Hypokalemia

Hypokalemia is a serum potassium concentration <3.5 mEq / l, which is caused by a reduction of the data stored in the body total amount of potassium or pathological shift of potassium into the cells. The most common cause is excessive loss of potassium through the kidneys or the gastrointestinal tract. Clinical indications are muscle weakness and polyuria. In severe hypokalemia may also occur in the occurrence of cardiac excitability. Diagnosis is made by determination of serum values. The treatment consists in a potassium administration and in the treatment of the cause.

(See also overview of disorders of potassium concentration.)

Hypokalemia is a serum potassium concentration <3.5 mEq / l, which is caused by a reduction of the data stored in the body total amount of potassium or pathological shift of potassium into the cells. The most common cause is excessive loss of potassium through the kidneys or the gastrointestinal tract. Clinical indications are muscle weakness and polyuria. In severe hypokalemia may also occur in the occurrence of cardiac excitability. Diagnosis is made by determination of serum values. The treatment consists in a potassium administration and in the treatment of the cause. (See also overview of disorders of potassium concentration.) Etiology A hypokalaemia can be caused by a decreased potassium intake, but is caused by excessive loss of potassium in the urine or via the gastrointestinal tract in general. Losses via the gastrointestinal tract in the following situations occurs pathological gastrointestinal potassium loss Chronic diarrhea including chronic laxative abuse or Malrotation the intestine intake of clay (bentonite), potassium binds and the absorbance greatly reduced rare villous adenomas of the colon, resulting in a massive loss of potassium lengthy vomiting or Magenabsaugung (the volume of hydrochloric acid and flies) cause kidney potassium losses due to metabolic alkalosis and stimulation of aldosterone due to volume depletion; Aldosterone and metabolic alkalosis cause both the kidneys potassium auszuscheiden.Intrazelluläre displacement A transcellular shift of potassium into the cells can also cause hypokalemia. At this shift may occur in the following cases: glycogenesis overeating as part of a parenteral nutrition or enteral (the insulin release stimulated) After administration of insulin stimulation of the sympathetic nervous system, in particular by beta-2 agonists (e.g., albuterol, terbutaline). which increases cellular potassium intake. Thyrotoxicosis (occasionally) due to excessive beta-sympathetic stimulation (hypokalemic periodic paralysis thyrotoxic) on. Familial periodic paralysis The familial periodic paralysis is a rare autosomal dominant disease that is characterized by transient episodes clearly Hypokalämien which are believed to be caused by sudden, pathologic potassium shifts into the cells. During these episodes often occur paralysis of varying degrees. They are formed usually by a high-carbohydrate meal or a strenuous Übung.Renale potassium losses Various disorders can increase the urinary excretion of potassium. The excretion of potassium may directly be increased in the distal nephron due to a Mineralokortikoidüberschusses (i.e., aldosterone); he comes in the following situations: Adrenal Mineralokortikoidüberschuss in Cushing's syndrome, the primary aldosteronism, on rare renin-secreting tumors, glucocorticoid a Sensitive aldosteronism (a rare, inherited disorder in which an abnormal Aldosteronstoffwechsel can be found), and in congenital adrenal hyperplasia , Ingestion of substances such as glycyrrhizin (which occurs in natural licorice and is used in the manufacture of chewing tobacco), which inhibit the enzyme 11-beta-hydroxysteroid dehydrogenase (11?-HSDH), which the conversion of cortisol which has a mineralocorticoid activity, cortisone, the activity has not prevented; This leads to high levels circulating cortisol and to a high loss of potassium through the kidneys. Bartter's syndrome, a rare genetic change that is characterized by a renal potassium and sodium loss and an excessive production of renin and aldosterone in normotensive blood pressure values. The Bartter syndrome is caused by a mutation in an ion transport mechanism in the Henle's loop responsive to loop diuretics. The Gitelman syndrome is a rare genetic change that is characterized by a renal potassium and sodium loss and an excessive production of renin and aldosterone in normotensive blood pressure values. The Gitelman syndrome is caused by mutations in a thiazidsensitiven ion transport mechanism in the distal nephron, which thereby loses its function. The Liddle's syndrome is a rare autosomal dominant disorder that is characterized by severe hypertension and hypokalaemia. The Liddle's syndrome is caused by increased sodium reabsorption in the distal nephron. This is due to one or more mutations that encode subunits of the epithelial sodium channel. An unduly high sodium reabsorption results in both hypertension and a renal potassium loss. A renal potassium loss can thus be triggered by a variety of inherited and acquired disorders of the kidney tubular. Further examples are the renal tubular acidosis and Fanconi syndrome, also a rarely occurring syndrome, which leads to a loss of renal potassium, glucose, phosphate, uric acid and amino acids. Hypomagnesemia often correlated with hypokalemia. Much of this correlation to common causes (d. H. Diuretics, diarrhea) due, but hypomagnesemia itself can also lead to increased potassium loss through the kidneys führen.Arzneimittel diuretics are the most widely used by far medications that can produce hypokalemia. Kaliumverlierende diuretics that block sodium reabsorption proximal the distal nephron are, thiazides, loop diuretics osmotic diuretics By triggering a diarrhea can also laxatives, especially if they are used improperly, lead to hypokalemia. The secret diuretics and / or laxatives is a common cause of persistent hypokalemia, particularly in patients with a pathological attitude to weight loss and people who work in health care and have access to prescription drugs. Other drugs that can cause hypokalaemia, amphotericin B are penicillins, which are active against Pseudomonas (z. B. carbenicillin) penicillin in high doses theophylline ((in acute and chronic intoxication) symptoms and discomfort during a mild hypokalemia serum potassium 3-3 5 mEq / l) rarely show up symptoms. Serum potassium <3 mEq / l cause muscle weakness in general and can lead to paralysis and respiratory failure. Other muscular disorders are cramps, fasciculations, paralytic ileus, hypoventilation, hypotension, tetany, and rhabdomyolysis. Persistent hypokalemia may affect the renal concentration and lead to polyuria with secondary polydipsia. Diagnostic determination of serum potassium EKG In clinically unclear mechanism potassium in the 24-hour urine and serum magnesium concentration A hypokalemia (serum potassium <3.5 mEq / l) can be detected during routine determination of serum electrolytes. They should be adopted in patients with typical ECG changes or muscular symptoms and risk factors and confirmed by blood tests. ECG An ECG should be taken in patients with hypokalemia. The cardiac effects of hypokalemia are usually minimal, until the serum potassium concentrations decrease to <3 mEq / l. Hypokalaemia leads to ST-segment depression, decrease in the T-wave and U-wave increase. With increasing hypokalemia the T-wave is always smaller and the U wave correspondingly larger. Occasionally, to fuse a flat, positive T-wave with a positive U-wave, which may result with a prolonged QT interval to confusion (ECG changes during hypokalemia and hyperkalemia.). Hypokalemia can cause premature ventricular and atrial contractions, ventricular and atrial tachyarrhythmias and lead to second and third degree AV block. The heavier the hypokalemia, the more severe the arrhythmia, which can progress to ventricular fibrillation in rare cases. Patients with pre-existing heart disease and Glykosidtherapie have to get as a result of low-grade hypokalemia an increased risk of cardiac arrhythmias. Clinical calculator: QT interval correction (EKG) diagnosis of the causes of the cause can usually be found out by the history (in particular by the drug history); this is not possible, further studies need to be performed. After exclusion of causes of acidosis and other intracellular potassium displacement (increased beta-adrenergic effect, hyperinsulinemia) potassium in the 24-hour urine and serum magnesium concentration. In a hypokalemia potassium excretion is normally <15 mEq / l. Extrarenal potassium losses (z. B. via the gastrointestinal tract) or a reduced potassium intake is suspected in an otherwise unexplained chronic hypokalemia, when the renal excretion of potassium is <15 mEq / l. Excretion> 15 mEq / L directs the suspected renal potassium loss. An unexplained hypokalemia with increased potassium excretion, and hypertension is suggestive of a tumor or aldosteronsezernierenden Liddle syndrome. An unexplained hypokalemia with increased renal potassium losses and normal blood pressure indicates a Bartter syndrome or Gitelman syndrome. However, hypomagnesemia, recurrent vomiting and diuretics abuse frequent causes and should also be considered. ECG changes during hypokalemia and hyperkalemia. (Serum potassium in mEq / L.) Treatment Oral potassium replacement intravenous potassium replacement in severe hyperkalemia persist potassium losses There are many oral medications for potassium replacement. Since high single doses irritation in the gastrointestinal tract and may also cause bleeding occasionally, the deficits are usually compensated by multiple doses. Liquid, orally administered potassium chloride increases the concentrations within 1-2 hours, but it has a bitter taste and is poorly tolerated mEq particularly at doses> 25-50. Wax-impregnated potassium chloride preparations are safe and are better tolerated. Under therapy with potassium chloride preparations in microcapsules gastrointestinal bleeding occur less frequently. Various preparations have Dosages of 8 or 10 mEq / capsule. Since a decrease in serum potassium to 1 mEq / l to about a deficit of 200-400 mEq correlated in total body potassium memory, can be estimated the total deficit and balanced with 20-80 mEq / day for several days. If the hypokalemia is heavy (z. B. with ECG changes or severe symptoms) is not responsive to oral therapy, or in hospitalized patients taking digoxin or which have a significant heart disease or ongoing losses, potassium must be replaced intravenously. Since potassium solutions can irritate the peripheral vein, the concentration should not exceed 40 mEq / l. The rate of correction of hypokalemia is limited, because of the delayed motion of potassium from the extracellular space into the cells. The routine infusion rate should not exceed 10 mEq / hour. In the case of an arrhythmia caused by hypokalemia the potassium chloride solution is to be infused more rapidly, simultaneously either a single access or a plurality of peripheral veins. The infusion rate may be up to 40 mEq of potassium chloride / hour, but should be monitored by means of continuous cardiac monitoring and hourly determination of serum potassium levels. Glucose solutions should be avoided as the increase in serum insulin concentrations can lead to a temporary worsening of hypokalemia. Even in the event of a severe potassium deficiency, it is rarely necessary to substitute more than 100 to 120 mEq of potassium within 24 hours, unless the potassium loss continues. With a potassium deficiency with high serum potassium concentrations, for. B. at a diabetic ketoacidosis, the i.v. Potassium supplements postponed until the serum potassium levels start to fall. If a hypokalemia together with hypomagnesaemia on, both the potassium and the magnesium deficiency must be corrected in order to prevent progression of renal potassium losses. Prevention In most patients with diuretics is not necessary a routine substitution with potassium. However, the serum potassium levels should be monitored during treatment with diuretics, if the risk of hypokalemia or its complications is high. Is a high risk in patients with impaired left ventricular function, patients who take digoxin patients with diabetes (which can vary the insulin concentration) patients with asthma, beta-2 agonists take Therapy with triamterene 100 mg p.o. 1 times daily or spironolactone 25 mg p.o. 4 times a day does not increase the excretion of potassium and is therefore well suited for patients who need diuretics, but during treatment with other drugs developed hypokalemia. If hypokalaemia shows, they must usually be treated with oral potassium chloride. Summary An hypokalemia may be caused by a reduced potassium intake or displacement of extracellular potassium into cells, but is generally caused by excessive loss of potassium in the urine or via the gastrointestinal tract. Clinical symptoms include muscle weakness, cramps, fasciculations, paralytic ileus and severe hypokalemia hypoventilation and hypotension. To the ECG changes, the <3 mEq / l usually occur at a serum potassium level include ST-segment depression, decrease in the T-wave and U-wave increase. With increasing hypokalemia the T-wave is always smaller and the U wave correspondingly larger. Hypokalemia can cause premature ventricular and atrial contractions, ventricular and atrial tachyarrhythmias and lead to second and third degree AV block; possibly ventricular fibrillation can occur. Potassium is replaced orally with 20-80 mEq / day, unless the patient show changes in ECG have severe symptoms. In hypokalämischer arrhythmia potassium chloride is given intravenously via a central vein with a maximum of 40 mEq / hour and only with continuous monitoring of cardiac function; intravenous standard infusion should be no more than 10 mEq / hour.

Health Life Media Team

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