Potassium is the predominant intracellular cation. Hypokalemia occurs when the serum potassium falls below 3.4 meq/L and most commonly occurs secondary to profuse vomiting with or without diarrhea. Therapy with loop diuretics can also cause hypokalemia. In diabetic ketoacidosis, profound hypokalemia can result from osmotic diuresis, although, in the face of the hydrogen-potassium shift that accompanies acidemia, serum levels may be normal or falsely elevated. Uncommon causes of hypokalemia are renal tubular acidosis and familial hypokalemia-induced paralysis.

Severe potassium depletion can result in skeletal muscle weakness, ileus, and cardiac conduction disturbances. A prominent electrocardiographic (ECG) manifestation is the U wave. Clinical manifestations generally reflect the rate of fall of serum potassium rather than the absolute level.

In most cases, hypokalemia occurs slowly, and it is difficult to predict whole body stores based on the serum level. In general, oral replacement over several days is adequate. Dehydration must be corrected. If intravenous therapy is necessary, 0.2 to 0.3 meq/kg/h is adequate. In extremely urgent situations, such as hypokalemia-induced respiratory insufficiency, 1 meq/kg/h can be administered, with continuous ECG monitoring. This is usually done via a central line. In diabetic ketoacidosis, potassium repletion should begin early in the course of therapy, since diuresis-induced depletion can result in profound hypokalemia as acidosis is corrected and serum potassium shifts into cells.

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