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Last reviewed: 11.04.2020

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Hyperkalemia is the concentration of a potassium in serum 5.5 mEq/L, which develops as a result of an excess of total body potassium or due to abnormal movement of potassium from the cells.

A common cause is impairment of renal excretion; but it may also occur in patients with metabolic acidosis, like in the case of uncontrolled diabetes. Usually clinical manifestations are neuromuscular characterized by muscle weakness and cardiotoxicity, which with severe treatment can lead to ventricular fibrillation or asystole. Diagnostics is based on determining the level of K (potassium) in the plasma or serum. The treatment is insertion of the cation and in extreme cases calcium gluconate, insulin or dialysis.

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Causes of hyperkalemia

The main causes of hyperkalemia are redistribution of potassium from the intracellular to the extracellular space and the delay of potassium in the body. However, so-called false increase potassium in the blood is worth mentioning, which is detected by hemolysis, high leukocytosis (white blood cells including over 200 000/ml of blood) and thrombocytosis. Hyperkalemia in these cases is caused by the release of potassium from the blood cells.

Redistribution of potassium from the intracellular to the extracellular space observed during the development of acidosis, insulin deficiency and the introduction of beta-blockers. Fast exit of potassium from the cells to the development of severe hyperkalemia occurs with severe trauma or crush syndrome. Chemotherapy of lymphoma, leukemia and multiple myeloma is accompanied by increased levels of potassium in the blood serum. Redistribution of potassium can also be caused by alcohol intoxication and the insertion of drugs that change potassium ratio between the cell and its environment. These drugs include cardiac glycosides, depolarizing muscle relaxants (succinylcholine). Hyperkalemia can be caused by severe or long exercise stress.

Hyperkalemia due to the delay of potassium by kidney is one of the most common causes of potassium imbalance with nephrological diseases. Isolation of potassium by the kidney depends on the number of nephrons, adequate delivery of sodium and fluid to the distal nephron, normal aldosterone secretion and condition of distal tubule epithelium. Renal insufficiency on its own doesn’t lead to the development of hyperkalemia until GFR falls to 15-10 ml/min or diuresis decreases to less than 1 l/sec. Under these conditions, homeostasis is maintained by increased secretion of potassium in the remaining nephrons. The exceptions are patients with interstitial nephritis or hyporeninemic hypoaldosteronism. This situation is most commonly seen in elderly patients (diabetics) who use drugs, which directly or indirectly (through the renin) blocking aldosterone synthesis (indomethacin, heparin sodium, captopril, etc.).

The main causes of renal origin hyperkalemia are oliguric renal failure (acute or chronic), mineralocorticoid insufficiency (Addison's disease, hyporeninemic hypoaldosteronism); drugs that violate the renal excretion of potassium (spironolactone, triamterene, amiloride, ACE inhibitors, heparin sodium).

Tubular Defects in Renal Excretion of Potassium

The rapid development of hyperkalemia in acute renal failure and chronic oliguric renal failure due to decreased GFR, reduced intake of fluid in the distal of nephron, direct damage of the distal tubules in acute tubular necrosis.

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Mineralocorticoid Deficiency

Aldosterone stimulates the secretion of potassium in the cortical collecting ducts and increases its cellular uptake. Aldosterone deficiency regardless of the reason of its development predisposes to the development of hyperkalemia. Hypoaldosteronism may be the result of a primary adrenal glands lesion (Addison's disease), or develop as a result of genetic defects in the biosynthesis of aldosterone (adrenal syndrome, or 21-hydroxylase deficiency). During the Addison's disease it often reveals salt depletion and overall reduction in body tone, like with hyperkalemia.

Hypoaldosteronism combined with low plasma renin is known as hyporeninemic hypoaldosteronism. This syndrome is often detected with chronic tubulointerstitial kidney disease, diabetes, obstructive nephropathy, sickle-cell anemia. Drugs may be the cause of hyporeninemic hypoaldosteronism development. We describe the development of this syndrome in the application of indomethacin and heparin sodium. Typically, the syndrome occurs in elderly patients, half of whom developed hyperchloraemic metabolic acidosis as a response to caused by hyperkalemia inhibition of the formation of ammonia in the kidney and impaired secretion of H + because of low level of aldosterone. Doctors detect arterial hypertension in half of the cases; the vast majority of patients are diagnosed with kidney failure.

Drugs that violate the renal potassium excretion

Spironolactone inhibits the secretion of potassium in the cortical collecting ducts. It operates as antagonists of aldosterone binding protein mineralocorticoid receptors in the target cells, forming a spironolactone-receptor complex. This leads to inhibition of dependent on aldosterone sodium reabsorption in the cortical collecting ducts with the corresponding inhibition of distal tubular secretion of potassium. Amiloride and triamterene inhibit the secretion of potassium through aldosterone independent mechanism. ACE inhibitors cause an increase in the level of blood serum potassium through the blockade of the angiotensin II effect and indirect by this suppression of the aldosterone production. Intensity of hyperkalemia, particularly sharp, increases during renal insufficiency. Heparin effects like a direct inhibitor of the synthesis of aldosterone, which requires careful use of this drug to patients with diabetes and renal failure.

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Tubular Potassium Renal Secretion Defects

Tubular potassium renal secretion defects are found in patients with normal or elevated levels of renin and aldosterone in blood serum. These patients haven’t had any effect during mineralocorticoid assigning; normal kaliuresis doesn’t develop as a response to the introduction of sodium sulfate, furosemide or potassium chloride. These defects are detected in patients with sickle cell disease, systemic lupus erythematosus, obstructive nephropathy and patients with transplanted kidney.

Symptoms of hyperkalemia

Symptoms of hyperkalemia manifest  themselves by cardiac arrhythmias; the electrocardiogram reveals an increased T-wave, the expansion of the complex QRS, prolongation of the PR interval and further flattening appears biphasic wave QRS-T. In addition, there may be arrhythmias (supraventricular tachycardia, sinoatrial block, atrio-ventricular dissociation, ventricular fibrillation or asystole).

Although sometimes there is flaccid paralysis, hyperkalemia is usually asymptomatic until the progress of cardiotoxicity. ECG changes appear when the plasma K level is more than 5.5 mEq/L and characterized by shortening of the interval QT, high, symmetrical, peaked T-wave. K-level more than 6.5 mEq/L causes nodal and ventricular arrhythmias, a wide range of QRS, prolongation of the interval PR, the disappearance of P-wave. As a result, it may develop ventricular fibrillation or asystole.

In case of rare hyperchloraemic family periodic paralysis, muscle weakness develops progress to severe paralysis.

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Diagnostics of hyperkalemia

Hyperkalemia diagnosed with plasma K level more than 5.5 mEq/L. It should be considered that severe hyperkalemia requires immediate treatment, so it’s important with patients at high risk, which include patients with renal insufficiency; progressive heart failure, ACE inhibitors and K-sparing diuretics; or with symptoms of renal obstruction, especially with arrhythmias or other ECG evidence of hyperkalemia.

Determining the cause of hyperkalemia includes examining drugs, determination of electrolytes, blood urea nitrogen, creatinine. It is necessary to do extra tests (including ultrasound of the kidneys to eliminate the obstruction etc) if you have renal failure.

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What do need to examine?

Treatment of hyperkalemia

Treatment of hyperkalemia requires orientation in the content of potassium in blood serum and ECG data.

Mild Hyperkalemia

Doctors can apply reduction of K consumption or stop the drug, increasing the level of K, to patients with plasma K levels less than 6 mEq/L and absence of changes in the ECG. Adding loop diuretics increases the K excretion. It’s possible to apply sodium polystyrene sulfonate sorbitol (1530 g in 3070 ml 70% sorbitol orally every 4-6 hours). It acts as a cation exchange resin and removes K through the gastrointestinal mucus. Sorbitol is assigned with cation to allow the passage through the digestive tract. Patients who can’t take oral due to ileus, or other reasons, the same dose may be administered in the form of an enema. About 1 mEq K injected per gram of cation. Cation exchange therapy passes and often has no significant effect on the reduction of plasma potassium level hyperkatabolis states. Excess of Na may be observed (especially, patients with oliguria, and ECF volume increased before) during using sodium polystyrene sulphonate because of exchanged Na to K.

Moderate and Severe Hyperkalemia

K level in plasma more than 6 meq/l (especially with the ECG changes) require aggressive therapy to transfer K inside cells. The first two of the following measures should be carried out immediately.

It is necessary to introduce 10-20 ml of 10% calcium gluconate solution (or 5.10 mL of 22% solution of calcium gluceptate) intravenously in 5-10 minutes. Calcium antagonizes the effects of hyperglycemia on the excitability of the heart muscle. Doctor should be care when appointing calcium to patients, who are taking digoxin, because of the risk of arrhythmias associated with hypokalemia. If there is a sinusoidal wave or asystole registered on the ECG, calcium gluconate administration can be accelerated (5-10 ml intravenously in 2 minutes). It is also possible to use calcium chloride, but it may have an irritating effect and must be administered through a central venous catheter. The effect develops in several minutes, but lasts only 20-30 minutes. The introduction of calcium is a temporary measure while waiting for the effects of other treatments and can be repeated if necessary.

The second move is introduction 5-10 units of regular insulin intravenously with immediately subsequent or simultaneous rapid infusion of 50 ml of 50% glucose solution. Introduction 10% dextrose should be carried out at a rate of 50 ml per hour to prevent hypoglycemia. The maximum effect on the plasma levels of potassium developed after 1 hour and lasts for several hours.

High-dose of beta-agonist (e.g. albuterol 10-20 mg) inhaled in 10 minutes (concentration 5 mg/ml) can safely reduce plasma potassium by 0.5-1.5 meq/liter. The best effect is observed after 90 minutes.

Intravenous injection of NaHCO is controversial. It can reduce the serum potassium level for several hours. Reduction may develop as a result of alkalinity or hypertonicity due to concentrations of sodium in the preparation. Hypertonic sodium contained in the product can be harmful for patients on dialysis, who can also have ECF volume increase. The usual dose is 45 meq (1 vial of 7.5% solution of NaHCO), it injects for 5 minutes and then procedure repeats after 30 minutes. This treatment has a small effect if we use it for patients with advanced renal failure (except epidemic).

In addition to the above-mentioned strategies of reducing the level of potassium into cells by changing the treatment of severe or symptomatic hyperkalemia attempts of potassium excretion from the body should be applied. Potassium can be outputted through the gastrointestinal tract with applying polystyrene sulfonate or with the application of hemodialysis. Peritoneal dialysis is relatively ineffective in removing potassium.

Severe hyperkalemia with concomitant changes on the electrocardiogram is a threat to the patient’s life. It is necessary to perform urgent intensive correction of electrolyte abnormalities in this situation. Patients with renal insufficiency by his health data get hemodialysis which able to withdraw excess potassium from the blood.

Intensive treatment of hyperkalemia includes the following steps:

  • Stabilization of myocardial activity; injection intravenously of 10% calcium gluconate solution (10 ml for three minutes, if necessary repeat the procedure after 5 min);
  • stimulate movement of potassium from the extracellular space into the cell; intravenously 500 ml of 20% glucose solution with 10 units of insulin in one hour; 20 mg of albuterol inhalation in 10 minutes;
  • injecting sodium bicarbonate if there are expressed forms of metabolic acidosis (for bicarbonate values in the blood serum less than 10 mmol/l).

After the acute phase, or the absence of changes on the electrocardiogram using diuretics, and the cation exchange resin.

In order to prevent the development of severe hyperkalemia is recommended following treatment of hyperkalemia:

  • limit the potassium in the diet to 40-60 mmol/day;
  • exclude drugs that can reduce the excretion of potassium from the body (potassium-sparing diuretics, NSAIDs, ACE inhibitors);
  • exclude prescriptions that can move the potassium out of the cell into the extracellular space (beta-blockers);
  • use loop and thiazide diuretics for intensive excretion potassium in the urine, if there aren’t contraindications;
  • apply specific pathogenetic treatment of hyperkalemia in each case.

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