Overdose : מינון יתר

4.9 Overdose

Clinical Symptoms
The clinical symptoms of an acute potassium overdose (poisoning) are mainly characterised by hyperkalaemia with cardiovascular and neuromuscular disorders. Renal insufficiency may already occur after relatively low doses of the medicinal product.

Cardiovascular system
Ventricular arrhythmias, bundle branch block with ventricular fibrillation accompanied by a decrease in blood pressure and states of shock ranging up to cardiac arrest may occur.
In addition to the increase of the K+ serum concentration, the following ECG changes are typical: increased t-wave amplitude and t-wave peaking, p-wave disappearance, widening of QRS complex and ST segment reduction.

Central nervous system
Paraesthesia, seizures, loss of reflex, atonia of the striated muscle, which may range up to symptoms of respiratory paralysis.

Treatment
In acute cases of poisoning the excess potassium must be removed from the body or inactivated through:
- Induced vomiting
- Stomach flushing
- Administration of cation exchange resins, either orally or by stomach instillation, e.g. 20 g Polystyrene sodium sulfonate with 20 mL of a 70% sorbitol solution, 3-4 times a day.

For moderate hyperkalaemia (Plasma K+ concentrations between 6.5 and 8 mmol/L and t- wave peaking as the only ECG change):
- Stimulation of transcellular potassium transportation through intravenous administration of 300 to 500 mL/hour of a 10% dextran solution with an insulin content of 10 to 20 units/L - Correction of a possible acidosis through intravenous sodium bicarbonate administrations (44 to 132 mmol/L in a glucose solution)
- Correction of a possible hyponatraemia and hypovolemia.

In severe cases of hyperkalaemia (Plasma K+ concentrations > 8 mmol/L or in case of considerable ECG changes including missing p-wave ,widening of the QRS complex, t-wave disappearance or the occurrence of ventricular arrhythmias):
- Glucose solution (with insulin) and/or bicarbonate infusions, as described above (leading to an extracellular to intracellular potassium displacement, onset after 30 mins) - Correction of a possible acidosis through intravenous sodium bicarbonate administrations (44 to 132 mmol/L in a glucose solution)
- Intravenous administration of 10 to 30 mL of a 10% potassium gluconate solution for 1 to 5 minutes under ongoing ECG control (leading to a reversal of the potassium effect on the cell membranes)
- Administration of cation exchange resins through high retention enemas and namely as follows:
30 to 50 g sodium polystyrene sulfonate in 100 mL of warm watery sorbitol solution, if possible, should be held in the sigmoid colon for a few hours. The colon will then be flushed with a sodium free solution in order to remove the resin. The enemas can be repeated, or oral ion-exchangers may be administered repeatedly so the normalised K+ concentration is maintained.
- Haemodialysis or peritoneal dialysis may be particularly useful for patients with renal insufficiency.

When treating hyperkalaemia it should be considered that for patients under well-controlled treatment with digitalis a quick reduction of the K+ serum levels can lead to digitalis intoxications.