Hyponatremia in the form of extracellular ﬂuid excess can be seen in patients with renal or cardiac failure and in conditions such as nephrotic syndrome, in which total body salt and water are increased, with a relatively greater increase in the latter. Administration of hypertonic saline to correct the hyponatremia would be inappropriate in this setting. The treatment should include, in addition to correcting the underlying disease process, water restriction with diuretic therapy. Inappropriate secretion of antidiuretic hormone (ADH) can occur with head trauma, pulmonary or cerebral tumors, and states of stress. The abnormally elevated ADH results in excess water retention. Treatment includes water restriction and, if possible, correction of the underlying cause. Demeclocycline, a tetracycline antibiotic, is effective in this disorder via its action in the kidney. The introduction of vasopressin receptor antagonists, such as tolvaptan, may replace demeclocycline as the drug of choice for the syndrome of inappropriate ADH secretion (34).
Inappropriate replacement of body salt losses with water alone will result in hyponatremia.
This situation will typically occur in patients who lose large amounts of electrolytes secondary to vomiting, nasogastric suction, diarrhea, or gastrointestinal fistulas, and who received replacement with hypotonic solutions. Simple replacement with isotonic ﬂuids and potassium will usually correct the abnormality. Rarely, rapid correction of the hyponatremia is necessary, in which case hypertonic saline (3%) can be administered. Hypertonic saline should be administered very cautiously to avoid a rapid shift in serum sodium, which will induce central nervous system dysfunction.
Hypernatremia is an uncommon condition that can be life-threatening if severe (serum sodium greater than 160 mEq/L). The pathophysiology is extracellular ﬂuid deficit. The resultant hyperosmolar state leads to decreased water volume in cells in the central nervous system, which, if severe, can cause disorientation, seizures, intracranial bleeding, and death. The causes include excessive extrarenal water loss, which can occur in patients who have a high fever, have undergone tracheostomy in a dry environment, or have extensive thermal injuries; who have diabetes insipidus, either central or nephrogenic; and who have iatrogenic salt loading. The treatment involves correction of the underlying cause (correction of fever, humidification of the tracheostomy, administration of desmopressin for control of central diabetes insipidus) and replacement with free water either by the oral route or intravenously with D5W. As with severe hyponatremia, marked hypernatremia should be corrected slowly, no faster than 10 mEq per day, unless the patient is symptomatic from severe acute hypernatremia (35).
Hypokalemia may be encountered preoperatively in patients with significant gastrointestinal ﬂuid loss (prolonged emesis, diarrhea, nasogastric suction, intestinal fistulas) and marked urinary potassium loss secondary to renal tubular disorders (renal tubular acidosis, acute tubular necrosis, hyperaldosteronism, prolonged diuretic use). It can arise from prolonged administration of potassium-free parenteral ﬂuids in patients who are restricted from ingesting anything by mouth. The symptoms associated with hypokalemia include neuromuscular disturbances, ranging from muscle weakness to ﬂaccid paralysis, and cardiovascular abnormalities, including hypotension, bradycardia, arrhythmias, and enhancement of digitalis toxicity. These symptoms rarely occur unless the serum potassium level is less than 3 mEq/L. The treatment is potassium replacement. Oral therapy is preferable in patients who are on an oral diet.
If necessary, potassium replacement can be given intravenously in doses that should not exceed 10 mEq per hour.