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KEY POINTS
A careful assessment of the patient's osmolality and volume status are vital to appropriately evaluate the patient with either hypernatremia or hyponatremia.
The syndrome of inappropriate antidiuretic hormone is characterized by inappropriately concentrated urine in the setting of a low serum osmolality and a normal plasma volume.
Treatment strategies for syndrome of inappropriate antidiuretic hormone include fluid restriction to 1 to 1.5 L of free water per day, sodium chloride tablets, isotonic saline along with furosemide or hypertonic saline (2% or 3%) alone, and vasopressin-2 (V2) receptor antagonists (conivaptan and tolvaptan).
For patients with symptomatic and/or severe hyponatremia (mental status changes, seizures, coma, sodium < 115mEq/L), 3% normal saline should be used to correct the sodium deficit with close monitoring of their neurologic status and serum sodium values.
The goals in treating hypernatremia include identifying correcting any reversible factors (hypercalcemia, hypokalemia, and hypertonic solutions); correcting volume depletion if present; and replacing the calculated free water deficit.
The clinical signs and symptoms of hyperkalemia are predominantly neuromuscular (weakness, and muscle paralysis) and cardiac (electrocardiographic [EKG] changes—peaked T waves, prolonged PR interval, widened QRS, arrhythmias, and asystole).
The most rapid way to lower serum potassium is with the use of inhaled beta agonists (nebulized albuterol 10-20 mg over 15 minutes) and insulin (50 s of D50W and 10U regular insulin over 15-30 minutes). Other treatments include IV sodium bicarbonate, isotonic saline infusion, loop diuretics alone or in combination with saline infusion, and sodium polystyrene given as a rectal suppository or orally in combination with sorbitol for faster delivery to its site of action at the colonic mucosa.
Clinical manifestations of hypokalemia are predominantly cardiac (arrhythmias, EKG changes [flattening of the T wave, and U wave]) and neuromuscular (muscle weakness, paralysis, ileus, and constipation).
Symptoms of severe hypocalcemia include tetany, seizures, a prolonged QT interval, and ventricular arrhythmias. For acute correction of symptomatic hypocalcemia, IV calcium gluconate, or calcium chloride (10 mL of a 10% solution) can be administered over 10 minutes.
For patients with symptomatic hypercalcemia, aggressive volume expansion with 0.9% normal saline at rates needed to promote a urine output of 100 to 150 cc/h is recommended. Other treatments include furosemide after adequate volume resuscitation is achieved, calcitonin, bisphosphonates (pamidronate and zoledronate), and dialysis.
Hypophosphatemia may be associated with decreased myocardial contractility, respiratory failure due to diaphragmatic paralysis, dysphagia, ileus, paresthesias, seizures, rhabdomyolysis, and myopathy.
Hyperphosphatemia may result from tumor lysis syndrome, massive blood transfusions, rhabdomyolysis, acute extracellular shifts of phosphorus (lactic and diabetic ketoacidosis), ingestion of large amounts of phosphorus containing laxatives, hypoparathyroidism, and vitamin D toxicity.
Clinically important manifestations of hypomagnesemia include EKG changes (arrhythmias and torsades de pointes), neuromuscular problems (tetany and seizures), electrolyte disorders (hypokalemia and hypocalcemia) and impaired parathyroid hormone release and action.
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Fluid and electrolyte disorders are ubiquitous in the intensive care unit (ICU) setting. This text will focus on common clinical scenarios in the ICU and assumes a basic fund of knowledge about fluid and electrolyte disorders.
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