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  • Image not available. Hypovolemic hypotonic hyponatremia is relatively common in patients taking thiazide diuretics. Thiazide-induced hyponatremia is usually mild and relatively asymptomatic. Hyponatremia rarely if ever occurs with loop diuretics.
  • Image not available. The syndrome of inappropriate secretion of antidiuretic hormone causes euvolemic hypotonic hyponatremia. Common causes of this syndrome include lung cancer, central nervous system disorders, pulmonary disorders, and a variety of drugs.
  • Image not available. Symptoms of hyponatremia are usually neurologic in nature and symptom severity depends both on the magnitude of the decrease in serum sodium concentration and the rate at which it developed. Treatment of hyponatremia is associated with a risk of osmotic demyelination syndrome, a severe neurologic complication that can develop if the rate of serum sodium correction exceeds 8 to 12 mEq/L (8–12 mmol/L) within 24 hours.
  • Image not available. Asymptomatic or mildly symptomatic hyponatremic patients should generally be managed conservatively with treatment directed at the underlying cause. A 0.9% sodium chloride infusion can be cautiously used to correct the serum sodium in patients with hypovolemic hypotonic hyponatremia and moderate to severe symptoms. A 3% sodium chloride infusion can be cautiously used in patients with euvolemic or hypervolemic hypotonic hyponatremia and moderate to severe symptoms.
  • Image not available. Hypernatremia most commonly occurs when increased water or hypotonic fluid losses are not offset by increased water intake or administration. For example, patients with diabetes insipidus excrete large volumes of dilute urine, but usually develop hypernatremia only if their water intake does not increase to offset the increased water losses.
  • Image not available. Symptoms of hypernatremia are usually neurologic in nature, and range in severity from weakness, lethargy, restlessness, irritability, and confusion to twitching, seizures, coma, and death. The severity of symptoms depends on both the magnitude of the increase in serum sodium and the rate at which it developed.
  • Image not available. The treatment goals in patients with hypernatremia include cautious correction of the serum sodium concentration and, when appropriate, restoration of a normal extracellular fluid volume. Too rapid correction of the serum sodium can result in cerebral edema, seizures, neurologic damage, and possibly death. To minimize the risk of these complications, the serum sodium concentration should be corrected at a maximum rate of 0.5 to 1 mEq/L (0.5–1 mmol/L) per hour, depending on the rate of hypernatremia development, and be limited to no more than 10 mEq/L (10 mmol/L) per day.
  • Image not available. Patients with central diabetes insipidus should be treated with intranasal desmopressin acetate, with goals of decreasing urine volume to less than 2 L per day while maintaining the serum sodium concentration between 137 and 142 mEq/L (137 and 142 mmol/L). Patients with nephrogenic diabetes insipidus should be treated by correcting the underlying cause when possible, and sodium chloride restriction in conjunction with a thiazide diuretic to decrease the extracellular fluid volume by approximately 1 to 1.5 L.
  • Image not available. Edema can develop as a primary defect in renal sodium handling or as a response to a decreased effective circulating volume. It is usually first detected in the feet or pretibial areas of ambulatory patients. Pulmonary edema, evidenced by auscultatory crackles, can be life-threatening.
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