Hyperkalemia

Hyperkalemia, also spelled hyperkalaemia, is an elevated level of potassium (K+) in the blood serum. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically this results in no symptoms. Occasionally when severe it results in palpitations, muscle pain, muscle weakness, or numbness. An abnormal heart rate can occur which can result in cardiac arrest and death. Common causes include kidney failure, hypoaldosteronism, and rhabdomyolysis. A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors. The severity is divided into mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L), and severe (>6.5 mmol/L). High levels can also be detected on an electrocardiogram (ECG). Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out. Initial treatment in those with ECG changes is calcium gluconate. Medications that might worsen the condition should be stopped and a low potassium diet should be recommended. Other medications used include dextrose with insulin, salbutamol, and sodium bicarbonate. Measures to remove potassium from the body include furosemide, polystyrene sulfonate, and hemodialysis. Hemodialysis is the most effective method. The use of polystyrene sulfonate, while common, is poorly supported by evidence. Hyperkalemia is rare among those who are otherwise healthy. Among those who are in hospital, rates are between 1% and 2.5%. It increases the overall risk of death by at least ten times. The word 'hyperkalemia' is from hyper- meaning high; kalium meaning potassium; and -emia, meaning 'in the blood'. The symptoms of an elevated potassium level are nonspecific, and generally include malaise, palpitations, shortness of breath, and muscle weakness. Hyperventilation may indicate a compensatory response to metabolic acidosis, which is one of the possible causes of hyperkalemia. Often, however, the problem is detected during screening blood tests for a medical disorder, or after hospitalisation for complications such as cardiac arrhythmia or sudden cardiac death. High levels of potassium (> 5.5 mmol/L) have been associated with cardiovascular events. Decreased kidney function is a major cause of hyperkalemia. This is especially pronounced in acute kidney injury where the glomerular filtration rate and tubular flow are markedly decreased, characterised by reduced urine output. This can be further intensified by active cellular breakdown which causes increase in serum potassium levels. In chronic kidney disease, hyperkalemia occurs as a result of reduced aldosterone responsiveness and reduced sodium and watery deliveries in distal tubules. Medications that interferes with urinary excretion by inhibiting the renin–angiotensin system is one of the most common causes of hyperkalemia. Examples of medications that can cause hyperkalemia include ACE inhibitors, angiotensin receptor blockers, beta blockers, and calcineurin inhibitor immunosuppressants such as ciclosporin and tacrolimus. For potassium-sparing diuretics, such as amiloride and triamterene; both the drugs block epithelial sodium channels in the collecting tubules, thereby preventing potassium excretion into urine. Spironolactone acts by competitively inhibiting the action of aldosterone. NSAIDs such as ibuprofen, naproxen, or celecoxib inhibit prostaglandin synthesis, leading to reduced production of renin and aldosterone, causing potassium retention. The antibiotic trimethoprim and the antiparasitic medication pentamidine inhibits potassium excretion, which is similar to mechanism of action by amiloride and triamterene. Mineralocorticoid (aldosterone) deficiency or resistance can also cause hyperkalemia. Primary adrenal insufficiency are: Addison's disease and congenital adrenal hyperplasia (CAH) (including enzyme deficiencies such as 21α hydroxylase, 17α hydroxylase, 11β hydroxylase, or 3β dehydrogenase).