Common Electrolyte

Disturbances
Dr TEKIY
Na disorders
• Disorders of fluid and Na+ balance occur daily in the intensive care unit (ICU)
This is because of patients have
• Multiple organ system failure
• Usually denied of self-regulation of water balance, and
• are administered medications that disturb fluid and electrolyte status.
Hyponatremia,
• , is one of the most common electrolyte disorders and implies excess body
water.
• Hyponatremia, defined as a serum Na+ concentration less than 135 mEq/L
• The manifestations of hyponatremia range from the subtle to the profound
symptoms
• But generally symptoms are proportional to the magnitude of the
hyponatremia and the speed with which it develops.
• Symptoms span the spectrum from muscle cramps, nausea, vomiting, and
anorexia to confusion, lethargy, coma, and seizures
CONT…
• In combination with a thorough history, medication review, and physical
examination
• the serum osmolality
• glucose, creatinine, and
• albumin provide essential data for determining the etiology of hyponatremia.
• Because Na+ is the predominant osmotically active extracellular cation, serum
osmolality is normally determined largely by the relative proportions of water
and Na+
Categories of Hyponatremia

Hypertonic hyponatremia
• Results from infusion or spontaneous generation of (nonsodium) osmotically active
substances.
• Hyperglycemia and therapeutic administrations of hypertonic glucose, mannitol, or
glycine can cause hypertonicity while depressing Na+ levels.
• (Although urea also increases osmolality, it fails to affect serum Na+ concentration
because it freely traverses cell membranes, dissipating any potential osmotic gradient.)
• Extracellular hypertonicity draws water from cells in an attempt to reduce the osmotic
gradient.
CONT…
Hypotonic Hyponatremias
• Hypotonic hyponatremia:
• The most common form of hyponatremia
• Can be subclassified into three categories based upon the estimation of the
patient's volume status.
• Hypotonic hyponatremia almost never develops unless the patient has
unrestricted access to water or receives a hypotonic fluid
• Isotonic Hyponatremia
Hyponatremia with normal serum osmolality occurs when large volumes of
isotonic, non-salt-containing solutions (glucose, hydroxyethyl starch, mannitol,
glycine, etc.) are retained in the extracellular space.
• This volume expansion does not cause a transcellular shift of water.
• One of the most common settings for the syndrome occurs following
transurethral prostatectomy. Massive absorption of bladder irrigants
containing 5% mannitol can cause isotonic hyponatremia
MANAGMENT
• Regardless of etiology, hyponatremia primarily affects the CNS.
• As the Na+ concentration acutely drops below 125 mEq/L, changes in cognition and
motor function occur commonly.
• Confusion and seizures often occur at serum values less than 120 mEq/L, particularly if
the decline occurs abruptly.
• The severity of the complications increases rapidly with further declines of Na+
concentration; many patients with severe hyponatremia (Na+ < 105 mEq/L) die.
• While clearly there are risks from hyponatremia, there are also risks of treating it..
CONT…
• Even though there are no definitive studies of the topic, it is generally agreed
that the speed of correction should be adjusted for the chronicity of the
problem.
• Unfortunately, the clinician often does not know the duration of hyponatremia.
• Practically, most symptomatic hyponatremic patients should have the Na+
corrected to an initial level of 120 to 130 mEq/L over a 12- to 24-hour period,
at an hourly rate not to exceed 1 to 2 mEq/L.
• Correction should not exceed 12 mEq/L/day.
CONT…
• Slower correction (i.e., 0.5 mEq/L/h) is prudent in patients with chronic
hyponatremia.
• Rapid correction of longstanding hyponatremia is associated with serious
neurologic sequelae—central pontine myelinolysis (CPM).
• CPM is a CNS demyelinating syndrome characterized by weakness, dysarthria,
dysphagia, coma, and risk of death.
• Predispositions include not only the rate of hyponatremia correction but also
severity of the hyponatremia, advanced age, preexisting liver or CNS
disorders, diuretic use, and alcoholism. CPM affects the pons and other areas
of the CNS
Hypernatremia

• Hypernatremia, defined as a serum Na+ level more than 145 mEq/L, occurs when more
water than Na+ is lost from the body or when highly concentrated Na+ solutions are
administered or ingested.
• Hypernatremia is relatively uncommon, both in the overall hospital population (1%) and
among critical care patients (9%).
• Hypernatremia is rare in patients with intact ADH secretion, a sensitive thirst
mechanism, and access to free water.
• Hence, it is primarily a disease of patients who are unable to obtain and drink fresh
water (e.g., infants, elderly, bedridden, and critically ill), particularly those
simultaneously sustaining increased water losses (e.g., diuretics, sweating).
• Hypernatremia implies hyperosmolarity, which is the major mediator of toxicity.
CONT…
• Like hyponatremia, the problem can logically be thought of in three
categories: high, normal, or low extracellular volume.
• Hypervolemic hypernatremia occurs from ingestion or infusion of hypertonic
Na+- containing solutions.
• For example, “normal” saline (0.9% NaCl) is modestly hypertonic (Na+ 154
mEq/L, 308 mOsm/L) and therefore tends to raise the serum Na+
concentration while expanding extracellular volume.
• Hypernatremia is much more common when osmolarity is intentionally
increased by hypertonic (3%) saline (Na+ 513 mEq/L, 1,026 mOsm/L) or
unintentionally by multiple ampules of sodium bicarbonate (Na+ of 595 mEq/L
and 1,190 mOsm/L).
Management
• Three percent saline is now a widely used therapy for intracranial
hypertension from cerebral edema.
• In this setting, serum hypertonicity attracts water from cerebrospinal fluid and
brain cells, reducing intracranial pressure and facilitating cerebral blood flow.
• For this effect, serum Na+ is typically maintained in the 145- to 155-mEq/L
range (roughly 300 to 320 mOsm/L).
• Hypernatremia can be an unintended consequence of NaHCO3 if large
volumes are administered to treat metabolic acidosis or cyclic antidepressant
overdose.
• For patients with impaired Na+ clearance, the Na+-K+ ion exchange resin,
Kayexalate, can raise serum Na+ by transferring significant salt loads across
the bowel wall.
CONT..
• Na+ accumulation from primary hyperaldosteronism or salt or seawater
ingestion are rare causes of hypernatremia.
• Extracellular volume is normal, at least initially, in a number of hypernatremic
conditions.
• For example, both central and nephrogenic diabetes insipidus (DI) produce
hypernatremia by preventing appropriate water reabsorption by the distal
convoluted tubules and collecting ducts of the kidney
• In central DI, ADH secretion is inadequate, and in nephrogenic DI, the kidney
does not respond normally to the secreted ADH
DIAGNOSIS
• Common symptoms of all forms of hypernatremia are
• Thirst, nausea, and vomiting progressing to agitation, stupor, and coma.
• All of these symptoms are nonspecific, and their cause many go unrecognized.
• History and physical examination typically identify the correct diagnosis.
MANAGMENT
• Treatment of hypernatremia consists of replacement of water either
• Enterally
• intravenously as D5W or a hypotonic NaCl solution, with frequent evaluation of
electrolytes and osmolality.
• The speed of correction depends on the chronicity of the problem and the severity of
neurologic symptoms.
• If endogenous ADH is deficient or ineffective, it may be replaced with desmopressin
(DDAVP), an ADH analog.
• In the less common cases of hypernatremia resulting from Na+ gain, such as after the
NaHCO3 administration in cardiac arrest, the use of loop diuretics or addition to Na+
poor fluid may be appropriate.
CONT..
• As a general rule, correction of serum sodium at the rate of 0.5 to 1 mEq/L
each hour is an appropriate target.
• It is also appropriate to limit correction rates to 12 mEq/L per day or 18 mEq/L
over 2 days.
• Like hyponatremia, very rapid correction, particularly of long-standing
hypernatremia, may precipitate CPM or cerebral edema.
• The latter condition results from rapid swelling of neurons that have
accumulated “idiogenic osmoles” in an attempt to match the tonicity of serum
during hypernatremia
POTASSIUM DISORDERS

• Ninety-eight percent of the total body potassium is intracellular.

• As the most abundant intracellular cation,
• Potassium is a strong determinant of intracellular osmolality.
• Muscle contractability and heart and nerve electrical conduction depend upon the ratio
between intracellular and extracellular potassium, a relationship that determines cell
membrane polarization.
• Most intracellular potassium resides in muscle cells.
• Body potassium stores in a typical adult total about 3,500 mEq.
• A true alteration in extracellular potassium measured as a decrease or increase in the
measured level of 1 mEq/L indicates a change in total body potassium of 100 to 200
mEq.
Hypokalemia

• Hypokalemia may result from decreased intake, increased losses, or

redistribution of K+
• Measurement of urinary K+ and chloride (Cl-) concentrations and pH is very
helpful in determining the etiology of hypokalemia
CONT…
• Severe enough to produce symptomatic hypokalemia. (Exceptions include cholera-like
illnesses, cathartic abuse, and villous adenomas.)
• Likewise, losses of K+ directly from gastric fluid are minimal.
• Thus, vomiting induces hypokalemia—not through direct losses but by promoting renal
K+ wasting as a result of volume depletion and hypochloremic metabolic alkalosis.

• ECG changes:
TREATMENT
• Total body deficits of K+ usually exceed 200 mEq in patients with hypokalemia.
• Hence, it should not be surprising that the common practice of administering a small
KCl replacement dose (i.e., 20 to 40 mEq) almost always is inadequate for correction.
• However, because the intracellular space must be accessed via the small intravascular
compartment, K+ therapy (especially intravenous replacement) must be cautiously
undertaken and closely monitored to avoid potentially dangerous hyperkalemia.
Hyperkalemia

• Pseudohyperkalemia may occur if venous blood is analyzed after prolonged tourniquet

application or if the blood is hemolyzed.
• Serum K+ values are normally 0.5 mEq/L higher than the plasma values because K+ is
released from platelets during clotting.
• However, marked hemolysis, severe leukocytosis (>100,000/mm3), or thrombocytosis
(>106/mm3) also may raise the K+ of the clotted specimen to extraordinary levels.
• The diagnosis of clot-related “pseudohyperkalemia” is confirmed by detecting a
disparity between simultaneous determinations of plasma and serum K+.
• Hemolysis can usually be confirmed by simple visual inspection of the sample.
SIGN AND SYMPTOMS
• Hyponatremia, hypocalcemia, hypermagnesemia, and acidosis potentiate the
neuromuscular effects of hyperkalemia.
• Therefore, levels of Na+, calcium, and magnesium should be evaluated and corrected
concurrently.
• Functional impairment of skeletal muscle rarely occurs at K+ levels less than 7.0
mEq/L.
• Hyperkalemia usually spares the respiratory muscles, cranial nerves, and deep tendon
reflexes but commonly causes weakness of the proximal lower extremities.
• The most devastating effect of hyperkalemia is cardiac arrhythmia; however, the
myocardial-impairing and vasodilatory effects of severe hyperkalemia may precipitate
refractory hypotension
CONT…
CONT…
• An electrocardiogram (ECG) should be obtained for every patient with a K+ more than
5.5 mEq/L
• Narrowing and peaking of T waves and QT interval shortening are typically seen with
levels of 5.5 to 7 mEq/L.
• Lengthening of the PR interval and widening of the QRS complex (because of delayed
depolarization) are often seen when concentrations reach 6.5 to 8.5 mEq/L.
• Atrial activity usually is lost shortly before the characteristic sine wave hybrid of
ventricular tachycardia/fibrillation appears at levels greater than 8 mEq/L
ECG changes of Hyperkalemia
Treatment
(1) stop all K+ administration
(2) expand intravascular volume
(3) begin removing K+ from the body
(4) administer drugs to shift K+ into the cellular compartment, and

(5) stabilize neuromuscular and cardiac function with calcium

Hypercalcemia

Causes:
• Three basic mechanisms:
• Increased gut absorption
• Decreased renal excretion, or
• Redistribution of Ca2+ from bone to serum.
• Relatively few disorders are responsible for most cases of hypercalcemia, and the list can be
rapidly culled by taking a careful history and obtaining a few basic laboratory tests.
• Neoplasia and primary hyperparathyroidism together account for 80% to 90% of cases, with
all other causes constituting the remainder.
• Specific malignancies include squamous cell cancer, breast cancer, myeloma, and renal cell
carcinoma. Some tumors produce PTH-related peptide, which may stimulate hypercalcemia.
Thiazide
Clinical features
• The signs and symptoms of hypercalcemia are nonspecific but most commonly result
from the two major pathophysiologic derangements.
• Dehydration and depressed neuromuscular function.
• Hypercalcemia induces an osmotic diuresis, but if fluid intake is unrestricted, severe
Ca2+ elevations are unlikely.
• Unfortunately, the decreased gut motility of hypercalcemia often produces nausea,
vomiting, abdominal pain, and constipation, negating this mode of compensation.
CONT…
• The most common manifestations of hypercalcemia are neuromuscular
disturbances (lethargy, weakness, fatigue, delirium, and coma).
• Symptoms correlate poorly with Ca2+ concentrations, but severe
manifestations are rare unless levels exceed 13 mg/dL.
• The ECG reflects the altered cellular electrical potential when it demonstrates
a truncated QT or increased PR interval
CONT…
• Rarely, complete heart block occurs. Ca2+ salts form and are deposited in the
tissue when a critical calcium-phosphate product (usually >60) is reached.
• In the kidney, renal stones and renal insufficiency may result from these
complexes; skin deposits may induce pruritus.
• Muscle and other soft tissue also may be affected by this “metastatic”
calcification.
• Pancreatitis or peptic ulcer diseases are less common presentations.
• Hypercalcemia may produce hypertension by increasing the peripheral
vascular resistance, an effect that is usually offset by significant volume
depletion
Management
• Initial therapy for hypercalcemia includes administration of isotonic saline at 200 to
300 mL/h to correct intravascular volume depletion.
• After rehydration, furosemide (20 to 200 mg to avoid volume overload and enhance
urinary calcium excretion) is given if GFR is greater than 30 mL/min.
• Zoledronic acid (4 mg as a 15-minute infusion) or pamidronate (60 to 90 mg as a 1- to
2-hour infusion) may be given if hypercalcemia persists after hydration.
• Salmon calcitonin (4 IU/kg) given subcutaneously or intravenously over 12 hours may
be administered until biphosphonates (above) take effect.
• Hydrocortisone (200 to 300 mg/IV) or prednisone (20 to 40 mg) is appropriate if
hypercalcemia is caused by hematologic malignancy or granulomatous disease.
• Hemodialysis is appropriate for serum Ca2+ greater than 14 mg/dL or in patients with
impaired renal function or heart failure due to volume overload.
CONT…
• Mild hypocalcemia occurs commonly during acute illness even in the absence of
causative drugs, but it is rarely symptomatic. Overt hypocalcemia is less common than
symptomatic hypercalcemia but is also life threatening. The urgency of evaluation and
treatment depends on the severity of symptom
• Hypocalcemia usually is asymptomatic if ionized Ca2+ remains normal despite
low total Ca2+ levels, especially if hypocalcemia develops slowly. Alkalosis
lowers the fraction of ionized Ca2+, aggravating the symptoms
clinical Manifestations

• At normal pH, the usual threshold at which symptoms develop in hypocalcemia is 0.7
mg/dL for ionized calcium and 7.5 mg/dL total calcium;
• Most symptoms are due to neuromuscular irritability.
• The most common complaints are paresthesia, cramps, or tetany. Dyspnea or stridor
may occur if ventilatory or upper airway muscles are affected.
• Tetany also may develop
CONT…
• Rare but more specific signs of neuromuscular irritability, including
carpopedal spasm (Trousseau sign) or facial muscle hyperreflexia (Chvostek
sign), may be elicited in patients with hypocalcemia.
• Other potential CNS effects include seizures, hallucinations, confusion, and
depression.
• In humans, the relationship between hypocalcemia and impaired circulatory
system performance is reduction in perfusion by lowering the systemic
vascular resistance and decreasing the cardiac contractility.
• The QT prolongation seen with hypocalcemia may result in a variety of
arrhythmias (most significantly, torsades de pointes)
CONT…
• There are four mechanisms of hypocalcemia
(1) decreases in serum protein concentration,
(2) binding and sequestration of Ca2+
(3) inability to mobilize bone Ca2+, and
(4) decreased Ca2+ intake or absorption.

Because most Ca2+ is bound to the serum proteins, reductions in protein concentration
result in hypocalcemia.
A reduction in albumin of 1 g/dL reduces the serum Ca2+ level by approximately 0.8
mg/dL.
Management of hypocalcemia
• Management of hypocalcemia is dictated by magnitude of deficiency and clinical
impact.
• In general, symptoms occur below ionized calcium concentrations of 0.7 mg/dL or total
serum calcium concentrations of 7.5 mg/dL Short-term therapy is intended to reverse
clinical effects rather than normalize serum calcium levels. Emergent therapies are
needed in the setting of seizures and tetany.
CONT…
• For severe symptomatic hypocalcemia, administer 10 to 20 mL of 10% calcium
gluconate or 10 mL of 10% calcium chloride intravenously over 10 minutes
and repeat every 60 minutes until clinical manifestations resolve
• Avoid bicarbonate or phosphate administration during calcium administration.
• For moderate to severe hypocalcemia (ionized calcium < 1 mg/dL) without
seizures or tetany, administer calcium gluconate 4 g/IV over 4 hours.
• Mild hypocalcemia (ionized calcium 1 to 1.2 mg/dL) is treated with calcium
gluconate 1 to 2 g/IV over 4 hours. Assess progress with ionized calcium
determinations.
CONT..
• In general, calcium gluconate is the preferable intravenous agent because it is less
phlebitic and, thus, less likely to cause tissue injury or necrosis if extravasation occurs.
• Hypomagnesium must also be corrected if present.
• Patients receiving calcium, particularly those on digoxin, should have cardiac
monitoring to reduce the risk of adverse cardiac events that include asystol.
• Patients receiving digoxin should also be monitored closely for digitalis toxicity
precipitated by calcium replacement.
• Hemodialysis is an option in patients with renal failure.
• In the setting of hypocalcemia and hyperphosphatemia, a phosphate binder should be
administered along with calcium infusion to reduce the calcium times phosphorus
product and the risk of calcium phosphate precipitation in tissues
The END