells: (glucose, insulin, hyperventilation, bicarbonate, and β-adrenergic
agonists) => Redistribution of potassium from the plasma into cells.
 Intravenous regular insulin, 5 to 10 U, administered with dextrose at a dose of 25 to 50 g (i.e., one to
two 50-mL ampoules of 50% dextrose solution), reduces serum potassium levels within 10 to 20
minutes, and the effects last 4 to 6 hours.
 Salbutamol: 5 mg nebulized beware of tachycardia.
 Bicarbonate: 1-2mmol/Kg in 5-10min.
 Drugs and treatments to eliminate potassium from the body: (diuretics, aldosterone agonists, dialysis)=>
Remove K+ from the body.
 Resin exchange: Calcium resonium 15g PO TID; works over several days.
 Diuretics: furosemide, 20-40 mg IV
 Aldosterone agonists: fludrocortisones
 Dialysis

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Calcium (Ca): 4.5-5.5mEq/L
 Most abundant in body but: 99% in teeth and bones, and 50% is free ionised calcium which is
physiologically important (1.0-1.25mmol/L) and <0.01 ICF.
 Inverse relationship with Phosphorus.
 Vitamin D needed for Ca absorption from GIT.
 Its homeostasis is regulated by:-
Parathyroid hormone: Increase blood calcium by stimulating osteoclasts, GI absorption and renal
retention.
Calcitonin: from the thyroid gland
 Promotes bone formation, and increase renal excretion.
 Circulating calcium can be: protein bound fraction, chelated(comlexed)fraction or ionised
fraction(physiologically active)
o Acidemia: decrease protein bound calcium and increase ionized calcium.
o Alkalemia: increase protein bound calcium and decrease ionized calcium.
 Physiologic roles of calcium:
 Needed for nerve transmission, vitamin B12 absorption, muscle contraction, blood clotting, enzyme
function, cardiac pacemaker activity, cardiac action potential, bone structure
 Hypocalcemia: Serum Ca < 4.3mEq/L (Ionized Ca<1mmol/L)
 Results from low intake, loop diuretics, parathyroid disorders, renal failure.
 Clinical manifestations:
 Early sign-sensation of numbness and tingling (fingers, toes).
 Tonic contraction of respiratory muscles, Tetany, seizures, Chovstek Sign & Trousseau Sign
 Smooth muscle spasm-abdominal cramp, Osteomalacia, Mental status alteration: irritability, depression,
psychosis.
 CVS impairment: dysrythmias, hypotension and heart failure.
 ECG changes: prolonged QT interval, T wave inversion, heart blocks, ventricular fibrilation.
 Management:
 Correction of coexisting disorder: alkalemia

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 In emergent situation:-
o If symptomatic and if serum ca++ is low:
 Calcium gluconate 10 ml of 10% solution over 10 minutes followed by elemental calcium infusion
(0.2-0.3mg/kg/hr.), and continued until ionized calcium is within range of 1-1.2 mmol/L.
 If asymptomatic: Oral calcium 500-1000mg po/day.
 Hypercalcemia: Serum Ca > 5.3mEq/L.
 Results from hyperparathyroidism, some cancers, prolonged immobilization, excessive intake of Ca OR
Vitamin D.
 Clinical manifestation:
 Muscle weakness, renal calculi, fatigue, altered LOC, decreased GI motility,
 ECG changes: shortened QT interval, prolonged PR and QRS intervals, increased QRS voltage, T-wave
flattening widening, AV block and cardiac arrest
 Management:
 In hypercalcaemic crisis:
 Rehydrate
 Loop diuretics: furosemide 40 to 80 mg IV every 2 to 4 hours.
 Bisphosphonates: pamidronate 60mg in 500 ml saline over 4 hrs.
 Drug of choice for life threatening hypercalcaemia.
 Calcitonin: 3-4U/kg IV then 4U/kg SC BID
 This rapidly decreases the skeletal release of calcium and phosphorous but its effects are only
temporary.
 Life threatening levels of calcium >4.5 mmol/L
 Can be rapidly lowered with phosphate (500ml of 0.1M neutral solution over 6-8 hrs.)
 Forced saline diuresis
 2nd line Rx once the dehydration is corrected:
 Loop diuretics such as frusemide 40mg IV every 4hrs.
 Consider hydrocortisone: 200-400mg IV in malignancy induced hypercalcaemia although this is
ineffective in primary hyperparathyroidism.
 Haemodialysis: For patients with coexisting renal failure.
 Consider underlying cause treatment

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Summary:
Disorders of Na+ and K+ homeostasis are very common problems, encountered in clinical practice on an almost
daily basis. Surgical patients are frequently affected by electrolyte imbalance. In able to take, intravenous fluid
infusions, bowel obstruction or bowel preparation, fluid shifts, and a water-retaining state due to a stress
response and ADH secretion are major causes of imbalance. Understanding electrolytes distribution and
detection of electrolyte imbalance are important in perioperative electrolyte management.
References:
 MILLER’S ANESTHESIA, 8th EDITION
 Clinical anesthesia/ Paul G. Barash. – 8th ed
 Daniel Freshwater-Turner et al. Sodium potassium and the anesthetist, TOTW-030,2006
 Fluid and Electrolytes in Pediatrics, A Comprehensive Handbook-2010
 G.F. Lema et al. Evidence-based perioperative management of patients with high serum potassium level
in resource-limited areas: A systematic reviewInternational Journal of Surgery Open 21 (2019) 21-29
 NTHONY J. VIERA et al. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician.
2015 Sep 15;92(6):487-495.