Hypokalemia

Hypokalemia is the serum potassium concentration of less than 3.5 meq / l, caused by a deficiency in total K in the body or an abnormal K movement inside the cells. The most common causes include increased loss through the kidneys or the gastrointestinal tract. Clinical manifestations include muscle weakness, polyuria; Excessive excitability of the myocardium can develop with severe hypokalemia.

[1], [2], [3]

Causes of the hypokalemia

Conditionally hypokalemia is divided into so-called pseudohypokalemia, i.e. Flowing without loss of potassium, and hypokalemia with loss of potassium.

Pseudohypokalemia develops with inadequate intake of potassium in the body (depletion syndrome) or the movement of potassium from the extracellular space to the intracellular space. The movement of the electrolyte into the intracellular space is promoted by hormones (insulin and adrenaline). To hypokalemia leads to an increase in the level of insulin, caused by hyperglycemia or the introduction of exogenous insulin. Endogenous release of catecholamines in stress or the use of beta ₂ -adrenomimetics is also accompanied by a decrease in the concentration of potassium in the blood serum. Redistribution of potassium with its movement inside cells occurs with hereditary hypokalemic periodic paralysis, thyrotoxicosis (thyrotoxic hypokalemic paralysis).

In clinical practice, hypokalemia due to potassium loss is more common. Potassium losses are divided into extrarenal (usually through the gastrointestinal tract) and kidney. The distinction between these states is based on the determination of the chloride concentration in the urine. When urinary excretion of chlorides <15 mmol / l with a high degree of probability assume the loss of electrolytes through the gastrointestinal tract.

The main causes of extrarenal potassium losses: constant vomiting (neurogenic anorexia, gastrointestinal diseases), diarrhea (gastrointestinal diseases, excessive use of laxatives). In these situations, hypokalemia, as a rule, is accompanied by the development of metabolic alkalosis, which arises in connection with the depletion of chlorides in the body, which adaptively leads to an intensive reabsorption of chloride in the kidneys and an increase in renal excretion of potassium.

Diagnosis of renal losses of potassium in the case when patients with hypokalemia are diagnosed with "excessive state of excretion" of potassium and chloride in urine (potassium urium is more than 20 mmol / day, chloride excretion is more than 60 mmol / l). Diseases that occur with similar electrolyte disorders, differ in the level of blood pressure. In this connection, in the classification of the causes of renal losses of potassium, 2 groups of pathological conditions are distinguished: normotensive (group A) and hypertensive (group B) states. The latter group is further subdivided depending on the level of circulating aldosterone and plasma renin.

Normotensive conditions (group A):

• abuse of diuretics (loop, thiazide, acetazolamide);
• Bartter's syndrome;
• Gitelman's syndrome;
• immune potassium-interstitial nephritis;
• renal tubular acidosis type I and II.

Hypertensive conditions (group B):

• with a high level of aldosterone and renin (primary aldosteronism against adenoma and adrenal hyperplasia);
• with a high level of aldosterone and low level of renin (malignant hypertension, renovascular hypertension, tumor secreting renin);
• with a low level of aldosterone and renin (use of mineralocorticoids, glycyrisic acid, carbenesolone);
• with a normal level of aldosterone and renin (Isenko-Cushing syndrome).

Among the renal losses of potassium group A, abuse of diuretics and Gitelman syndrome predominate.

In clinical practice, hypokalemia often develops with the abuse of diuretics or laxatives. As a rule, this situation is typical for young women who strictly follow their figure in connection with the characteristics of the character or profession. The main clinical and laboratory manifestations are weakness, hypokalemia and hypochloraemia, metabolic alkalosis, high concentration of potassium and chlorine in the urine (chlorine concentration more than 60 mmol / l), normal blood pressure values. To diagnose this condition, it is necessary to carefully collect the patient's history and confirm the presence of diuretics in several urine samples.

The more rarely diagnosed Bartter's syndrome in its clinical and laboratory manifestations is hardly distinguishable from the abuse of diuretics. However, Bartter's syndrome is a pathology, usually of early childhood. Most often it is detected in children with violations of intrauterine development (intrauterine growth retardation, polyhydramnios), and often with preterm labor. The main clinical signs are hypokalemia, polyuria with potassium-induced fatigue, low blood pressure values, secondary hyperaldosteronism and metabolic alkalosis. The content of Mg ²⁺  in the blood and the excretion of Ca ²⁺  in the urine are within the normal range. With Bartter's syndrome, hyperplasia of the juxtammadullary apparatus is revealed, which is accompanied by a sharp increase in the production of renin and aldosterone. The pronounced electrolyte disturbances in this syndrome are due to gene disorders that are associated with the mutation of the TALH gene responsible for the reabsorption of chlorides in the distal straight tubule.

Gitelman's syndrome, described in the late 1960s, is currently considered the most common cause of hypokalemic renal involvement. More than 50% of all cases of hypokalemia is associated with this syndrome. The disease develops in adults and manifests moderately pronounced hypokalemia (potassium serum is in the range of 2.4-3.2 mmol / l), which does not reduce the quality of life, does not cause violations of heart rhythm and muscle weakness. The examination often reveals a decrease in the concentration of Mg ²⁺  in the blood, border hypochloraemia, poorly expressed metabolic alkalosis and secondary hyperaldosteronism. The functions of the kidneys of these patients remain intact for a long time. In the study of urine, attention is drawn to the increased excretion of chlorides, hypocalciuria. Diagnostically significant signs are a decrease in the level of magnesium in the blood serum and hypocalciuria. The reason for the development of Gitelman syndrome is associated with a mutation of the thiazide sensitive Na ⁺ -Q ~ cotransporter in the distal tubules of the nephron, which makes it possible to diagnose this condition by genotyping. For the correction of hypokalemia, products enriched with potassium and potassium supplements are used. The prognosis of patients with Gitelman syndrome is favorable.

Rare causes of hypokalemia are immune potassium-interstitial nephritis. This disease also reveals hypokalemia (from moderate to severe), hypercaliuria, metabolic alkalosis, moderate hyperaldosteronism. The concentration of calcium and phosphorus in the blood serum is usually within normal limits. A distinctive feature of the disease is the presence of concomitant autoimmune manifestations (iridocyclitis, immune arthritis or the detection of high-titer rheumatoid factor or autoantibodies). In kidney biopsies, lymphocytic infiltrates in interstitium are often found. The cause of electrolyte disturbances in this situation is associated with damage to ion transporters, but, in contrast to the syndromes of Bartter and Gitelman, not of genetically determined, but of immune genesis.

A common cause of hypokalemia development along with the above states is renal ductal acidosis of distal (I) and proximal (II) type. The prevailing clinical manifestations of the disease are pronounced hypokalemia and metabolic acidosis. A similar clinical picture is also caused by prolonged use of carbonic anhydrase inhibitors (acetazolamide).

In patients with loss of potassium in hypertensive states (group B), the main cause of hypokalemia is the excessive production of mineralocorticoid hormones, primarily aldosterone. Hypochloremic metabolic alkalosis usually develops in these patients. The combination of high aldosterone concentrations and low plasma renin activity is observed in primary aldosteronism, which develops in adenoma, hyperplasia or carcinoma of the glomerular zone of the adrenal cortex. Hyperaldosteronism with a high plasma renin level is usually detected in malignant hypertension, renovascular hypertension and renin-secreting tumors. Hypokalemia against a background of arterial hypertension with a normal level of aldosterone and plasma renin develops with  the Itenko-Cushing syndrome.

[4],

Symptoms of the hypokalemia

Light hypokalemia (plasma potassium level 3-3.5 meq / L) rarely causes symptoms. At a plasma potassium level of less than 3 meq / l, muscle weakness usually develops, which can lead to paralysis and respiratory arrest. Other muscular disorders include convulsions, fasciculations, paralytic intestinal obstruction, hypoventilation, hypotension, tetany, rhabdomyolysis. Persistent hypokalemia can lead to a violation of the concentration ability of the kidneys, causing polyuria with secondary polydipsia.

Cardiac effects of hypokalemia are minimal to potassium level  in plasma  <3 meq / L. Hypokalemia causes a decrease in the ST segment, a depression of the T wave, a rise in the U wave. With considerable hypokalaemia, the T wave progressively decreases, and U increases. Sometimes a flat or positive T merges with a positive U-tooth, which may be mistaken for a prolonged QT. Hypokalemia can cause premature contractions of the atria and ventricles, ventricular and atrial tachyarrhythmias, and atrioventricular blockades of the 2nd-3rd degree. Such arrhythmias are worse with more severe hypokalemia; as a result, ventricular fibrillation may develop. Patients with existing heart disease and / or taking digoxin have a high risk of cardiac conduction disorders even with mild hypokalemia.

Symptoms of hypokalemia are as follows:

• defeat of skeletal musculature (muscle weakness, fatigue, flaccid paralysis, rhabdomyolysis);
• defeat of smooth muscles (decreased motility of the stomach and small intestine);
• defeat of the heart muscle (decrease of the T wave, prolongation of the QT interval, appearance of the pronounced U-wave, expansion of the QRS complex and development of the atrioventricular blockade);
• defeat of peripheral nerves (paresthesias and rigidity of limbs);
• kidney damage with the development of polyuria, nocturia (due to a violation of the concentration ability of the kidneys) and primary polydipsia.

Long-term depletion of potassium reserves can cause interstitial nephritis and the development of renal failure, and in some cases - the formation of cysts in the kidneys.

[5], [6], [7]

Diagnostics of the hypokalemia

Hypokalemia is diagnosed at a K level in the plasma of less than 3.5 meq / l. If the cause is not obvious from an anamnesis (for example, taking medications), further examination is necessary. After excluding acidosis and other causes of the transition of K into the cells, a 24 hour level of K in the urine is measured. With hypokalemia, K secretion is usually less than 15 meq / L. The extrarenal loss of K or decrease in its intake with food is observed in cases of chronic unexplained hypokalemia, when renal secretion K <15 meq / L. Secretion> 15 meq / L testifies to the renal causes of loss of K.

Unexplained hypokalemia with increased renal K secretion and hypertension presupposes an aldosterone secreting tumor or Liddle syndrome. Hypokalemia with increased renal loss of K and normal BP suggests Barter's syndrome, but hypomagnesemia, secret vomiting and diuretic abuse are also possible.

[8]

Treatment of the hypokalemia

Symptoms of hypokalemia, confirmed by the detection of low levels of electrolyte in the blood serum, require immediate correction of the electrolyte balance, as a decrease in serum potassium content by 1 mmol / l (in the concentration range of 2-4 mmol / l) corresponds to a decrease in its total stores in the body on 10%.

There are various oral K preparations. Since they cause irritation of the gastrointestinal tract and occasional bleeding, they are usually given in divided doses. Liquid KCI when administered orally increases the K level for 1-2 hours, but is poorly tolerated at doses greater than 25-50 meq because of the bitter taste. KCI preparations coated with a coating are safe and better tolerated. Gastrointestinal bleeding is less common with microencapsulated drugs. There are several preparations containing 8-10 meq per capsule.

In severe hypokalemia, not responding to oral therapy, or inpatients in the active phase of the disease, compensation of K should be parenteral. Since solutions of K can exert an irritating effect on the peripheral veins, the concentration should not exceed 40 meq / l. The rate of correction of hypokalemia is limited by the period of K movement into the cells, the rate of administration should not exceed 10 meq / h.

In arrhythmias caused by hypokalemia, intravenous administration of KCI should occur faster, usually along the central vein or with the simultaneous use of several peripheral veins. 40 meq KCI / h can be administered, but only when monitoring the ECG and determining the K plasma level every hour. Glucose solutions are undesirable, as increasing plasma insulin levels can lead to transient deterioration of hypokalemia.

With a K deficiency with a high K concentration in the plasma, which is observed with diabetic ketoacidosis, intravenous administration of K is delayed until the K level in plasma begins to decrease. Even in the case of severe K deficiency, there is usually no need to administer more than 100-120 mekv K for 24 hours, except for cases of continued loss of K. When hypokalemia is combined with hypomagnesemia, correction of deficiency of K and Mg is necessary in order to avoid the continuing renal loss of K.

In patients taking diuretics, there is no need for constant admission K. However, when taking diuretics, control of plasma K level is necessary, especially in patients with decreased left ventricular function taking digoxin in the presence of diabetes mellitus in patients with asthma receiving beta-agonists. Triamterene in a dose of 100 mg orally once a day or spironolactone at a dose of 25 mg orally does not increase the excretion of K and can be taken by patients who develop hypokalemia, but who can not refuse to take diuretics. With the development of hypokalemia, compensation is required K. At a K level of less than 3 meq / l, oral KCI is needed. Since a decrease in the K plasma level by 1 meq / l correlates with a total K deficiency in the body of 200-400 meq, a dose of 20-80 meq / day is required for several days to correct the deficit. When you resume food after a prolonged fasting, you may need to take K preparations for several weeks.

Hypokalemia in the presence of diuretics and Gitelman syndrome is rarely expressed (from 3 to 3.5 mmol / l), and in patients who are not on digitalis, these changes rarely lead to serious complications. In connection with the concomitant loss of potassium in urine, the depletion of magnesium - an electrolyte that is involved in the functioning of many enzymes involving adenosine triphosphate (ATP) and, accordingly, involved in the regulation of the cardiovascular and nervous system, even an unsharpened degree of hypokalemia should be Corrected. In these situations, the doctor's tactics should be aimed at the abolition of potassium diuretics (if this is possible according to the condition of the patient) or the additional appointment of potassium-sparing diuretics in conjunction with the administration of potassium preparations. Low sodium content in the diet (70-80 mmol / day) also helps reduce the severity of hypokalemia.

With more pronounced and poorly corrected hypokalemia, the introduction of potassium chloride homeostasis in combination with potassium-sparing diuretics (amiloride, triamterene or spironolactone) is used to normalize potassium homeostasis.

Treatment of hypokalemia in metabolic alkalosis is the use of potassium chloride, and in the treatment of renal tubular acidosis, potassium hydrogen carbonate. Intravenous administration of these drugs is justified with a pronounced degree of hypokalemia (serum potassium concentration less than 2.5 mmol / l and the presence of clinical signs of potassium deficiency - changes in the electrocardiogram, muscle weakness). The said potassium preparations are administered intravenously at such doses that provide potassium intake in a concentration of 0.7 mmol / kg for 1-2 hours.

With severe hypokalemia (potassium serum below 2.0 mmol / l) or the development of arrhythmias, the dose of potassium administered is increased to 80-100 mmol / l. It should be remembered that the administration of potassium to the peripheral vein at a dose exceeding 60 mmol / l, even at a low rate of its administration (5-10 mmol / h), is extremely painful. If a rapid intravenous injection of potassium is necessary, a femoral vein can be used. With the development of urgent states, potassium solutions are administered at a rate exceeding the calculated loss of potassium (20 to 60 mmol / h). The introduced potassium is initially distributed in the extracellular fluid and then enters the cell. Intensive treatment of hypokalemia is discontinued when the degree of hypokalemia is no longer a danger to the life of the patient. Usually this is achieved by administering about 15 mmol of potassium in 15 minutes. In the future, the deficit of potassium is replenished more slowly under the constant control of the electrocardiogram and its serum level.