Potassium sparing diuretics as adjunct to mannitol therapy in neurocritical care patients with cerebral edema: effects on potassium homeostasis and cardiac arrhythmias.

Mannitol therapy to treat cerebral edema induces osmotic diuresis and electrolyte loss. In neurocritical care patients, potassium is the electrolyte that most often needs replacement. Objective of this study was to evaluate the effects of adding potassium sparing diuretic (canrenone) to mannitol therapy on potassium urinary excretion, potassium plasma levels, and incidence of new cardiac arrhythmias in patients receiving neurocritical care for cerebral edema. Fifty-six patients were prospectively assigned to mannitol or mannitol plus i.v. canrenone. Potassium urinary excretion, potassium plasma levels, urinary volume, and the incidence of new cardiac arrhythmias were recorded during the first 8 days of therapy. In patients treated with mannitol the potassium urinary excretion was stable over the first 3 days and significantly increased, compared to baseline, on day 4th to 8th (baseline 20.3 ± 10.6 mEq/l/die, day 8th 24.6 ± 10.6 mEq/l/die, P < 0.05); while potassium plasma levels significantly decreased. In patients receiving mannitol plus canrenone potassium urinary excretion decreased from day 3rd to 8th (baseline 21.9 ± 11.6 mEq/l/die, day 8th 15.9 ± 10.9 mEq/l/die, P < 0.015) and potassium plasma levels increased but remained within normal values range. The incidence of new cardiac arrhythmias was higher in the mannitol group than the mannitol plus canrenone group (35.7 vs. 10.7%; P < 0.01). Urinary volumes, potassium balance, and sodium plasma concentration were similar in the 2 study groups. In patients receiving neurocritical care for cerebral edema, the adjunct of a potassium sparing diuretic (canrenone) to mannitol therapy reduces potassium urinary loss, prevents hypokalemia, and reduces the incidence of new cardiac arrhythmias.