Perioperative fluid

management Part II:

Dyselectrolytemia: Sodium, Potassium, Calcium,
andMagnesium

PRESENTER: Dr. Ayush Shrestha

MODERATOR:
Department of Anesthesiology, PoAHS
Objectives

To discuss the physiology of electrolytes in our body.

To discuss the features and causes dyselectrolytemia

To discuss the management of dyselectrolytemia.

To know about anesthetic implication of dyselectrolytemia

Sodium Physiology

Na+ is the dominant extracellular cation, and major component of osmolality of

plasma.

The relatively free movement of water throughout the fluid compartments

means that Na+ is therefore the prime determinant of ECF volume.

Total body Na+ content is approximately 4000 mmol, of which only 10% is
intracellular.
 loss is predominantly by the renal route, with minor contributions from feces,

sweat, and skin (10 mEq/day each).

Na+ is freely filtered at the glomerulus, 99.5% absorbed in PCT.

 Serum Na+ concentrations within a tight range (138-142 mEq/L)

Plasma osmolality (mOsm/kg)

[Na+]×2+ BUN/2.8 + Glucose/18

where [Na+] is expressed as mEq/L and blood urea nitrogen (BUN) and glucose as
mg/dL.

Urea is an ineffective osmole because it readily permeates cell membranes.

So, Effective plasma osmolality = [Na + ] × 2 + Glucose/18

Regulation of ADH
ADH also called Arginine Vasopressin in humans is synthesized in supraoptic and
paraventricular nuclei of hypothalamus

ADH release are stimulated by hyperosmolality and inhibited by hypo osmolality.

Carotid body receptors as well as low pressure volume receptors in atria, venecava and
pulmonary arteries also influence ADH release.

 Hypothalamic osmoreceptor influence thirst and the release of antidiuretic hormone

(ADH).

ADH release causes increase in Urinary osmolality by causing water retention.

Hyponatremia

It is classified as:

 mild (130-134 mEq/L),

Moderate (120-130 mEq/L),

severe (<120 mEq/L)

 Moderate-to- severe hyponatremia, particularly of acute onset, is

associated with significant perioperative morbidity.
Pseudohyponatremia refers to a laboratory phenomenon by which a high
content of plasma proteins and lipids expands the nonaqueous portion of plasma
sample

This leads to an errant report of low ECF[Na+] in the setting of normal serum
osmolality.

This can be averted with Na+ sensitive electrodes and the normal ECF [Na+] with
a normal serum osmolality.
Hyponatremia cause cerebral edema and increased intracranial pressure, highly
dependent on how rapidly the hyponatremia occurred.

In acute onset, symptoms typically occur when Na+ concentrations are as low as
120 to 125 mEq/L common in children and premenopausal females.

Symptoms are headache, confusion, agitation, vomiting, and lethargy.

At Na+ concentrations less than 110 mEq/L, symptoms progress to seizures and
coma.

In the chronic setting, clinical features may be absent even at concentrations less
than 120 mEq/L.
Causes
Syndrome of inappropriate antidiuretic
hormone secretion(SIADH)
Inappropriate secretion of ADH is characterized by the activation of water conserving
mechanisms despite the absence of osmotic or volume related stimuli.

These patients are typically euvolemic as renal response to volume expansion remain
intact.

Causes are neuropsychiatric disorders such as meningitis, encephalitis, head trauma , etc.

Pulmonary diseases, malignant tumors eg small cell lung cancer, etc.

Drugs: Desmopressin, vasopressin, NSAIDs, Cyclophosphamide, Chlorpropamide,

carbamazepine,SSRI etc
It is characterized by:

 Plasma hypoosmolality

 Uosm more than 100 to 150 mOsm per kg

 Urinary Na+ concentration of more than 20 mEq per litre.

 Normal adrenal, renal and thyroid function.

 Normal potassium and acid base balance.

Cerebral salt wasting(CSW)

A rare disorder characterized by:

 Low plasma osmolality

 Urine osmolality above 100 to 150 mOsm/kg

 Urinary sodium concentration of greater than 20 mEq/L.

Unlike SIADH, evidence of volume depletion is present.

In affected individuals, the high urinary Na+ represents inappropriate salt wasting
rather than a response to normal tissue perfusion( as in SIADH patients)
Symptomatic hyponatremia (typically euvolemic or
hypervolemic)

In patients with moderate symptoms (confusion, lethargy, nausea, and vomiting),
hypertonic 3% saline may be used at an initial rate of 1 mL/kg/h with the goal of
increasing [Na+] by 1 mEq/L/h for 3 to 4 hours, after which electrolytes should be
rechecked.

The infusion rate should be modified to ensure that [Na+] is increased by no

more than 10 mEq/L in the first 24 hours of treatment.
Severely symptomatic hyponatremia (coma, seizures, often with [Na+] <120
mEq/L) is typically of acute onset and the risks of undertreating are more than
those of osmotic demyelination.

A bolus of 100 mL of 3% saline should initially be given with the aim of acutely
increasing [Na+] by 2 to 3 mEq/L.

If no improvement in neurologic status occurs, this approach may be repeated

once or twice at 10-minute intervals.
• The amount of NaCl necessary to raise plasma sodium to desired
value can be estimated by:
• Na+ deficit = TBW × (Desired [Na+] – Present [Na+])
TURP syndrome

 Symptomatic hyponatremia, excessive intravascular volume, and edema

resulting from IV absorption of hypotonic nonconductive (electrolyte-free)
irrigation fluid during TURP.

10% to 15% of TURP procedures, with onset between 15 minutes and 24

hours of resection.

Risk factors include increased intravesical pressure, prolonged resection,

hypotonic irrigants, and open prostatic sinuses.
TURP syndrome prevention

The use of conducting (isotonic saline) irrigant with bipolar diathermy.

Monitoring fluid absorption by comparing the amount instilled with the amount
removed.

 Surgery should be halted if 750 mL (for females) or 1000 mL (for males) has been
absorbed and the patient should be assessed for Na+ levels and neurologic status
(if awake).
Surgery should be terminated if 1000 to 1500 mL (for females) or more than
2000 mL (for males) has been absorbed.

 If saline irrigant is used, surgery should be terminated after 2500 mL has been
absorbed.
Limiting the duration of irrigation: irrigation should continue only for longer than
1 hour after careful assessment of the patient for possible TURP syndrome.

Limiting intravesical pressure to less than 15 to 25 mm Hg or 70 mm Hg for

endometrial procedures.
Treatment
Monitoring the patient’s neurologic status by using regional anesthetic
techniques.

Symptoms in the awake patient include nausea and vomiting, visual disturbance,
reduced level of consciousness, agitation, confusion, and seizures.

Taking account of the patient’s intravascular volume status, Na+ level, and
osmolality, but typically involves cessation of irrigation solutions and water
restriction.
A loop diuretic should be given to promote free water excretion if intravascular
volume overload is present.

 In severe hypoosmolar hyponatremia with neurologic symptoms, hypertonic

saline may be used.

When osmolality is normal or marginally decreased, hemodialysis is preferred.

Hypernatremia

Hypernatremia ([Na] >145 mEq/L) is less common than hyponatremia but may
affect up to 10% of critically ill patients caused by primary Na+ gain or water
deficit.

If severe ([Na] >160 mEq/L), a 75% mortality may occur depending on the
severity of the underlying disease process.
Anesthetic implication
• Plasma sodium concentration greater than 130 mEq/L is ususally
considered safe for patients undergoing general anesthesia.
• Lower concentration may result in significant cerebral edema
manifesting intraoperatively as decrease in MAC or post operatively
as agitation, confusion.
The major mechanisms are:
 excessive water loss with inadequate compensatory intake,

lack of ADH,

administration of exogenous sodium.

Diabetes insipidus (DI) is caused by a lack of ADH action as a result of impaired
production or release (central DI)

Reduced renal sensitivity to ADH (nephrogenic DI) with consequent failure to

concentrate urine and excretion of large quantities of inappropriately dilute
urine.
If the patient is unable to accept compensatory fluid orally (e.g., because of coma
or in the elderly with impaired thirst reflexes), they may rapidly become
hypovolemic.

Central DI is seen after pituitary surgery, subarachnoid hemorrhage, traumatic

brain injury (particularly skull base fractures), and brainstem death.
Nephrogenic DI may be due to renal disease, electrolyte disorders, or drugs
(lithium, foscarnet, amphotericin B, demeclocycline).

Clinical features of hypernatremia include altered mental status, lethargy,

irritability, seizures, hyperreflexia, and spasticity.

Diagnosis is based on assessment of intravascular volume status, urinary

osmolality, and Na+ concentration.
Diagnostic criteria include an inappropriately dilute urine (<300 mOsm/kg) in
combination with hypernatremia and high serum osmolality (>305 mOsm/kg).

Urine specific gravity (SG) may provide a rapid guide to urine osmolality where
urgent treatment is being considered;

Urine SG less than 1.005 in the context of hypernatremia and a potential

underlying cause is consistent with DI.
Treatment
Correction of the Na+ concentration should be no more rapid than 10 mEq/L/day
unless the onset has been very acute.

The mainstay of management is administration of water, preferably by mouth or

NG tube.

Alternatively, 5% dextrose in water (D5W) or quarter NS can be given via IV.

Free water deficit= TBW x (serum [Na] -140) / 140

TBW = wt (kg) x 0.6 (male) or 0.5 (female)

Hypovolemic hypernatremia:

Correction of intravascular volume deficit with isotonic saline and

correction of underlying cause.
Correction of water deficit with 0.45% Nacl, 5% dextrose or enteral
water to cover ongoing losses.
Euvolemic hypernatremia

Use of 0.45% saline, 5% dextrose, or enteral water to replace the deficit and

ongoing losses.

In central DI, with urine output > 250 mL/h and risk for hypovolemia, titrated IV

doses of desmopressin acetate 0.4 to 1 μg (1-deamino-8-d-arginine vasopressin

[DDAVP], an ADH analogue) is given to reduce the urine output.

 Higher acute doses may have a prolonged effect with the risk for water

intoxication.
Hypervolemic hypernatremia:

 Stop administration of exogenous Na+, give furosemide with 5% dextrose or

enteral water.

 Dialysis may be indicated in the presence of renal failure.

Anesthetic consideration

• Increases the minimum alveolar concentration for inhalational

anesthetic in animal studies.
• Hypovolemia accentuates vasodilation or cardiac depression form
anesthetic agents.
• Decrease in volume of distribution for drug necessitates dose reduction
for most IV agents.
• Decrease in cardiac output enhance the uptake of inhalational agents.
• Elective anesthetics should be postponed in patients with significant
hypernatremia (>150mEq/L)
Potassium physiology

Dominant intracellular cation, total body content of approximately 4000 mmol,

98% of which is intracellular, particularly in muscle, liver, and RBCs.

The ratio of ICF to ECF K+ balance is vital in the maintenance of cellular resting
membrane potential, and K+ therefore has role in all excitable tissues.
Term infants require 2 to 3 mEq/kg/day and adults 1 to 1.5 mEq/kg/day.

Nearly all ingested K+ is absorbed by the intestine, and minimal amounts are
excreted in feces.

Renal potassium handling is responsive to aldosterone.

The elimination of potassium occurs through renal excretion at distal nephron. K+

secretion is enhanced by distal Na+ absorption.
• Intercompartmental shifts of potassium are known to occur by
following ways:

• Changes in extracellular pH
• Circulating insulin level
• Circulating catecholamine
• Plasma osmolality
Potassium Disorders
K+ has key role on excitable tissue resting membrane potential.

Dyskalemia can lead to life-threatening cardiac arrhythmias in the perioperative

period.

Sampling artifacts occur in laboratory tests of K+ions.

Anticoagulated samples typically give results 0.4 to 0.5 mEq/L less than those
from clotted samples because of erythrocyte K+ release during clotting.
Hypokalemia

Hypokalemia (<3.5 mEq/L)

Moderate-to-severe hypokalemia (2-2.5 mEq/L) leads to muscle weakness,

electrocardiogram (ECG) abnormalities (ST segment depression, T wave
depression, U wave elevation), and arrhythmias (atrial fibrillation and ventricular
extrasystoles).

Hypokalemia (e.g., as low as 2.6 mEq/L) is associated with an increased rate of

perioperative morbidity or mortality.
Treatment

The treatment of hypokalemia depends on the presence and severity of any

associated organ dysfunction.

Significant ECG changes such as ST-segment changes or arrhythmias need

continuous ECG monitoring, particularly during intravenous K+ replacement.

Oral replacement safest and given over several days (60–80 mEq/d).

Intravenous replacement of potassium chloride is for patients with or risk for,

significant cardiac manifestations or severe muscle weakness.
Because of potassium’s irritative effect on peripheral veins, peripheral
intravenous replacement should not exceed 8 mEq/h.

More rapid intravenous replacement (10–20 mEq/h) requires central venous

administration and close ECG monitoring.

Intravenous replacement should generally not exceed 240 mEq/d.

Dextrose-containing solutions should be avoided because the resulting

hyperglycemia as secondary insulin secretion may worsen the low plasma [K+]
Kdeficit(mmol)=(Knormal lower limit-K measured)x weight(kg)x0.4

Potassium chloride is the preferred potassium salt when a metabolic alkalosis is also
present because it also corrects the chloride deficit.

Potassium bicarbonate or equivalent (K+ acetate or K+ citrate) is preferable for patients

with metabolic acidosis.

Potassium phosphate is a suitable alternative with concomitant hypophosphatemia (eg,

diabetic ketoacidosis).
Anesthetic implications
• Potassium level should be at least 3 mEq/L for elective surgery
• Mild hypokalemia (3-3.5 mEq/L) without ECG changes doesn’t
increase anesthetic risk.
• Intraoperative management:
• Vigilant ECG monitoring
• Intravenous potassium of atrial or ventricular arrhythmias develop
• Avoid hyperventilation
• Use glucose free IV solutions
• Increased sensitivity to neuromuscular blockers may occur
Hyperkalemia

Hyperkalemia (>5.5 mEq/L)

 It may result from excess intake, failure of excretion, or shift from the
intracellular to extracellular compartment.

Pseudohyperkalemia is an artificially elevated plasma [K+] due to K+ movement

out of cells immediately before or following venipuncture.

Contributed factors include repeated fist clenching, hemolysis and marked

leukocytosis or thrombocytosis.
Features:
Muscle weakness
Paralysis
Increased cardiac automaticity
Enhanced repolarization
ECG changes
Consquent ECG changes as K+ levels increase
 5.5 to 6.5 mEq/L: tall, peaked T-waves

 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

Anesthetic consideration

• ECG monitoring
• Succinylcholine contraindicated
• Avoid potassium containing IV solutions
• Avoid metabolic/respiratory acidosis
• Mild hyperventilation is desirable
• Hyperkalemia can accentuate effects of NMBs
Calcium Physiology

Its role is in the formation of bone structure, where 98% of body calcium (Ca2+) is
stored.

Nearly 50% of serum Ca is(ionized) free, 40% is bound to albumin and 10% with anions
like phosphate, HCO3-, lactate, citrate

Hypoalbuminia causes only decrease in total serum calcium

Corrected total Calcium concentration: add 0.8mg/dl per 1 g/dl decrease in albumin
concentration below 4 g/dl.

Acidemia increases ionized calcium 0.1 mEq/L per 0.1 decrease in pH

Intracellular Ca2+ entry may have direct effects in cardiac and skeletal muscle
contraction

Ca2+also plays a key role in coagulation by linking coagulation factors to the negatively
charged plasma membrane of activated platelets.

Serum Ca2+ concentrations are between 4.5 and 5 mEq/L (8.5-10.5 mg/dL), maintained
by vitamin D and parathyroid hormone (PTH).

Ionized Ca2+ is sensed by the extracellular domain of a G-coupled receptor expressed

on parathyroid cells (the Ca2+/Mg2+-sensing receptor), inhibiting PTH release.
Hypercalcemia

A serum calcium >10.3 mg/dl with a normal serum albumin or an ionized

calcium >5.2 mg/dl.

Clinically significant hypercalcemia typically requires both increase in ECF calcium

and a decrease in renal calcium clearance.
Clinical presentation

Clinical manifestation if serum Calcium >12 mg/dl.

Renal manifestations include polyuria and nephrolithiasis.

If serum Ca > 13 mg/dl, renal failure with nephrocalcinosis and ectopic soft tissue
calcification is possible.

Anorexia, vomiting, constipation and signs of pancreatitis occur rarely.

Weakness, fatigue, confusion, stupor, coma as neurologic signs.

Osteitis fibrosa cystica can develop when hyperparathyroidism is profound and prolonged,
Serum calcium should be interpreted with the knowledge of serum albumin, or
ionized calcium should be measured.

Corrected Ca2+= [Ca2+ +0.8x (4- albumin)]

Intact serum PTH are measured ( independent of renal functions)

Serum phosphorous- decreased in hyperparathyroidism

Urine calcium- elevated in primary hyperparathyroidism

ECG- shortened QT interval, prolonged PR interval, variable degree of AV block in

severe cases.
Treatment
Symptomatic hypercalcemia requires rapid treatment.

Rehydration followed by a brisk diuresis (urinary output 200–300 mL/h) utilizing

intravenous saline infusion and a loop diuretic to accelerate calcium excretion.

This causes reduction of calcium by 1-3 mg/dl in 1-2 days.

Premature diuretic therapy prior to rehydration exacerbates volume depletion and

aggravates hypercalcemia.

Renal loss of potassium and magnesium usually occurs during diuresis. So, laboratory
monitoring and intravenous replacement as necessary.
Severe hypercalcemia (>15 mg/dL) usually requires additional therapy after
saline hydration and furosemide .

Bisphosphonates or calcitonin are preferred agents.

Hemodialysis for correcting severe hypercalcemia may be necessary in the

presence of kidney or heart failure.
Anesthetic considerations
Ionized calcium level should be monitored.
Saline diuresis should be continued intraoperatively with care to
avoid hypervolemia if surgery must be performed.
Potassium and Magnesium must be monitored in anticipation of
diuresis related hypokalemia and hypomagnesemia.
Responses to anesthetic agents and NMBs are unpredictable.
Acidosis must be avoided.
Hypocalcemia

A serum Ca <8.4 mg/dl with normal serum albumin or ionized Ca <4.2 mg/dl.

Pseudohypocalcemia is the situation in which total calcium is reduced due to

hypoalbuminemia but corrected Ca2+ remains within normal range.

 Albumin level should be measured any time there is abnormality in serum

calcium levels to rule out pseudohypocalcemia.

Calcium is corrected by adding {0.8x (4- [albumin]} to the total calcium level.
Signs:
Neuromuscular irritability

 Circumoral and peripheral paresthesia

 Chvostek sign (facial twitching induced by tapping on the facial nerve)

Trousseau sign (forearm muscular spasm induced by inflating a pressure cuff)

 Muscle cramps

 Laryngospasm

Tetany

 Seizures
Cardiac:
 Impaired inotropy

Prolonged QT

 Ventricular fibrillation

Heart block
Coagulopathy occurs when hypocalcemia occurs at ionized Ca2+
concentrations less than 1.2 mEq/L
Treatment

Symptomatic hypocalcemia is a medical emergency and should be treated

immediately with intravenous calcium chloride (3–5 mL of a 10% solution) or
calcium gluconate (10–20 mL of a 10% solution).

Ten mL of 10% CaCl2 contains 272 mg of Ca2+, whereas 10 mL of 10% calcium

gluconate contains 93 mg of Ca2+.
To avoid precipitation, intravenous calcium should not be given with
bicarbonate- or phosphate-containing solutions.

Serial ionized calcium monitoring is mandatory.

Repeat intravenous boluses or a continuous infusion (Ca2+ 1–2

mg/kg/h) may be necessary.
Plasma magnesium concentration should be checked to exclude
hypomagnesemia.

In chronic hypocalcemia, oral calcium (CaCO3) and vitamin D

replacement are usually adequate.
Anesthetic considerations:
Serial ionized calcium level should be monitored intraoperatively in
patients with history of hypocalcemia
Alkalosis should be avoided.
Intravenous calcium may be necessary following rapid transfusion of
citrated blood products or large volumes of albumin products.
Responses to NMBs are inconstistant and require nerve stimulator
monitoring.
Magnesium Physiology

Primarily an intracellular ion.

Of total body Mg2+, 50% is within bone, 20% within muscle, and the rest in liver,
heart, and other tissues.

1% is found in ECF

Plasma total Mg2+ concentration ranges from 1.5 to 2.1 mEq/L.

65% is in the biologically active ionized form.

About 25% is protein (mostly albumin) bound.

The remainder is complexed to phosphates, citrates, and other anions.

Mg2+ has following three main cellular actions:
Energy metabolism

Nucleotide and protein production

Ion transport- physiologic antagonism of Ca2+.

Mg2+ is absorbed from GI tract by a transport system and passive diffusion.

Excretion is via the GI tract (∼60% of ingested) and kidneys.

75% is freely filtered at the glomerulus, and proximal tubule reabsorption is

minimal.

 60% to 70% is reabsorbed at the thick ascending loop of Henle and 10%
reabsorbed under regulation in the distal tubule.
The main determinant for magnesium reabsorption is the plasma Mg2+
concentration, sensed by Ca2+/Mg2+-sensor receptors present on the basal
aspect of thick ascending loop cells.

Mg2+ reabsorption is affected by PTH but also calcitonin, glucagon, acid-base

balance, Ca2+ and K+ levels.
Hypomagnesemia

A serum Mg <1.3 mEq/L.

Caused by impaired intestinal absorbtion and increased renal excretion.

Clinical presentation:

May be non specific and symptoms often relate to coexisting

hypocalcemia or hypokalemia
Neuromuscular: Trousseau and Chvostek signs, vertigo, seizures, weakness

Metabolic: Carbohydrate intolerance, hyperinsulinemia, atherosclerosis

Cardiovascular: Wide QRS, prolonged PR, T-wave inversion, ventricular

arrhythmias

Musculoskeletal: Osteoporosis and osteomalacia

Measurement of urine Mg excretion is helpful. 24 hour urine Mg of > 2mEq/L or >24 mg or
a fractional excretion of magnesium of > 4% during hypomagnesemia suggests increased

renal excretion.

FEMg = ((UMg x Cr)/(0.7 x Mg) x UCr) x 100

UMg = random urine magnesium

UCr = random urine creatinine

Mg = plasma or serum Mg

 Cr = plasma or serum creatinine)

Treatment

Asymptomatic patients with moderate-severe hypomagnesemia should receive

oral supplementation.
 Approximately 240 mg for mild deficiency
 More severe deficiency require 720 mg/d of elemental Mg.

In the presence of symptoms or Magnesium level below 1mg/dl IV magnesium

should be administered : 1-2 gm over 5-10 minutes

Co-existing hypocalcemia, hypokalemia should be corrected.

Anesthetic implications
• Co existing electrolyte disturbances must be corrected before surgery.
• Isolated hypomagnesemia should be corrected before elective
procedures because of its potential to cause arrhythmias.
Hypermagnesemia

 A serum magnesium >2.2 mEq/L

Causes:
Mostly due to excessive intake: magnesium containing antacids, laxatives, magnesium
sulphate therapy
Kidney impairment: GFR < 30 ml/min

Less commonly due to adrenal insufficiency, hypothyroidism, rhabdomyolysis, lithium

administration
Clinical symptoms are seen when serum Mg level is >4 mEq/L.

Neuromuscular abnormalities include hyporeflexia(1st sign), lethargy,

weakness, paralysis and respiratory failure.

Cardiac findings are hypotension, bradycardia and cardiac arrest.

The ECG may show bradycardia, prolonged PR, QRS and QT intervals with
magnesium levels of 5- 10 mEq/L.

Complete Cardiac heart block or asystole may occur with levels >15mEq/L
Treatment

Mild hypermagnesemia: Discontinue sources of magnesium intake

High magnesium level with clinical signs : 10% calcium gluconate 10-20 ml IV (1-2g)
over 10 minutes.

Forced diuresis with loop diuretics and IV fluids.

Hemodyalysis for significant renal insufficiency.

Mechanical ventilation for respiratory failure.

Temporary pacemakers for significant bradyarrythmias.

Anesthetic considerations

Serum Mg2+ levels should be monitored closely during therapeutic administration.

 Because excretion is renal, doses should be decreased for patients with kidney disease.

It should be used with extreme caution in patients with a background impairment of

neuromuscular transmission (myasthenia gravis, Lambert-Eaton myasthenic syndrome).

 NM blockers should be with caution because Mg2+ potentiates the effects of both depolarizing

and nondepolarizing neuromuscular blockers.

Potentiation of vasodilatory and negative inotropic properties of anesthetics should be expected.

References
Millers textbook of anesthesia 9th edition
Morgan’s and Mikhail’s Clinical Anesthesiology 6th edition
Take home message
• Acute hyponatremia or hypernatremia with symptoms is more
dangerous.
• Succinylcholine must be avoided in hyperkalemia.
• Ionized calcium must be monitored.
• NMB should be used carefully in cases of hypermagnesemia
Thank You!!