ESSENTIALS OF DIAGNOSIS
Serum potassium level greater than 5.2 mEq/L (5.2 mmol/L).
Check medications carefully. Hyperkalemia may develop from angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and potassium-sparing diuretics, most commonly in patients with kidney dysfunction.
The ECG may be normal despite life-threatening hyperkalemia.
Rule out pseudohyperkalemia and extracellular potassium shift from cells.
Hyperkalemia is a rare occurrence in normal individuals due to adaptive mechanisms designed to prevent accumulation of potassium in the extracellular fluid, mainly via rapid urinary excretion. Persistent hyperkalemia generally requires an impairment in renal potassium excretion due to impaired secretion of or hyporesponsiveness to aldosterone, impaired delivery of sodium and water to the distal nephron, or kidney disease (acute or chronic) (Table 21–4). Transient hyperkalemia suggests shift of potassium from inside cells into the extracellular fluid, which can occur in the context of tissue damage (rhabdomyolysis, tumor lysis, massive hemolysis, and trauma) or metabolic acidosis. Finally, pseudohyperkalemia is a laboratory artifact in which there is an elevation in serum potassium levels in the absence of true electrolyte imbalance as a result of tourniquet application or fist clenching during blood draw, or improper transport or processing of venous samples in patients with marked thrombocytosis or leukocytosis.
Table 21–4.Causes of hyperkalemia. |Favorite Table|Download (.pdf) Table 21–4. Causes of hyperkalemia.
Marked thrombocytosis or leukocytosis with release of intracellular K+
Repeated fist clenching during phlebotomy, tourniquet application, use of small-bore needles during lab draw
Shift of K+ out of the cell
Tissue injury (rhabdomyolysis, hemolysis, tumor lysis)
Hyperkalemic periodic paralysis
Drugs (digoxin overdose, succinylcholine)
Kidney disease, acute and chronic
Renal secretory defects (may or may not have reduced kidney function): kidney transplant, interstitial nephritis, systemic lupus erythematosus, sickle cell disease, amyloidosis, obstructive nephropathy
Type IV renal tubular acidosis
Drugs that inhibit potassium excretion: spironolactone, eplerenone, drospirenone, NSAIDs, ACE inhibitors, angiotensin II receptor blockers, triamterene, amiloride, trimethoprim, pentamidine, cyclosporine, tacrolimus
Excessive intake of K+
Especially in patients with diminished kidney excretion
The symptoms of hyperkalemia are a consequence of impaired neuromuscular transmission. The most serious manifestations are cardiac conduction abnormalities and neuromuscular manifestations, such as muscle weakness, which may be profound. This generally occurs with potassium concentrations above 7 mEq/L, though it can vary depending on the acuity in development of hyperkalemia. Hyperkalemic period paralysis is a rare genetic disorder characterized by episodes of painless muscle weakness precipitated by potassium ingestion, rest after heavy exercise, and cold exposure. Hyperkalemia additionally impairs urinary ammonium excretion and may lead to metabolic acidosis.
Electrocardiography is an unreliable method for detecting hyperkalemia; clinical studies show poor correlation between serum potassium levels ...