Hyperkalemia is a serum potassium concentration> 5.5 mEq / l, which is due to a reduced potassium excretion in renal or by a pathological shift of potassium into the extracellular space in the rule. There are usually several, concurrent causative factors, including the increase in potassium intake, drugs that interfere with potassium excretion by the kidneys, and acute renal disease or chronic kidney disease. Hyperkalemia may occur in the context of metabolic acidosis such as diabetic ketoacidosis. The clinical manifestations are usually neuromuscular cause. It show up muscle weakness and cardiac arrhythmias, which can at worst lead to ventricular fibrillation and asystole. The diagnosis results from the determination of serum potassium. The therapy can be done by reducing the potassium intake, adjusting the drug, administration of a cation exchange resin and in emergencies by the administration of calcium gluconate and insulin. The dialysis is a treatment option.
(See also overview of disorders of potassium concentration.)
Hyperkalemia is a serum potassium concentration> 5.5 mEq / l, which is due to a reduced potassium excretion in renal or by a pathological shift of potassium into the extracellular space in the rule. There are usually several, concurrent causative factors, including the increase in potassium intake, drugs that interfere with potassium excretion by the kidneys, and acute renal disease or chronic kidney disease. Hyperkalemia may occur in the context of metabolic acidosis such as diabetic ketoacidosis. The clinical manifestations are usually neuromuscular cause. It show up muscle weakness and cardiac arrhythmias, which can at worst lead to ventricular fibrillation and asystole. The diagnosis results from the determination of serum potassium. The therapy can be done by reducing the potassium intake, adjusting the drug, administration of a cation exchange resin and in emergencies by the administration of calcium gluconate and insulin. The dialysis is a treatment option. (See also overview of disorders of potassium concentration.) Etiology A common cause of an increased serum potassium concentration is probably a Pseudohyperkalämie, which is usually caused by hemolysis of red blood cells in the blood sample. This can occur during the venous blood even after prolonged use of a pressure bandage or by excessive clenching of the fist. Thrombocytosis can pseudohyperkalemia in serum (platelet potassium during blood clotting released) lead, as well as extreme leukocytosis. Normal kidneys are able to excrete large amounts of potassium. Shall provide a lasting, not artificial hyperkalemia to suspect a decreased renal potassium excretion. However, other factors are important. These include increased potassium intake and / or increased potassium release from the cells (see Table: Causes of hyperkalemia). For oral fast uptake of potassium chloride or an i.v. Potassium supplements can cause a normally transient hyperkalemia even with normal renal function. Causes of hyperkalemia category Examples Decreased excretion of potassium drug ACE inhibitor Angiotensin II receptor antagonists Direct renin inhibitor (aliskiren) cyclosporin heparin potassium arms diuretics lithium NSAIDs tacrolimus trimethoprim hypoaldosteronism adrenal insufficiency Acute Renal Nierenschä ending Chronic kidney disease closure Renal tubular acidosis type IV Other Decreased effective circulating volume increased potassium intake (usually iatrogenic) Oral food Oral potassium supplements Intravenous infusions blood transfusions with additional potassium Kaliumcitratlösungen potassium-containing drug (e.g.. As penicillin G) Total parenteral nutrition Increased potassium shift from the cells drug digoxin toxicity beta blockers Increased tissue catabolism Acute tumor lysis Acute intravascular hemolysis bleeding in soft tissue or gastrointestinal tract burns rhabdomyolysis juvenile diabetes mellitus fasting diseases Hyperkalemic family periodisc he paralysis (rare) Other causes training metabolic acidosis A hyperkalemia on the floor an increased total body amount of potassium is common in oliguric states, particularly in acute kidney injury, wherein rhabdomyolysis, burns, bleeding into soft tissues or in the gastrointestinal tract and adrenal insufficiency. In chronic kidney disease hyperkalemia is uncommon until the GFR falls to <10-15 ml / min, unless the food or intravenous potassium intake is massive. Symptoms and signs Although occasionally flaccid paralysis occurs, hyperkalemia is usually asymptomatic so long until making the Kardioarrhythmie noticeable. On the rare hyperkaliämischen familial periodic paralysis often a weakness, which may progress to a real paralysis developed during seizures. Diagnostic determination of the serum potassium value ECG medication review assessment of renal function Hyperkalemia (serum potassium level> 5.5 mEq / l) may be discovered during a routine determination of serum electrolytes. You should be suspected in patients with typical ECG changes or in patients at high risk, as is the case with kidney failure, advanced heart failure or urinary tract obstruction, or when treatment with ACE inhibitors and potassium sparing diuretics. Pseudohyperkalemia should be considered in patients with no risk factors or changes in the ECG. Hemolysis can be reported by the laboratory. If a pseudo-hyperkalemia is suspected, the potassium concentration should be repeated and measures are taken to avoid hemolysis of the sample (such as avoiding needles with small size or tourniquet use and limited ball of the thumb) and blood should promptly by the laboratory are processed. ECG An ECG should be taken in patients with hyperkalemia. ECG changes (ECG changes during hypokalemia and hyperkalemia.) Are often seen> 5.5 mEq / L in serum potassium levels. First, it can be seen a deceleration of the line, which is characterized by a prolonged PR interval and a shortened QT interval as well as high, symmetrical peak T-wave. Potassium values> 6.5 mEq / l cause a further slowing down of the line broadening of the QRS complex, the disappearance of P-wave and nodal and ventricular arrhythmias. Finally, the QRS complex degenerate to a sine wave, and ventricular fibrillation or asystole can be observed. ECG changes during hypokalemia and hyperkalemia. (Serum potassium levels in mEq / l.) Diagnosis of the causes of diagnosis of the cause of hyperkalemia requires a detailed medical history, including a review of medication, physical examination, with focus on the volume status, and measurement of electrolytes, blood urea nitrogen and creatinine. In the case of kidney failure further investigation including an ultrasound to determine the cause must be performed. Treatment Treating the cause In low-grade hyperkalemia, sodium polystyrene sulfonate case of medium or severe hyperkalemia intravenous insulin and glucose, intravenous calcium solution, possibly an inhaled beta-2 agonist and usually hemodialysis Mild hyperkalemia in patients with a serum potassium level <6 mEq / L and without ECG changes, it may be sufficient to reduce potassium intake and deposit kaliumerhöhende drugs. If no volume depletion is present, the administration of a loop diuretic improves renal potassium excretion. Sodium polystyrene sulfonate in sorbitol (weight 15-30 g in 30-70 ml of a 70% sorbitol solution p.o. every 4-6 hours) may be administered. It acts as a cation exchange resin and removes potassium on the mucosa of the Gastrointestinalrakts. Sorbitol is used together with the resin, to ensure the passage through the gastrointestinal tract. Patients who can orally take any medications for. B. nausea can receive similar doses as an enema. Enemas to reduce potassium are not as effective in patients with ileus. Enemas should not be given in suspected acute abdomen. about 1 mEq potassium be removed per gram of the resin. The resin therapy works very slowly and often the serum potassium levels can not be sufficiently reduced in hyper metabolic disorders. Since sodium is replaced by potassium, sodium polystyrene sulfonate is used when an additional overload can occur with sodium especially in patients with pre-oliguric volume overload. In patients with recurrent hyperkalemia, avoidance of medications that may provoke hyperkalaemia (see Table: Causes of hyperkalemia) is generally all that is needed. In patients taking ACE inhibitors and angiotensin receptor blockers (eg., Patients with chronic heart failure or diabetic nephropathy) require a newly available Polymerharzpatiromer can be taken daily to help to reduce the intestinal absorption of potassium and hyperkalemia to verhindern.Mittel- to severe hyperkalemia serum potassium 6 to 6.5 mEq / l require an immediate treatment, but the actual therapy depends on the clinical condition. If no ECG changes are present and the kidney function is intact, procedures are effective as low-grade hyperkalemia usually. More check-ups in serum potassium value are required to ensure that the hyperkalemia was successfully treated. Serum potassium> 6.5 mEq / l require a more aggressive therapy. After or together with the supply of 5-10 units of short-acting insulin i.v. a rapid infusion of 50 ml is added 50% glucose. An infusion of 10% dextrose at a sweep rate of 50 ml / hour should be followed in order to avoid hypoglycemia. The effects on serum potassium levels reached after 1 hour peak and hold for several hours. in the ECG when a disappearance of the P-wave or a widening of the QRS complex is seen, the treatment in intravenous calcium and in an insulin and glucose administration; 10-20 ml of 10% calcium gluconate (or 5-10 ml 22% Kalziumgluceptat) are injected i.v. given over 5-10 minutes. Calcium antagonizes the effects of hyperkalemia on the myocardium. Patients who receive a Glykosidtherapie, calcium should be administered with extreme caution because of the risk of triggering hypokalämieinduzierte arrhythmia. If the ECG is already showing a sine wave or an asystole, calcium may be added rapidly (5-10 ml i.v. over 2 minutes). Potassium chloride can also be used, but may lead to irritation of the peripheral veins and as it emerges subsequent tissue. Potassium chloride should only be administered via a correctly positioned central venous catheter. The effect of calcium occurs within minutes but lasts only 20 to 30 minutes. The infusion of calcium is a temporary measure, with which one gains time while waiting for the effects of other treatment options or the start of a hemodialysis. The administration of calcium may be repeated. A high dose of a beta-2-agonists such. B. albuterol 10-20 mg inhaled over 10 min (in a concentration of 5 mg / ml), the serum potassium level may be reduced by 0.5-1.5 mEq / L and is a valuable adjunct. The highlight of the effect is achieved after 90 minutes. However, beta-2 agonists in patients with unstable angina pectoris are contraindicated or acute myocardial infarction. The supply of sodium carbonate (NaHCO3) i.v. is controversial. It can lower serum potassium levels for several hours. The reduction may result from the alkalinization or from the hypertonicity of the high sodium content of the preparation. The amount of sodium in the solution can be harmful to dialysis patients who may already a volume overload. Another possible complication of iv is sodium bicarbonate that it acutely lowers the ionized calcium concentration, which increases the cardiac toxicity of hyperkalemia. When applied, the typical dose is 3 ampoules of 7.5% sodium bicarbonate in a liter of 5% D / W infused over 2 to 4 h. The bicarbonate therapy has, in itself, in patients with severe renal disease had little effect, unless there is a acidemia. In addition to the measures that will lead to a reduction of potassium by transport into cells, should include measures to be taken early in the treatment of severe or symptomatic hyperkalemia, which lead to a removal of the excess potassium from the body. Potassium can be removed through the GI tract by administration of sodium polystyrene sulfonate (Mild hyperkalemia), but because the rate of the potassium removal is somewhat unpredictable, close monitoring is required. Patiromer is not recommended because of its delayed onset of action for use as an emergency treatment to acutely reduce potassium. Hemodialysis should in patients with kidney failure after implementation of emergency measures or if the emergency measures do not show the desired effect, be carried out immediately. Dialysis should be considered in patients with ESRD and hyperkalemia considered early because they have a higher risk of progression to severe hyperkalemia and severe cardiac arrhythmias. Peritoneal dialysis is concerning acute potassium removal is not very effective. Summary Some common causes of hyperkalemia potassium restrained drug, renal insufficiency, adrenal insufficiency and disorders associated with cellular degradation include (z. B. rhabdomyolysis, burns, bleeding into soft tissue or GastrointestinaItrakt). Hyperkalemia is to the development of cardiotoxicity usually asymptomatic, although some patients have a weakness. ECG changes begin with a prolonged PR interval, a shortened QT interval and high, symmetrical, acute T-waves; with potassium values> 6.5 mEq / l widens the QRS complex and the P-wave disappears; ultimately, the QRS complex degenerated into a sine wave pattern and ventricular fibrillation or asystole occurs. In low-grade hyperkalemia sodium polystyrene sulfonate is given. For treatment of moderate to severe hyperkalemia is intravenous insulin, glucose and calcium and possibly given an inhaled beta-2 agonist. Hemodialysis is performed in patients with chronic kidney disease and in patients with significant ECG changes.