Most patients with hyponatremia are asymptomatic, and the diagnosis is made after incidental laboratory findings. Symptoms range from nausea and malaise, with mild reduction in the serum sodium level, to lethargy, decreased level of consciousness, headache, and (if severe) seizures and coma. Overt neurologic symptoms most often are due to very low serum sodium levels (usually < 115 mEq/L), resulting in intracerebral osmotic fluid shifts and brain edema.
Diuretics may induce hypovolemic hyponatremia. Note that thiazide diuretics, as opposed to loop diuretics, impair the diluting mechanism without limiting the concentrating mechanism, thereby impairing the ability to excrete a free water load. This is particularly so in elderly persons, who already have impaired diluting ability. Loop diuretics are not a common cause of hyponatremia.
Euvolemic hyponatremia is the most common form, accounting for 60% of cases. The most common cause is syndrome of inappropriate secretion of antidiuretic hormone (ISADH). Hypervolemic hyponatremia is characterized by clinically detectable edema or ascites that signifies an increase in total body water and sodium. Paradoxically, however, a decrease in the effective circulating volume, critical for tissue perfusion, stimulates the same pathophysiologic mechanism of impaired water excretion by the kidney that is observed in hypovolemic hypotonic hyponatremia. Commonly encountered examples include cirrhosis, congestive heart failure, nephrotic syndrome, and severe hypoproteinemia.
According to guidelines, in patients with chronic, severe symptomatic hyponatremia, the rate of correction should not exceed 0.5 mEq/L/h, with a total increase not to exceed 8-10 mEq/L in a 24-hour period. The sodium concentration must be corrected to a safe range (usually to ≤ 120 mEq/L) rather than to a normal value.
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Cite this: Vecihi Batuman. Fast Five Quiz: Electrolyte Disorders - Medscape - Mar 23, 2021.