Hyperkalemia

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}} Hyperkalemia (hyper is high, kalium is the Latinname for potassium) is an elevated blood level (above 5.0 mmol/L) of the electrolytepotassium. Extreme degrees of hyperkalemia are considered a medical emergencydue to the risk of potentially fatal arrhythmias.

Signs and symptoms

Symptoms are fairly nonspecific, and generally include malaise and muscle weakness; mild breathlessness may indicate metabolic acidosis, one of the settings in which hyperkalemia may occur. Often, however, the problem is detected during screening blood testsfor a medical disorder, or it only comes to medical attention after complications have developed, such as cardiac arrhythmiaor sudden death.

During the medical history taking, a doctor will dwell on kidney diseaseand medicationuse (see below), as these are the main causes. The combination of abdominal pain, hypoglycemiaand hyperpigmentation, often in the context of a history of other autoimmune disorders, may be signs of Addison's disease, itself a medical emergency.

Diagnosis

In order to gather enough information for diagnosis, the measurement of potassium needs to be repeated, as the elevation can be due to hemolysisof the material in the first sample. Generally, blood tests for renal function(creatinine, blood urea nitrogen), glucoseand occasionally creatine kinaseand cortisolwill be performed. Calculating the trans-tubular potassium gradientcan sometimes help in distinguishing the cause of the hyperkalemia.

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 gasmeasurements and renal ultrasoundwill be performed.

Differential diagnosis

Causes include:

Ineffective elimination from the body

• Renal failure
• Medication. Medication that can cause hyperkalemia (most are antihypertensives):
  • ACE inhibitors
  • Potassium-sparing diuretics(e.g. amilorideand spironolactone)
  • Angiotensin receptor blockers
  • Succinylcholine(also known as suxamethonium, a paralytic used in anesthesia)
• Metabolic acidosis
• Mineralocorticoiddeficiency 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, burnsor any cause of rapid tissue necrosis, including tumor lysis syndrome
• Massive blood transfusionor massive hemolysis
• Insulindeficiency

Excessive intake

• Intoxication(potassium-containing dietary supplements or salt replacement)

Pathophysiology

Potassium is the most important intracellularcationand participates in many cellular processes, including transmission of action potentialsin nerve cells. Its main dietary sources are vegetables(tomatoand potato), fruits (orangeand banana) and meat. Elimination is through the gastrointestinal tractand the kidney.

The renal elimination of potassium is passive (through the glomeruli), and resorption is active in the proximal tubuleand the ascending limb of the loop of Henle. In the distal tubule, there is active excretion of potassium in the distal tubuleand 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 aldosteronedeficiency) or due to causes in the renal parenchyma that impair excretion.

Increased extracellular potassium levels result in depolarizationof the membrane potentials of cells. This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinalorgan systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillationor asystole.

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.

• Calciumsupplementation (calcium gluconate10%, preferably through a central venous catheteras the calcium may cause phlebitis) does not lower potassium but decreases myocardialexcitability, protecting against life threatening arrhythmias.
• Salbutamolnebuliser (or intravenously) is a rapidly acting catecholamine. Catecholamines promote movement of K into cells, lowering the blood levels.
• Insulinand 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. Kayexelatecan 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 dialysisto remove the potassium from the circulation.
• When mineralocorticoid deficiency is contributing, high dose hydrocortisoneand intravenous salinesolution may be all that is necessary.

See also

• Hypokalemia
• Renal failure

Reference

• Kasper DL et al (Eds). Harrison's Principles of Internal Medicine, 16th ed, chapter 41, pages 258-61. ISBN 0071402357.de:Hyperkaliämie

References

• Schaefer TJ, Wolford RW (2005). Disorders of potassium. Emerg Med Clin North Am, 23(3), 723-47.

This article is licensed under the GNU Free Documentation License.
It uses material from the http://en.wikipedia.org/wiki/Hyperkalemia Wikipedia article Hyperkalemia.