Abstract
BackgroundHypokalemia has been rarely attributed to tizanidine, although the precise mechanism is unclear. Severe hypokalemia is a well-established cause of abnormalities involving cardiac conduction. Given this agent’s well-known cardiac arrhythmogenic potential, awareness of potential concomitant electrolyte abnormalities is important.Case presentationElectrolyte disorders, including hypokalemia, are rare complications of the antispasmodic medicine tizanidine when taken in doses as outlined by the manufacturer’s prescribing instructions. Although cases of severe hypokalemia have also been described in the literature in association with this agent, such reports are few. We report a Caucasian case of an intentional overdose involving a very large ingestion of tizanidine. In addition to the characteristic abnormalities on the electrocardiogram, our patient developed electrolyte derangements as well as self-limited acute kidney injury. These biochemical abnormalities included profound hypokalemia that was refractory to aggressive replacement over the ensuing several days, before eventually dissipating. A thorough assessment of the etiology of this hypokalemia was consistent with a defect in renal potassium handling.ConclusionIn our patient with intentional tizanidine overdose, severe and refractory hypokalemia appears to have been due to a transient potassium wasting nephropathy.
Highlights
Drug-induced hypokalemia is a complication often encountered in clinical practice, caused by a variety of therapeutics
In our patient with intentional tizanidine overdose, severe and refractory hypokalemia appears to have been due to a transient potassium wasting nephropathy
It has been suggested that the mechanism by which tizanidine results in hypokalemia is through a defect in renal potassium handling, which was confirmed in our case
Summary
Drug-induced hypokalemia is a complication often encountered in clinical practice, caused by a variety of therapeutics. The patient’s urine potassium level was abnormally elevated at 38 mEq/L (should be < 20 mEq/L in the setting of severe hypokalemia), alluding to a defect in renal potassium handling, and not losses of gastrointestinal secretions which would have led to renal potassium conservation. Since he had achieved resolution of his acute kidney injury (creatinine was down to 0.81 mg/dL), oral spironolactone 25 mg twice daily was started. On hospital day 5 he was transferred to the inpatient psychiatry service, at which time his electrolyte levels and renal function were normal He was maintained on spironolactone 25 mg twice daily with no supplemental potassium requirements. The aldosterone to plasma renin activity ratio was reported as 7.7, which is not suggestive of primary hyperaldosteronism
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