Hyperkalemia

Hyperkalemia is a serum potassium concentration of 5.5 mEq/L, resulting from excess total body potassium or from abnormal movement of potassium out of cells. Impaired renal excretion is a common cause; it may also occur with metabolic acidosis, as in uncontrolled diabetes. The clinical manifestations are usually neuromuscular, characterized by muscle weakness and cardiotoxicity, which, if severe, may lead to ventricular fibrillation or asystole.

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Causes hyperkalemia

The main causes of hyperkalemia are the redistribution of potassium from the intracellular space to the extracellular space and the retention of potassium in the body.

At the same time, it is necessary to mention the so-called false increase in potassium in the blood, which is detected with hemolysis of erythrocytes, high leukocytosis (the number of leukocytes above 200,000 in 1 μl of blood) and thrombocytosis. Hyperkalemia in these cases is caused by the release of potassium from blood cells.

Redistribution of potassium from the intracellular to the extracellular space is observed during the development of acidosis, insulin deficiency, and the introduction of beta-blockers. Rapid release of potassium from cells with the development of severe hyperkalemia occurs in severe injuries and crush syndrome. Chemotherapy of lymphomas, leukemia, and myeloma is accompanied by an increase in the level of potassium in the blood serum. Redistribution of potassium can also be caused by alcohol intoxication and the introduction of drugs that change the ratio of potassium between the cell and the environment. Such drugs include cardiac glycosides, depolarizing muscle relaxants (succinylcholine). Hyperkalemia can be caused by very severe acute or prolonged physical exertion.

Hyperkalemia due to renal potassium retention is one of the most common causes of potassium imbalance in nephrological diseases. Renal potassium excretion depends on the number of functioning nephrons, adequate delivery of sodium and fluid to the distal nephron, normal secretion of aldosterone, and the state of the epithelium of the distal tubule. Renal failure itself does not lead to the development of hyperkalemia until the SCF is below 15-10 ml/min or diuresis decreases to values less than 1 l/day. Under these conditions, homeostasis is maintained due to increased secretion of potassium into the remaining nephrons. The exceptions are patients with interstitial nephritis and hyporeninemic hypoaldosteronism. This situation most often occurs in elderly people with diabetes mellitus, when taking drugs that directly or indirectly (via renin) block the synthesis of aldosterone (indomethacin, sodium heparin, captopril, etc.).

The main causes of hyperkalemia of renal genesis are oliguric renal failure (acute and chronic), mineralocorticoid deficiency ( Addison's disease, hyporeninemic hypoaldosteronism), drugs that impair renal excretion of potassium (spironolactone, triamterene, amiloride, ACE inhibitors, sodium heparin).

Tubular defects of renal potassium excretion

Rapid development of hyperkalemia in acute renal failure and oliguric chronic renal failure is due to decreased SCF, decreased fluid flow into the distal nephron, and direct damage to 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 uptake by cells. Aldosterone deficiency, regardless of the cause, predisposes to the development of hyperkalemia. Hypoaldosteronism may result from primary adrenal gland damage (Addison's disease) or develop as a result of hereditary defects in aldosterone biosynthesis (adrenogenital syndrome or C ₂₁ -hydroxylase deficiency). In Addison's disease, along with hyperkalemia, salt depletion and a general decrease in body tone are often detected.

Hypoaldosteronism in combination with low plasma renin levels is known as hyporeninemic hypoaldosteronism. This syndrome is often found in chronic tubulointerstitial kidney diseases, diabetes mellitus, obstructive nephropathy, and sickle cell anemia. It can also be caused by medications. We have described the development of this syndrome with the use of indomethacin and sodium heparin. As a rule, the syndrome occurs in elderly patients, half of whom develop hyperchloremic metabolic acidosis as a response to hyperkalemia-induced inhibition of renal ammonia formation and impaired H ⁺ secretion due to low aldosterone levels. Arterial hypertension is found in half of the cases; renal failure is diagnosed in the vast majority of patients.

Drugs that impair renal potassium excretion

Spironolactones inhibit potassium secretion in the cortical collecting duct. They act as aldosterone antagonists by binding to mineralocorticoid protein receptors in target cells, forming a spironolactone-receptor complex. This results in inhibition of aldosterone-dependent sodium reabsorption in the cortical collecting duct with corresponding inhibition of distal tubular potassium secretion. Amiloride and triamterene inhibit potassium secretion by an aldosterone-independent mechanism. ACE inhibitors cause an increase in serum potassium by blocking the action of angiotensin II and the resulting suppression of aldosterone production. The severity of hyperkalemia increases especially sharply in the presence of renal failure. Heparin acts as a direct inhibitor of aldosterone synthesis, which requires caution in patients with diabetes mellitus and renal failure.

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Tubular defects of renal potassium secretion

They are found in patients with normal or elevated serum renin and aldosterone levels. These patients do not respond to mineralocorticoids and do not develop normal kaliuresis in response to sodium sulfate, furosemide, or potassium chloride. These defects are found in patients with sickle cell anemia, systemic lupus erythematosus, obstructive nephropathy, and in patients with a transplanted kidney.

Symptoms hyperkalemia

Symptoms of hyperkalemia are manifested by disturbances of the heart rhythm: the electrocardiogram reveals an elevated T wave, widening of the QRS complex, prolongation of the P-R interval, and later the appearance of smoothing of the biphasic QRS-T wave. In addition, rhythm disturbances may occur (supraventricular tachycardia, sinoatrial block, atrioventricular dissociation, ventricular fibrillation and/or asystole).

Although flaccid paralysis is sometimes observed, hyperkalemia is usually asymptomatic until cardiotoxicity develops. ECG changes appear when plasma K levels are greater than 5.5 mEq/L and are characterized by shortening of the QT interval and tall, symmetrical, peaked T waves. K levels greater than 6.5 mEq/L cause nodal and ventricular arrhythmias, a wide QRS complex, prolongation of the PR interval, and disappearance of the P wave. Ventricular fibrillation or asystole may eventually develop.

In the rare case of hyperkalemic familial periodic paralysis, muscle weakness develops during attacks and may progress to full-blown paralysis.

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Diagnostics hyperkalemia

Hyperkalemia is diagnosed when the plasma K level is greater than 5.5 mEq/L. Since severe hyperkalemia requires immediate treatment, this should be considered in high-risk patients, including those with renal insufficiency; advanced heart failure taking ACE inhibitors and K-sparing diuretics; or with symptoms of renal obstruction, especially in the presence of arrhythmia or other ECG signs of hyperkalemia.

Determining the cause of hyperkalemia involves checking medications, determining the level of electrolytes, blood urea nitrogen, creatinine. In the presence of renal failure, additional studies are necessary, including ultrasound of the kidneys to exclude obstruction, etc.

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Treatment hyperkalemia

Treatment of hyperkalemia requires orientation in serum potassium levels and electrocardiogram data.

Mild hyperkalemia

In patients with plasma K levels less than 6 mEq/L and no changes on the ECG, it is enough to reduce K intake or discontinue drugs that increase K levels. The addition of a loop diuretic increases K excretion. Sodium polystyrene sulfonate in sorbitol (1530 g in 3070 ml of 70% sorbitol orally every 4 to 6 hours) can be used. It acts as a cation exchange resin and removes K through the gastrointestinal mucus. Sorbitol is given with a cation exchange resin to ensure passage through the gastrointestinal tract. In patients who cannot take drugs orally because of intestinal obstruction or for other reasons, the same doses can be given as an enema. About 1 mEq of K is removed for each gram of cation exchange resin. Cation exchange therapy is slow and often has no significant effect on lowering plasma K in hypercatabolic states. Since sodium polystyrene sulfonate is used to exchange Na for K, an excess of Na may be observed, especially in patients with oliguria, in whom oliguria was preceded by an increase in the volume of the ECF.

Moderate - severe hyperkalemia

Plasma K levels greater than 6 mEq/L, especially in the presence of ECG changes, require aggressive therapy to move K into cells. The first 2 of the following measures should be implemented immediately.

Administration of 10-20 ml of 10% calcium gluconate solution (or 5-10 ml of 22% calcium gluceptate solution) intravenously over 5-10 minutes. Calcium counteracts the effect of hyperglycemia on cardiac excitability. Caution is required when administering calcium to patients taking digoxin due to the risk of developing arrhythmias associated with hypokalemia. If the ECG shows a sinusoidal wave or asystole, the administration of calcium gluconate can be accelerated (5-10 ml intravenously over 2 minutes). Calcium chloride can also be used, but it can have an irritating effect and must be administered through a central venous catheter. The effect develops within a few minutes, but lasts only 20-30 minutes. Calcium administration is a temporary measure while waiting for the effects of other treatments and can be repeated if necessary.

Administration of regular insulin 5-10 U intravenously with immediate or simultaneous rapid infusion of 50 ml of 50% glucose solution. Administration of 10% dextrose solution should be carried out at a rate of 50 ml per hour to prevent hypoglycemia. The maximum effect on plasma potassium level develops after 1 hour and lasts for several hours.

A high dose of a beta-agonist, such as albuterol 10-20 mg inhaled over 10 minutes (concentration 5 mg/mL), can safely reduce plasma potassium by 0.5-1.5 mEq/L. The peak effect is seen at 90 minutes.

Intravenous administration of NaHCO is controversial. It may decrease serum potassium within a few hours. The decrease may result from alkalinization or hypertonicity due to the concentration of sodium in the preparation. The hypertonic sodium contained in the preparation may be harmful to patients on dialysis, who may also have an increase in ECF volume. When administered, the usual dose is 45 mEq (1 ampoule of 7.5% NaHCO ), administered over 5 minutes and repeated after 30 minutes. Treatment with NCO has little effect when used in patients with advanced renal failure, unless there is an epidemic.

In addition to the above intracellular potassium-lowering strategies, treatment of severe or symptomatic hyperkalemia should include attempts to remove potassium from the body. Potassium can be removed via the gastrointestinal tract by using sodium polystyrene sulfonate or by hemodialysis. In patients with renal failure or when emergency measures are ineffective, hemodialysis should be started immediately. Peritoneal dialysis is relatively ineffective in removing potassium.

Severe hyperkalemia with accompanying changes in the electrocardiogram poses a threat to the patient's life. In this situation, it is necessary to perform urgent intensive correction of electrolyte disturbances. A patient with renal failure undergoes hemodialysis sessions for vital indications, which can remove excess potassium from the blood.

Intensive treatment of hyperkalemia includes the following measures:

• stabilization of myocardial activity - a 10% solution of calcium gluconate is administered intravenously (10 ml over 3 minutes, if necessary, the drug is administered again after 5 minutes);
• stimulate the movement of potassium from the extracellular space into cells - intravenously 500 ml of 20% glucose solution with 10 units of insulin for 1 hour; inhalation of 20 mg of albuterol for 10 minutes;
• administration of sodium bicarbonate in case of severe manifestations of metabolic acidosis (with serum bicarbonate values less than 10 mmol/l).

After the acute phase or in the absence of changes on the electrocardiogram, diuretics and cation exchange resins are used.

To prevent the development of severe hyperkalemia, the following treatment for hyperkalemia is recommended:

• limiting 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 the use of drugs that can move potassium from the cell to the extracellular space (beta-blockers);
• in the absence of contraindications, use loop and thiazide diuretics to intensively excrete potassium in the urine;
• apply specific pathogenetic treatment of hyperkalemia in each individual case.