Electrolyte Disturbance

outline
• Hyponatremia
• Hypernatremia
• Hyperkalemia
• Hypokalemia
• Hypocalcemia
• Hypercalcemia
• hypo/ Hypermagnesaemia
Introduction Electrolyte Disturbance
• When altered, fluids and electrolytes should be corrected in the
following order
• volume;
• pH
• potassium
• calcium, and magnesium; and sodium and chloride.
• Reestablishment of tissue perfusion often equilibrates the fluid-
electrolyte and acid-base balances.
Hyponatremia ([Na + ] < 135 mEq/L)
• The clinical manifestations of hyponatremia occur when the [Na + ]
drops below 120 mEq/L;
• They include
nausea, weakness, headache, agitation,
hallucinations, cramps, confusion, lethargy, and seizures.
Diagnosis and Differential
• Evaluate volume status
• True hyponatremia presents with reduced osmolarity and is further
differentiated based on volume status and urine [Na + ].
• Factitious hyponatremia (false low measurement of the serum
sodium) is due to
hyperglycemia,
 hyperproteinemia,
hyperlipidemia
Cont’d

• The syndrome of inappropriate antidiuretic hormone, characterized

by hyponatremia, inappropriately elevated urine

• osmolality despite low serum osmolarity, elevated urine sodium, and

• clinical euvolemia, is a diagnosis of exclusion.

Emergency Department Care and Disposition

Correct existing volume or perfusion deficits with NS.

In euvolemic or hypervolemic patients, restrict fluids (500 to 1500 mL

of water daily

In severe hyponatremia ([Na + ] <120 mEq/L) that has developed

rapidly with central nervous system (CNS) changes

give hypertonic saline, 3% NS (513 mEq/L), at 25 to 100 mL/h.

Cont’d

• [Na+ ] should not be corrected faster than 0.5 mEq/L/h in chronic

hyponatremia or 1.0 mEq/L/h in acute hyponatremia.

• The [Na + ] correction hould not exceed 12 mEq/L/day.

• The sodium dose can be calculated as follows: weight (kilograms) ×

0.6 ×(desired [Na + ] − measured [Na + ]) = sodium deficit (mEq).
Cont’d

• Complications of rapid correction include congestive heart failure

(CHF) and central pontine myelinolysis

Causes of Hyponatremia

• Hypotonic (true) hyponatremia (P osm < 275)

• Hypovolemic hyponatremia

Extra renal losses (urinary [Na + ] < 20 mEq/L)

Volume replacement with hypotonic fluids

Sweating, vomiting, diarrhea, fistula

Third-space sequestration (burns, peritonitis,

Renal losses (urinary [Na+] > 20 mEq/L)

• Diuretic use

• Aldosterone deficiency

• Salt-wasting nephropathies; renal tubular acidosis

• Osmotic diuresis (mannitol, hyperglycemia, hyperuricemia

Cont’d

 Euvolemic hyponatremia (urinary [Na+] usually > 20 mEq/L)

• Inappropriate ADH secretion (CNS, lung, or carcinoma disease)

• Physical and emotional stress or pain

Cont’d

 Euvolemic hyponatremia (urinary [Na+] usually > 20 mEq/L)

• Inappropriate ADH secretion (CNS, lung, or carcinoma disease)

• Physical and emotional stress or pain

• Myxedema
Cont’d
• Hypervolemic hyponatremia
 Urinary [Na+] > 20 mEq/L
Renal failure (inability to excrete free water)
 Urinary [Na+] < 20 mEq/L
Cirrhosis
Congestive heart failure
Nephrotic syndrome
Hypernatremia ([Na + ] > 150 mEq/L)
An osmolarity increase of 2% stimulates thirst to prevent
hypernatremia

Symptoms of hypernatremia are usually noticeable at a serum

osmolarity> 350 or [Na + ] > 158 mEq/L.

Initial symptoms include irritability, tremulousness, and ataxia.

Cont’d

• Lethargy, coma, and seizures may be seen with osmolarities above

400.

• Morbidity and mortality are highest in infants and the elderly who
may be unable to respond to increased thirst.
Diagnosis and Differential

• Hypernatremia is most commonly caused by a decrease in total body

water due to decreased intake or excessive loss

• Common causes are GI loss, hyperpyrexia, and excessive sweating.

• An important etiology of hypernatremia is diabetes insipidus (DI),

which results in the loss of hypotonic urine.
Cont’d
• Central DI (no antidiuretic hormone secreted) results from

CNS disease,

surgery, or

trauma.
CON’D
• Nephrogenic DI (unresponsive to antidiuretic hormone) results from

congenital disease,

Drugs

hypercalcemia,

hypokalemia, or

 renal disease
Causes of Hypernatremia
Loss of water

• Reduced water intake

• Defective thirst drive

• Unconsciousness

• Inability to drink water

• Lack of access to water

Cont’d
 Water loss in excess of sodium
Vomiting, diarrhea
Sweating, fever
Diabetes insipidus
Drugs including lithium, phenytoin
Dialysis
Osmotic diuresis, renal concentrating defects
Thyrotoxicosis
Severe burns
Cont’d
 Gain of sodium

• Increased intake

• Increased salt use, salt pills

• Hypertonic saline ingestion or infusion

• Sodium bicarbonate administration

Emergency Department Care and Disposition
1. Correct existing volume or perfusion deficits with NS or Lactated
Ringer solution. Free water deficits are corrected with ½NS. Avoid
lowering the [Na + ] more than 10 mEq/L/day

2. Each liter of water deficit causes the [Na + ] to increase 3 to 5

mEq/L. Use the formula to calculate the free water deficit: water
deficit (L) = (measured [Na+ ]/desired [Na + ]) − 1.
Cont’d

3. If no urine output is observed after NS or lactated Ringer solution

rehydration, rapidly switch to ½ NS: unload the body of the extra
sodium by using a diuretic (eg, furosemide 20 to 40 milligrams IV).

4. Central diabetes insipidus DI is treated with desmopressin with

careful monitoring of electrolytes, urine osmolarity, and specific gravity.
Hypokalemia ([K + ] < 3.5 mEq/L)
Clinical Features

• The signs and symptoms of hypokalemia usually occur at levels below

• 2.5 mEq/L and affect the following body systems:

• the CNS (weakness, cramps, hyporeflexia, paresthesias), gastrointestinal

system (ileus),

• Cardiovascular system (dysrhythmias, worsening of digoxin toxicity,

hypotension or hypertension, U waves, ST-segment depression, and
prolonged QT interval),
Cont’d
renal system

metabolic alkalosis and

 increased ammonia production;

glucose intolerance also can develop

Causes of Hypokalemia
 Shift into the cell

• Alkalosis and sodium bicarbonate

• β-Adrenergics

• Administration of insulin and glucose

 Increased loss

Primary & secondary hyperaldosteronism

Diuretics, osmotic disuresis, postobstructive diuresis

Renal tubular acidosis

Renal artery stenosis

Diagnosis and Differential

• Causes can be grouped by

decreased [K + ] intake,

increased [K + ] excretion, or

transcellular shift.

 The most common cause is the use of loop diuretics.

Emergency Department Care and Disposition

1. 20 mEq/dose [K + ] will raise the [K + ] by 0.25 mEq/L.

2. In stable patients, oral replacement is preferred (safe and rapid); a

20 to 40 mEq [K + ] dose is used.

3. In unstable patients, IV Potassium chloride (KCl in doses of 10 to 20

mEq/h may be given)
Cont’d

Add no more than 40 mEq of KCl to each liter of IV fluid. Infusion

rates should not exceed 40 mEq/hr.

Doses greater than 20 mEq/h should be given through a central line.

Patients should be monitored continuously for dysrhythmias
Hyperkalemia ([K + ] > 5.5 mEq/L)
Clinical Features
• The most concerning and serious manifestations of hyperkalemia are
the cardiac effects.
• At levels of 6.5 to 7.5 mEq/L, the electrocardiogram (ECG) shows
peaked T waves (precordial leads) and prolonged PR and short QT
intervals.
• At levels of 7.5 to 8.0 mEq/L, the QRS widens and the P wave flattens.
Con’d

• At levels above 8 mEq/L, a sine-wave pattern, ventricular fibrillation,

and heart blocks occur.

• Neuromuscular symptoms include weakness and paralysis.

• Gastrointestinal symptoms include vomiting, colic, and diarrhea

Diagnosis and Differential

• Beware of pseudohyperkalemia, which is caused by hemolysis after

blood draws.

• Renal failure with oliguria is the most common cause of true

hyperkalemia.

• Appropriate tests for management include an ECG, electrolytes,

calcium, magnesium, arterial blood gases (check for acidosis)
Emergency Department Care and Disposition

Symptomatic patients are treated in a stepwise approach:

stabilize the cardiac membrane with CaCl 2 or Ca-gluconate;

shift [K + ] into the cell using glucose and insulin and/or bicarbonate
and/or albuterol;

enhance [K+ ] excretion by using sodium polystyrene sulfonate

(Kayexalate), diuretics, or dialysis in severe cases.
cont’d
• In acidotic patients, consider giving 50 to 100 mEq of sodium
bicarbonate slow IV.

• In children 1 to 2 mEq/kilogram is given slow IV.

• Give 50 mL (25 grams) of D50W with 10 to 20 units regular insulin IV

push (5 to 10 units in dialysis patients).

• In children, give 0.5 to 1 gram/kilogram of glucose as D10W plus

insulin 0.1 units/kilogram
• Diuresis is maintained with furosemide 20 to 40 milligrams IV.

• Kayexalate (PO or rectal [PR]) 1 gram binds 1 mEq [K + ]. Administer

Kayexalate 15 to 30g PO with sorbitol or 30 to 50 grams PR with sorbitol.

• In patients with acute renal failure, consult a nephrologist for emergent

dialysis

• Albuterol 5 to 10 milligrams by nebulization may also be used to lower K +

Cont’d

• Kayexalate and insulin/glucose therapies last several hours;

all other therapies (except hemodialysis) have transient
effects. Frequent monitoring of [K + ] should occur
 Hypocalcemia
• ([Ca 2+ ] < 8.5 mEq/L or ionized level < 2.0 mEq/L

 Clinical Features

• The signs and symptoms of hypocalcemia are usually seen with

ionized [Ca2+ ] levels below 1.5 mEq/L.

• Symptoms include paresthesias, increased deep tendon reflexes

(DTRs), cramps, weakness, confusion, and seizures.
Cont’d

• Patients also may demonstrate the Chvostek sign (twitch of the corner
of mouth on tapping with finger over cranial nerve VII at the zygoma)

• The Trousseau sign (more reliable; carpal spasm when the blood
pressure cuff is left inflated at a pressure above the systolic blood
pressure for longer than 3 min)
Cont’d

• Alkalosis decreases the ionized [Ca 2+ ] fraction (physiologically active

form) without changing the total calcium level.

• Low [Ca 2+ ] decreases myocardial contractility, so patients may

present with CHF or prolonged QT intervals on the ECG.
Diagnosis and Differential
Causes include:

• hypoparathyroidism,

• hyperphosphatemia,

• vitamin D deficiency,

• hypomagnesemia, and fluoride poisoning

Emergency Department Care and Disposition
• If asymptomatic, use calcium gluconate tablets 1 to 4 grams/d PO
divided every 6 hours with or without vitamin D (calcitriol 0.2
micrograms two times a day). Milk is not a good substitute.

• In symptomatic patients or those with severe hypocalcemia, give

calcium gluconate, or calcium chloride, 10 mL 10% solution IV slowly
over 10 min

• Replace magnesium in conjunction with [Ca 2+ ].

Hypercalcemia
• [Ca 2+ ] > 10.5 mEq/L or ionized [Ca 2+ ] > 2.7 mEq/L)

• Several factors affect the serum calcium level:

• parathyroid hormone increases calcium and decreases phosphate; .

• Decreased [H + ] causes a decrease in ionized [Ca 2+ ].

• A decrease in albumin causes a decrease in [Ca 2+ ] but not in the

ionized portion
Clinical Features
• Clinical signs and symptoms develop at levels above 12 milligrams/dL.
Patients often have profound volume depletion; concomitant
electrolyte abnormalities are frequent

• A mnemonic to aid recall of common hypercalcemia symptoms is

stones (renal calculi), bones (osteolysis), psychic moans (lethargy,
weakness, fatigue, and confusion), and abdominal groans (abdominal
pain, constipation, polyuria, and polydipsia).
ECG finding

• ECG changes include depressed ST segments, widened T

waves, shortened QT intervals, and heart blocks
Diagnosis and Differential

• Most cases of hypercalcemia are due to hyperparathyroidism or

malignancy.

• A mnemonic to aid recall of the common causes is PAM P. SCHMIDT

arathyroid hormone, Addison disease, multiple myeloma, Paget

disease, sarcoidosis, cancer, hyperthyroidism, milk-alkali syndrome,
immobilization, excess vitamin D , and thiazides
Emergency Department Care and Disposition

Initiate treatment in patients with severe symptoms, [Ca 2+ ] above

14 milligrams/dL, or significant dehydration. Restore fluid deficits,
enhance calcium elimination, and decrease osteoclastic activity

Correct fluid deficits with NS; several liters may be required. Correct
concomitant electrolyte abnormalities cautiously
Cont’d

Drugs that inhibit osteoclastic activity include the bisphosphonates,

calcitonin, and glucocorticoids. Recommendations for initiating
therapy in the ED are lacking;
Cont’d

Loop diuretics inhibit the renal resorption of [Ca 2+ ], but worsen

dehydration and other electrolyte abnormalities. They are no longer
recommended for malignancy-related hypercalcemia. In isolated
cases, furosemide (10 to 40 milligrams IV) may be administered after
fluid deficits are corrected, with careful attention to avoid
dehydration.
Hypomagnesemia

• Plasma magnesium concentration of 1.4 to 1.7 mEq/L

• [Mg 2+ ], [K + ], and PO 4 move together intra- and extracellular.

• Hypomagnesemia presents with CNS symptoms (depression, vertigo,

ataxia, seizures, increased DTR, or tetany) or cardiac symptoms
(arrhythmias, prolonged PR, QRS and QT, or worsening of digitalis
effects)
Diagnosis and Differential

• In adults, the most common cause is alcoholism, followed by poor

nutrition, cirrhosis, pancreatitis, correction of diabetic ketoacidosis
(DKA), excessive gastrointestinal losses, and renal wasting (especially
diurectic use).

• Severe [Mg 2+ ] depletion can occur before significant laboratory

changes are seen.
Emergency Department Care and Disposition

• Correct volume deficits and other electrolyte abnormalities. Oral [Mg

2+ ] replacement is sufficient for most patients.

• In patients with severe symptoms and normal renal function,

administer 2 grams magnesium sulfate IV over an hour, followed by 6
grams over the first 24 hours.

• Continuous cardiac monitoring and frequent DTR checks are

recommended.
Hypomagnesaemia
Clinical Findings

• Signs and symptoms manifest progressively: nausea and somnolence

occur first, followed by muscle weakness and loss of DTRs.

• Respiratory depression, hypotension, heart block, and cardiac arrest

occur at progressively higher magnesium levels.
Diagnosis and Differential

• Hypermagnesemia is rare. Common causes are renal failure with

concomitant ingestion of [Mg 2+ ]-containing preparations (antacids)
and lithium ingestion.

• Serum levels are diagnostic.

• Hyperkalemia, hypercalcemia, and hyperphosphatemia often present

concurrently.
Emergency Department Care and Disposition

1. In many patients, stopping [Mg 2+ ] intake is sufficient. More

aggressive therapy includes rehydration with NS.

2. In severely symptomatic patients, give 5 mL (10% solution) of

calcium chloride IV to antagonize the effects of magnesium
Reference
• Tintinallis 7th edition.
• Up-to-date 2022