Hyperkalemia

Potassium is a monovalent cation whose presence is essential for life. All cells in the human body have a transporter on the surface of the cell whose specific function is to ferry potassium inside the cell. This transporter is called the sodium-potassium ATPase, and utilizes energy stored in the form of ATP to actively push sodium outside of cells and potassium into cells. This process is continuous, and cells would cease to function if this transporter stopped working.

Hyperkalemia is an electrolyte disturbance where a person's serum potassium is elevated. Potassium is a major contributor to the cell's membrane voltage gradient, and an increase in extracellular potassium can disturb that gradient and cause multisystem effects. Cells that rely heavily upon the membrane voltage gradient, such as neurons and muscle cells are especially vulnerable to such disturbances. Hyperkalemia can be a medical emergency and can result in death from arrhythmias and cardiac arrest.

Causes

There are two basic causes of true hyperkalemia:

-Decreased excretion of potassium by the kidneys

-Transcellular shifts

Decreased Excretion

Like most electrolytes, the kidneys play a vital role in regulating potassium levels. Therefore, any cause of kidney failure can cause potassium levels to rise. Patients who have end-stage renal disease are especially susceptible to hyperkalemia.

However, even people with normal renal function can have situations where there is decreased potassium excretion. Because potassium homeostasis is controlled in great part by aldosterone (with aldosterone acting at the distal tubule of the kidney to increase potassium excretion), situations where aldosterone is low can lead to hyperkalemia. These include primary adrenal insufficiency and medications that interfere with the renin-angiotensin-aldosterone system. Such medications include ACE inhibitors, ARBs, and potassium sparing diurectics such as spironolactone.

Transcellular shifts

Certain conditions can cause potassium to shift in and out of cells. Things that will cause potassium to shift out of cells include:

-Acidosis, where there are extra protons in the serum (decreased pH)

-Beta-blockers such as metoprolol

-Digitalis

-Cellular lysis (such as seem in tumor lysis syndrome or rhabdomyolysis)

Pseudohyperkalemia

Pseudohyperkalemia is when serum testing for potassium is artificially high. This is caused by hemolysis, where cells in the blood sample collected burst open and release their intracellular potassium. Because the concentration of potassium is very high within cells, a few cells lysing can dramatically increase the perceived potassium level.

Pseudohyperkalemia can also be seen in situations where clot is formed in the specimen vial. The act of forming clots releases potassium, and pro-thrombotic situations can cause this after collection of a sample. These include very high white cell counts (WBC > 50,000) and very high platelet counts (platelets > 1 million).

Signs and Symptoms

The primary symptoms of hyperkalemia result from disturbances of cells that most rely on the cellular membrane gradient (e.g. neurons and muscle cells). These symptoms include weakness, paresthesias, and palpitations.

Signs include changes on EKG: peaked T waves is the classic sign of hyperkalemia. Left untreated one can see an increase in the PR interval (including the spectrum of first degree heart block to complete heart block), an increased QRS duration, ventricular fibrillation, and PEA.

Diagnosis

Diagnosis of hyperkalemia is made chiefly by serum testing of potassium levels. A high potassium level in a patient with no clear reason to be hyperkalemic and no symptoms of hyperkalemia should raise suspicion of pseudohyperkalemia and should be retested.

EKG changes, such as peaked T waves or new AV blocks represent life-threatening hyperkalemia and should be treated immediately.

Treatment

The ultimate goal of treatment should be to fix the underlying cause, however, the immediate goal of treatment is to prevent serious cardiac events. Medications that should be administered include:

Calcium gluconate

Calcium gluconate stabilizes cardiac myocytes' membrane gradients and can prevent the progression of T wave inversions to more serious arrhythmias. This is a temporary measure until definitive treatment can be obtained.

Insulin and glucose

Insulin promotes a transcellular shift of potassium into cells. The glucose does not directly affect potassium levels but should be given to prevent hypoglycemia (low blood sugar). This is also a temporary measure as the shifted potassium will eventually be released by the cells.

Beta-agonists

As mentioned above, beta blockers will facilitate potassium release from cells, and beta agonists such as albuertol will promote potassium shifts into cells. Like insulin, this is a temporary measure as the potassium will eventually shift back into the serum.

Kayexalate

Kayexalate is a sodium exchange resin that is given orally or an an enema. It works by exchanging potassium for sodium within the intestine. As it permanently removes potassium from the system, it is a more definitive treatment for hyperkalemia.

Loop diuretics

Loop diuretics such as furosemide (Lasix) will increase the renal excretion of potassium. This is also a definitive treatment of hyperkalemia; however, it will not work in patients with severe renal insufficiency or end-stage renal disease.

Dialysis

Hemodialysis is the most definitive treatment for hyperkalemia, and its use should be employed if available and cardiotoxicity is demonstrated.

Prevention

Hyperkalemia is chiefly a problem of end-stage renal disease patients. Patients are advised to consume diets low in potassium and will attend dialysis regularly (or perform continuous ambulatory peritoneal dialysis, or CAPD at home) to prevent the accumulation of potassium.