Potassium is the most common intracellular cation, but only a small portion is found in the extracellular fluids. Potassium plays an important role in cellular function, neuromuscular activity, and cardiac conduction. Because the body does not store potassium, it requires a minimum intake of 40 to 60 mEq/day. Most potassium (80%) is excreted through the kidneys in response to hyperkalemia and/or the hormone aldosterone; 15% is excreted through the gastrointestinal tract, and 5% is lost through the skin. (Smith, 2000)

Potassium levels normally are regulated by two mechanisms in response to variation in potassium intake. In the first mechanism, ingested potassium enters the hepatic portal circulation, which stimulates the pancreas to release insulin. The elevated levels of insulin cause the rapid transport of potassium from the extracellular space into cells. In the second mechanism, increased potassium in the circulation causes the release of renin from the renal juxtaglomerular cells; this stimulates hepatic activation of angiotensin I, which is converted to angiotension II in the lungs (Hollander-Rodriguez & Calvert, 2006).

The most common cause of hypokalemia is potassium depletion, which results from an inadequate intake or abnormal losses. Hypokalemia can also occur without actual loss of total body potassium, through processes that result in a shift from the extracellular fluid to the intracellular spaces (e.g., acidosis). In acidosis, potassium moves out of the cell in exchange for hydrogen; as the kidneys continue to excrete potassium, hypokalemia becomes evident. In metabolic acidosis, severe potassium depletion usually is seen as a result of increased bicarbonate reabsorption. Hypovolemia stimulates the rennin-angiotensin system, which leads to the secretion of aldosterone and the excretion of potassium through the kidneys (Smith, 2000).

When trauma or severe injury occurs, anabolic cellular activity increases the demand for intracellular potassium, and this can cause hypokalemia. Pseudohypokalemia can occur with leukocytosis because of an increased uptake of potassium by white blood cells after a specimen has been drawn (Smith, 2000).

Hypokalemia is an exceptionally common electrolyte abnormality in clinical practice. More than 20% of hospitalized patients have been reported to have some degree of hypokalemia (Schaefer & Wolford, 2005).

As mentioned, the most common cause of hypokalemia is potassium depletion caused by inadequate intake or abnormal losses. Although loss of electrolytes through vomiting, diarrhea, or nasogastric drainage does not cause potassium depletion, it does cause significant chloride depletion, which alters the renal signals for potassium secretion and promotes renal potassium losses (Gennari, 2002).

Increased excretion of potassium can occur through renal losses caused by diuretics, metabolic alkalosis, mineralocorticoid excess, magnesium depletion, and renal tubular acidosis.

A variety of tumors may ectopically synthesize ACTH and cause Cushing’s syndrome; this can be rapidly fatal with fast-growing tumors. The patient may complain of weakness, and hypokalemia and metabolic acidosis may be severe (Casciato, 2004).

The prognosis for hypokalemia depends entirely on the underlying cause. Hypokalemia caused by diarrhea has an excellent prognosis. Hypokalemia caused by a rapidly growing tumor that is producing ACTH has a poor prognosis.