Hyperkalemia (hyper is high, kalium is the Latin name for potassium) is an elevated blood level (above 5.0 mmol/L) of the electrolyte potassium. Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of arrhythmia.

Signs and symptoms

Symptoms are fairly nonspecific, and generally include malaise. Often, the problem is detected during screening blood tests for a medical disorder. Often, it only comes to medical attention after resuscitation due to arrhythmia or sudden death.

During the medical history taking, a doctor will dwell on kidney disease and medication use (see below), as these are the main causes. Abdominal pain, hypoglycemia and brown pigmentation, together with a history of autoimmune disorders, may be signs of Addison's disease.

Medication that can cause hyperkalemia (note that most are antihypertensives):

• ACE inhibitors
• Potassium-sparing diuretics
• Angiotensin receptor blockers
• Spironolactone
• Suxamethonium (muscle relaxant)

Diagnosis

In order to gather enough information for diagnosis, the measurement of potassium needs to be repeated, as the elevation can be due to hemolysis of the material in the first sample. Generally, blood tests for renal function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol will be performed.

Electrocardiography (ECG) is generally done early to identify any influences on the heart. High, tent-shaped T-waves, a small P wave and a wide QRS complex (that becomes sinusoidal) all identify the influence of excess potassium on the heart. This finding alone is an important reason for treatment, as it may forewarn ventricular fibrillation.

Often arterial blood gas measurements and renal ultrasound will be performed.

Differential diagnosis

• Ineffective elimination from the body:
  • Renal failure
  • Medication
  • Metabolic acidosis
  • Mineralocorticoid deficiency or resistance (many types)
    • Addison's disease
    • Aldosterone defiency
    • Congenital adrenal hyperplasia
  • Liddle syndrome , pseudohypoaldosteronism, other defects of renal tubular K excretion
• Excessive release from cells:
  • Rhabdomyolysis, burns or any cause of rapid tissue necrosis, including tumor lysis syndrome
  • Massive blood transfusion or massive hemolysis
  • Insulin deficiency
• Excessive intake:
  • Intoxication (potassium-containing dietary supplements or salt replacement)

Pathophysiology

Potassium is the most important intracellular cation and participates in many cellular processes, including transmission of action potentials in nerve cells. Its main dietary sources are vegetables (tomato, orange and banana) and meat. Elimination is through the gastrointestinal tract and the kidney.

The renal elimination of potassium is passive (through the glomeruli), and resorption is active in the proximal tubule and the ascending limb of the loop of Henle. In the distal tubule, there is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.

Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.

Treatment

When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower K levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.

• Calcium supplementation (calcium gluconate 10%, preferably over a central line as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against arrhythmia.
• Salbutamol nebuliser (or intravenously) is a rapidly acting catecholamine. Catecholamines promote movement of K into cells, lowering the blood levels.
• Insulin and dextrose (e.g. 20 Units of insulin and 50 ml 50% dextrose) act similarly, leading to a shift of potassium ions into the intracellular compartment. Some of the glucose transport mechanisms bring a K ion into the cell with each glucose molecule transported.
• Polystyrene sulfonate (Calcium Resonium, Kayexalate) is a binding resin that binds K within the gut and removes it from the body by defecation. Calcium Resonium (15g three times a day in water) can be given by mouth. Kayexelate can be given by mouth or as an enema. In both cases, the resin absorbs K within the gut and carries it out of the body by defecation.
• Refractory or very severe cases may need dialysis to remove the potassium from the circulation.
• When mineralocorticoid deficiency is contributing, high dose hydrocortisone and intravenous saline solution may be all that is necessary.

See also

• Hypokalemia
• Renal failure