Hyperkalemia is a potentially life-threatening metabolic problem caused by the inability of the kidneys to excrete potassium, impairment of the mechanisms that transfer potassium from the circulation into the cells, or a combination of these factors (Hollander-Rodriguez & Calvert, 2006). Hyperkalemia in patients with or without cancer usually occurs as a consequence of renal failure.

Normal serum potassium (K+) ranges from 3.5 to 5.5 mEq/L. Hyperkalemia is defined as a serum potassium level greater than 5.5 mEq/L (Smith, 2000; Wallach, 2000). Potassium is the most common intracellular cation, and only a small percentage is found in the extracellular fluids. Potassium plays a critical role in cellular function, neuromuscular activity, and cardiac conduction, including maintenance of intracellular osmolality, maintenance of a balance between hydrogen and sodium within the cell, and maintenance of a stable resting membrane potential for transmitting and conducting nerve impulses. Potassium also plays a role in glycogen deposition in skeletal and liver cells in response to insulin (Smith, 2000).

The body does not store potassium, thercefore a minimum daily intake of 40 to 60 mEq is required. The typical Western diet provides an average of 50 to 100 mEq a day (Murphy-Ende, 2006). Most potassium (80%) is excreted through the kidneys in response to hyperkalemia and/or aldosterone. Fifteen percent is excreted through the gastrointestinal tract, and 5% is lost through the skin (Smith, 2000).

Potassium levels normally are regulated by two mechanisms, which are activated 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 rennin from the renal juxtaglomerular cells; this stimulates hepatic activation of angiotensin I, which is converted to angiotensin II in the lungs (Hollander-Rodriguez & Calvert, 2006). Angiotensin II causes the secretion of aldosterone from the kidney, and elevated aldosterone causes the kidney to excrete potassium and retain sodium, thereby lowering the serum potassium. A balance of GI intake and renal excretion results in long-term potassium balance (Garth, 2006).

Disorders of potassium are the most commonly encountered electrolyte abnormalities in hospitalized patients. Hyperkalemia occurs in up to 8% of hospitalized patients (Garth, 2006; Gennari, 2006) as a result of an imbalance in normal potassium handling. It most often occurs when potassium excretion is impaired by a medical condition or by medications taken by a patient with some degree of underlying renal dysfunction (Schaeffer & Wolford, 2005). The most common causes of hyperkalemia are kidney dysfunction, adrenal gland disease, shifting of potassium out of the cells into the circulation, and medication side effects (Stoppler, 2005). Hyperkalemia can result from:

The primary cause of mortality with hyperkalemia is potassium’s effect on cardiac function. The mortality rate can exceed 65% if severe hyperkalemia is not treated rapidly and effectively (Garth, 2006). Most patients can expect a full resolution with correction of the underlying etiology (Garth, 2006).