[Hypokalemic paralysis in furosemide therapy and simultaneous laxative abuse]

Clinical signs of hypokalemia are not directly related to the extent of the electrolyte imbalance, and therefore monosymptomatic cases may be observed.

Following an acute gastroenteritis with considerable diarrhea, a 47-year-old male patient was admitted to hospital for progressive painful paraparesis. Upon admission, the patient complained of painful paresthesias in both legs, and a moderate flaccid paraparesis with widespread fasciculations and loss of leg tendon reflexes was found. Serum potassium level on admission was 1.7 mmol/l. Other signs of hypokalemia were absent, and the ECGs showed a slow sinus rhythm without disturbances of de- or repolarisation or cardiac arrhythmias. Hypokalemic paralysis was diagnosed and was considered to be primarily drug-induced, as the patient had a history of laxative abuse and was on a continuous medication with furosemide (80 mg/d) without regular assessment of serum electrolytes. The additional electrolyte loss following the gastroenteritis precipitated the development of clinical signs of hypokalemia. In parallel to the rise in serum potassium levels, both painful paresthesias and muscle weakness disappeared, and electromyography documented the amelioration of the myopathic syndrome.

The prominent clinical symptom of hypokalemia was a dyskalemic paralysis in the absence of other sequelae of electrolyte imbalance, such as cardiac arrhythmias or vegetative disturbances.