Hyperkalemia is a condition of elevated serum potassium concentration (> 5.5 mmol/L) due primarily to reduced excretion of urinary potassium, increased potassium release from cells, and excess potassium intake.
Signs and symptoms include muscle weakness, paralysis, and cardiac abnormalities (irregular conduction and arrhythmias). Hyperkalemia is most commonly seen in individuals with:
Concurrent use of beta blockers, angiotensin-converting enzyme (ACE) inhibitors / angiotensin II receptor blockers (ARBs), and potassium-sparing diuretics.
ECG changes of hyperkalemia do not reliably correlate with potassium levels, but mild elevation (5.5-6.5 mmol/L) may cause peaked T waves, shortened QT interval, and ST-segment depression. At higher levels of potassium (< 8.0 mmol/L), the ECG may demonstrate peaked T waves, PR prolongation with decreased P waves, and widening QRS.
Codes
ICD10CM: E87.5 – Hyperkalemia
SNOMEDCT: 14140009 – Hyperkalemia
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Differential Diagnosis & Pitfalls
In the process of treating hyperkalemia, it is important to determine what is causing the elevation in potassium. In general, there are 3 mechanisms by which hyperkalemia occurs: increased potassium release from cells, increased potassium intake, and decreased potassium excretion.
Increased potassium release from cells
Pseudohyperkalemia – This is a diagnosis of exclusion. It most often occurs with hemolysis during blood draws. The intracellular fluid containing a higher concentration of positively charged potassium ions (K+) is exposed to the collected sample, resulting in an artificially elevated K+ level on the laboratory results. This can be considered when the patient has no symptoms of hyperkalemia and no changes on ECG, or in cases of difficult blood draws with longer tourniquet times.
Metabolic acidosis – K+ transcellularly shifts out of the cells to maintain electroneutrality as the increasing number of positively charged hydrogen ions (H+) accumulates in the cells.
Insulin encourages K+ entry into cells. In diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS), insulin depletion (either compromised insulin secretion or insulin resistance) and concurrent hyperosmolality secondary to hyperglycemia lead to marked hyperkalemia.
As the plasma osmolality increases, the osmotic gradient favors water excretion out of the cell. Potassium exits the cells via 2 different mechanisms. As water exits the cell, the potassium gradient becomes more potent, favoring potassium excretion via K+ channels in the cell membrane. The other mechanism involves the concept of solvent drag, as K+ ions are carried out of the cell via water excretion.
Any mechanism that depletes insulin (octreotide or fasting) or that raises the serum osmolality (hypernatremia, mannitol, contrast) can cause hyperkalemia via these same mechanisms.
Beta blockers – Beta-2 agonists promote K+ entry into cells. Beta blockers, primarily nonselective beta blockers, prevent this effect. The typical rise in K+ is approximately lower than 0.5 mEq/L, and true hyperkalemia is rare.
Exercise – K+ is released during exercise, most likely to promote vasodilation. This mechanism is thought to contribute to pseudohyperkalemia via excessive hand clenching during blood draws. Hyperkalemia during exercise can be compounded by patients taking nonselective beta blockers and in patients who are in end-stage renal disease (ESRD).
Hyperkalemic periodic paralysis – This autosomal dominant disorder involves a point mutation in the skeletal muscle cell sodium channel. It occurs when episodes of weakness or paralysis are precipitated by stress (eg, cold exposure, exercise, fasting, and ingestion of potassium).
Red blood cell transfusion – K+ leaks out of cells while in storage
Increase in potassium intake
Excess consumption of potassium-rich foods, such as bananas, potatoes, melons, citrus, and avocados
Intake of salt substitutes (common in patients with chronic kidney disease)
Reduced urinary potassium excretion
Acute or chronic kidney disease – Potassium excretion is mainly mediated by the kidneys. In both acute kidney injury and chronic kidney disease, potassium excretion is decreased and hyperkalemia may develop.
Hyporeninemic hypoaldosteronism – Aldosterone promotes sodium ion (Na+) reabsorption and K+ excretion. In hyporeninemic hypoaldosteronism, there is decreased renin secretion and, therefore, decreased aldosterone secretion, allowing for K+ to accumulate in the blood.
Type 4 renal tubular acidosis and cortical collecting duct defects – Type 4 renal tubular acidosis forms from decreased aldosterone responsiveness in the cortical collecting duct due to defects in the collecting duct or decreased aldosterone secretion.
Drugs, including angiotensin inhibitors, NSAIDs, calcineurin inhibitors (cyclosporine, tacrolimus), heparin, and potassium-sparing diuretics.
Calcineurin inhibitors (cyclosporine, tacrolimus) are nephrotoxic drugs that decrease the kidney's ability to excrete K+.
Heparin – Heparin-induced hypoaldosteronism can cause hyperkalemia.
K+-sparing diuretics – In the collecting duct, the blockage of epithelial sodium channels (ENaCs) (amiloride, triamterene) or the blockage of aldosterone receptors (spironolactone, eplerenone) cause a decrease in K+ excretion.
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Drug Reaction Data
Below is a list of drugs with literature evidence indicating an adverse association with this diagnosis. The list is continually updated through ongoing research and new medication approvals. Click on Citations to sort by number of citations or click on Medication to sort the medications alphabetically.
