What are the clinical symptoms of hyperkalemia

Hyperkalemia in everyday practice

Hyperkalemia in clinical practice


The article summarizes the diagnosis and treatment of acute and chronic hyperkalaemia and also takes a position on new treatment options.


This article summarizes diagnostics and therapy of acute and chronic hyperkalemia under consideration of new treatment options.

With an incidence of 2–3% in the normal population, hyperkalemia is one of the most common electrolyte disorders in everyday clinical practice. In patients with chronic kidney disease, the incidence is even between 40–50% (1). The general practitioner plays a key role, particularly in the management of chronic hyperkalemia in polymedicated patients. The frequent coincidence of chronic kidney failure, heart failure and diabetes mellitus and their therapies favor the development of hyperkalemia. The question arises: stop taking important medication or treat a drug side effect with another medication?

Most hyperkalemia is asymptomatic. Occasionally find each other unspecific symptoms such as nausea and diarrhea, muscle weakness up to paresis, paresthesia and palpitations. The potassium level is classically classified as follows: mild hyperkalemia 5.0-5.4 mmol / l, moderate hyperkalemia 5.5-5.9 mmol / l, severe hyperkalemia 6.0-6.4 mmol / l and life-threatening hyperkalemia> 6, 5 mmol / L (2).

By far the most common Incorrect measurement Hyperkalemia results from excessive venous congestion when taking blood, for example in the case of difficult venous conditions. Therefore, in the event of unexpected hyperkalaemia, a control sample is recommended in order to decide whether there is real hyperkalaemia or just pseudo-hyperkalaemia. Some laboratories state whether the material sent was haemolytic; this should be checked in any case, e.g. B. on an ionometer in whole blood without prior centrifugation (3).

Often times, hyperkalemia results from the combination of a clinical risk factor and one or more drugs that increase potassium. Medicationthat promote the development of hyperkalemia are listed in Table 2.

ACE inhibitors, for example, are (partly) responsible for 10–38% of hyperkalemia in hospitalized patients (5).

Acute hyperkalemia

The relevance of the serum potassium varies depending on the accompanying illnesses, the speed at which it occurs and the level. EKG changes are very variable and can occur with low levels of hyperkalaemia or fail with severe increase (2). Typical ECG changes are a tent-like raised T-wave, a reduced height of the P-wave, a lengthened P-R interval, and a widening of the QRS (see Figure 1). In very severe cases, a "sinus pattern" occurs. Due to the poor correlation with the potassium level, however, the changes are only very unsuitable for risk assessment. In a prospective study, typical ECG changes were found in only 46% of patients with potassium levels> 6 mmol / l (6). However, if these ECG changes can be seen, this is always an emergency. In addition, lethal arrhythmias can occur without prior ECG changes.

The therapy acute as well as severe, possibly life-threatening hyperkalemia requires acute admission to a hospital with the option of hemodialysis. There, the potassium level in the whole blood is determined in the emergency room without centrifugation in order to obtain immediate results. This should be followed by a 12-lead ECG and monitor monitoring on the 3-lead ECG (3). Thereafter, therapy must begin immediately.

If severe ECG changes occur, calcium gluconate can be administered i.v. can be applied to stabilize the cardiac membrane potential. It doesn't lower potassium levels. The application should only be carried out under monitor supervision due to the proarrhythmogenic potential (2).

The application of glucose and insulin, as well as nebulized salbutamol, leads to an influx of potassium into the cell. The onset of action of insulin and glucose shows a little earlier, but lasts shorter. The combination of both therapies is more effective than monotherapy and leads to an average reduction of 1.21 mmol / l (3; 7). Afterwards, however, the elimination of potassium from the body should be stimulated in order to permanently lower the serum potassium. This is possible, for example, by increasing the physiological renal excretion of potassium by means of non-potassium-sparing diuretics. Thiazides are more effective at eliminating potassium (4) in GFR < 30="">2 however, loop diuretics should be used. In the case of desiccated patients, this measure is combined with volume administration, preferably 0.9% NaCl. This therapy is no longer effective in shock because the mean arterial perfusion pressure of the kidneys is reduced and there is an excess of catecholamines.

The administration of 8.4% bicarbonate is indicated at most in the case of metabolic acidosis, since the studies on the potassium-lowering effect are very weak (3; 7). An overview of the conservative therapy for hyperkalemia is shown in Table 3.

Emergency hemodialysis therapy is the preferred treatment for vitally endangered patients, particularly those with anuria or severe renal insufficiency. This is possible even under resuscitation. In this case, intensive medical monitoring is recommended after the initiation of therapy.

Chronic hyperkalemia

The goal of treating chronic hyperkalemia is to avoid costly inpatient admissions and life-threatening complications such as arrhythmias or asystole. It is also important to avoid recurrences of acute hyperkalemia. In the case of a gradual, slow increase in potassium up to a moderate level, acute intervention is rarely necessary. Measures to lower a chronically elevated potassium level should, however, be initiated, since the chronically elevated value reduces the safety margin to very high potassium values.

One of the basic measures in outpatient care is first of all the nutritional training of patients with regard to low-potassium diet. In general, a low-potassium diet with an importation is recommended < 40="" mmol/l.="" die="" compliance="" wird="" deutlich="" erhöht,="" wenn="" der="" patient="" über="" die="" möglicherweise="" lebensbedrohlichen="" konsequenzen="" einer="" hyperkaliämie="" aufgeklärt="" wird.="" diese="" maßnahme="" ist="" einfach="" und="" kosteneffektiv,="" nimmt="" jedoch="" viel="" zeit="" in="" anspruch.="" trotzdem="" sollte="" dieser="" wichtige="" schritt="" nicht="" übersprungen="" werden,="" da="" so="" eventuell="" folgemedikationen="" zur="" kaliumsenkung="" und="" ihre="" nebenwirkungen="" reduziert="" werden="" können.="" weiterhin="" ist="" die="" überprüfung="" der="" medikation="" entscheidend.="" die="" kombination="" mehrerer="" medikamente,="" welche="" das="" serumkalium="" erhöhen="" (siehe="" tabelle="" 2),="" ist="" insbesondere="" bei="" patienten="" mit="" chronischer="" niereninsuffizienz="" kritisch="" zu="" betrachten.="" es="" gilt="" den="" potenziellen="" nutzen,="" zum="" beispiel="" von="" aldosteronantagonisten="" bei="" herzinsuffizienz,="" gegen="" die="" gefahr="" der="" potenziellen="" nebenwirkung="" abzuwägen.="" insbesondere="" das="" ansetzen="" von="" spironolacton="" ohne="" nachkontrolle="" der="" elektrolyte="" führt="" immer="" wieder="" zu="" bedrohlichen="" kaliumerhöhungen.="" bei="" einer="" gfr="">< 30="">2 and re-preparation of an AT1 antagonist, ACE inhibitor or aldosterone antagonist, potassium checks should be carried out regularly, initially weekly. The prescribing doctor is primarily responsible for this.

Occasionally, mineralocorticoids (e.g. fludrocortisone) are also used to lower potassium. However, an effect could not be proven in studies (7).

Oral potassium binders such as polystyrene sulfonate (CPS powder) are very often given. However, the evidence on its effectiveness is poor. In the original study from 1961, only 32 patients were included (8). According to today's approval standards, this study would be unsuitable due to the small number of patients. A Cochrane review showed no reduction in potassium after a single dose (9). The potassium-lowering effect only sets in after 1–5 days. In addition, it has not been proven whether the lowering of potassium is actually triggered by the CPS powder or the laxative comedication (previously mostly sorbitol). Furthermore, drug safety must be guaranteed, which is to be viewed as questionable in the case of CPS powder. The most common adverse drug reactions include constipation, hypomagnesaemia, and hypercalcemia. A very rare but serious adverse drug reaction (ADR) is intestinal necrosis, which is associated with considerable mortality. In the meantime, the theory has been favored that intestinal necrosis is triggered by the addition of sorbitol. Therefore, other laxatives, such as lactulose, are preferred, although this side effect can occur without sorbitol. It is possible to apply orally or rectally. Oral administration is unsuitable in patients with vomiting or diseases of the upper gastrointestinal tract.

A newly approved oral potassium binder is Patiromer (Veltassa®). It is a non-absorbable polymer that binds potassium in the intestine in exchange for calcium. The effect begins after approx. 7 hours and reaches its maximum after 48 hours (10). In the OPAL-HK study with 237 patients with chronic kidney disease (CKD) III and IV, RAAS inhibitor therapy and hyperkalaemia between 5.1–6.5 mmol / l, an average reduction in serum potassium of 1 mmol / l ( 95% confidence interval [CI] 1.07 to -0.95; p < 0,001)="" nachgewiesen="" werden="" (11).="" in="" der="" amethyst-dn-studie="" wurden="" sowohl="" die="" optimale="" dosis="" als="" auch="" die="" uaw="" über="" 52="" wochen="" untersucht.="" es="" zeigten="" sich="" hypomagnesiämien="" bei="" 8,6="" %,="" hypokaliämien="">< 3,5="" mmol/l)="" bei="" 5,6="" %="" und="" obstipation="" oder="" diarrhoe="" bei="" 7–11="" %="" (12).="" außerdem="" besteht="" interaktionspotenzial="" mit="" ciprofloxacin,="" levothyroxin,="" metformin="" und="" quinidin,="" welche="" mindestens="" drei="" stunden="" vor="" oder="" nach="" patiromer="" eingenommen="" werden="" sollten.="" ebenfalls="" sollte="" ein="" vorsichtiger="" umgang="" in="" kombination="" mit="" substanzen="" geringer="" therapeutischer="" breite="" erfolgen,="" da="" zu="" den="" meisten="" keine="" untersuchungen="" zu="" interaktionen="" vorliegen.="" nachteilig="" ist="" die="" relativ="" geringe="" patientenzahl="" der="" studien="" und="" die="" bisher="" fehlende="" klinische="" langzeiterfahrung.="" außerdem="" liegen="" keine="" studien="" bezüglich="" klinischer="" endpunkte="" vor,="" wie="" kardiovaskuläre="" mortalität="" oder="" hospitalisation.="" man="" hofft,="" durch="" dieses="" medikament="" mehr="" ras-blockierende="" subtanzen="" in="" hoher="" dosierung="" und="" aldosteronantagonisten="" in="" der="" indikation="" herzinsuffizienz="" einsetzen="" zu="" können,="" um="" dadurch="" die="" prognose="" dieser="" patienten="" zu="" verbessern.="" gerade="" dieser="" nachweis,="" also="" die="" verbesserung="" harter="" klinischer="" endpunkte,="" ist="" aber="" noch="" nicht="" erbracht.="" wenn="" ein="" medikament="" nur="" mit="" einem="" zweiten="" medikament="" gegeben="" werden="" kann,="" um="" nebenwirkungen="" zu="" mindern="" (hyperkaliämie),="" braucht="" es="" dafür="" gewichtige="" argumente,="" die="" über="" die="" verbesserung="" von="" laborparametern="">

Another new drug that has not yet been approved in Germany is sodium zirconium cyclo-silicate (ZS-9). It is also a non-absorbable polymer that binds potassium in the intestine. By mimicking the physiological potassium channels, it binds potassium relatively selectively (5). Compared to the other potassium binders, the advantage lies in the faster onset of action and the low ADRs, which according to previous studies should be at the placebo level. A double-blind placebo-controlled study with 753 patients showed a dose-dependent potassium reduction of 0.7 mmol / l at the maximum dose of 10 g (13).

conclusion for practice

The benefits of potassium-increasing drugs and possible side effects of the subsequent potassium-lowering medication must be weighed up in everyday clinical practice. In the case of chronic hyperkalemia, the first step is to train the patient on a low-potassium diet. In the case of acute, severe hyperkalemia, hospitalization should be carried out immediately. New potassium-lowering drugs offer further treatment options for acute and chronic hyperkalemia. So far, however, there is a lack of long-term experience and studies with clinically important endpoints that show that it makes sense to administer another drug because of side effects of one drug.

Conflicts of Interest

The author denies a conflict of interest.


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online in advance

This article was pre-published online on October 12, 2018.

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