American Family Physician - Initial evaluation of vertigo
Hyperkalemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors. Acute episodes of hyperkalemia commonly are triggered by the introduction of a medication affecting potassium homeostasis; illness or dehydration also can be triggers. In patients with diabetic nephropathy, hyperkalemia may be caused by the syndrome of hyporeninemic hypoaldosteronism. The presence of typical electrocardiographic changes or a rapid rise in serum potassium indicates that hyperkalemia is potentially life threatening. Urine potassium, creatinine, and osmolarity should be obtained as a first step in determining the cause of hyperkalemia, which directs long-term treatment. Intravenous calcium is effective in reversing electrocardiographic changes and reducing the risk of arrhythmias but does not lower serum potassium. Serum potassium levels can be lowered acutely by using intravenous insulin and glucose, nebulized beta2 agonists, or both. Sodium polystyrene therapy, sometimes with intravenous furosemide and saline, is then initiated to lower total body potassium levels. (Am Fam Physician 2006;73:283-90. Copyright
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The prevalence of hyperkalemia in hospitalized patients is between 1 and 10 percent. (1) Although the exact prevalence of hyperkalemia in community-based medical practice is unknown, potassium elevation is a common, potentially life-threatening problem most often occuring in patients with chronic renal failure or other illnesses that reduce renal potassium excretion (Table 1 (2,3)). In these patients, acute hyperkalemia often is precipitated by stressors such as illness, dehydration, or initiation of medicines that alter potassium homeostasis (Table 24-10). (4-7)
Normal Potassium Physiology
Two mechanisms normally regulate potassium levels in response to variation of potassium intake. First, ingested potassium rapidly enters the portal circulation, stimulating the pancreas to release insulin. Elevated insulin levels induce rapid transport of potassium from the extracellular space into cells via cellular sodium-potassium adenosine triphosphatase. Second, increased potassium in the circulation causes the renal juxtaglomerular cells to release renin. This stimulates hepatic activation of angiotensin I that is then converted in the lungs to angiotensin II. Angiotensin II stimulates the adrenal zona glomerulosa to secrete aldosterone. Elevated serum aldosterone causes the renal cortical collecting ducts to excrete potassium and retain sodium, further lowering serum potassium.2
Causes of Hyperkalemia
The first step in the evaluation of a patient with elevated serum potassium is to exclude spurious potassium elevation (Table 3 (2,3)). If the elevation is shown to be real, the next step is to consider: (1) the effects of medications, including increased potassium intake (Table 2 (4-10)); (2) the impaired distribution of potassium between the intracellular and extracellular space; or (3) the impaired renal excretion of potassium. All three factors often are present (e.g., the stress of illness induces hyperkalemia in a patient rendered susceptible by impaired homeostatic mechanisms and the presence of a medication that impairs normal potassium regulation).
PSEUDOHYPERKALEMIA
Pseudohyperkalemia occurs when laboratory reports of potassium do not reflect actual values. The most common cause is lysis of red cells in a phlebotomy specimen. Other causes are listed in Table 3 (2,3). Potassium released from platelets can lead to spuriously high levels of potassium in a blood sample allowed to clot to collect serum. Pseudohyperkalemia can be excluded by repeating the sample collection as atraumatically as possible and obtaining serum and plasma potassium levels. In patients with pseudohyperkalemia, the plasma potassium will be normal in the face of an elevated serum potassium.
HYPERKALEMIA CAUSED BY DECREASED EXCRETION OF POTASSIUM
Effective excretion of potassium is dependent on aldosterone and sufficient distal delivery of sodium and water within the nephron. Hyperkalemia may occur when one of these mechanisms is impaired because of renal failure, renal hypoperfusion (e.g., volume depletion, congestive heart failure), or hypoaldosteronism. Hypoaldosteronism may be the cause of hyperkalemia in patients who do not have advanced renal failure or hypoperfusion. (11)
Hyporeninemic hypoaldosteronism, a syndrome associated with type IV renal tubular acidosis, may be part of the mechanism behind hyperkalemia in patients with mild renal failure, particularly diabetic nephropathy. Hyporeninemic hypoaldosteronism can cause patients who have diabetic nephropathy to develop acute elevations of potassium because of medications or stress (e.g., dehydration, acute illness). (12)
MEDICATION-INDUCED HYPERKALEMIA
The factors that decrease potassium excretion also increase the risk of medication-induced hyperkalemia. Because of the relative decline in renal function with age, family physicians should use caution when prescribing medications that alter potassium metabolism in older patients. Judicious monitoring of potassium levels is important in at-risk patients receiving these medicines.
