Torsemide injection

Hepatic Disease With Cirrhosis and Ascites
Torsemide should be used with caution in patients with hepatic disease with cirrhosis and ascites, since
sudden alterations of fluid and electrolyte balance may precipitate hepatic coma. In these patients,
diuresis with torsemide (or any other diuretic) is best initiated in the hospital. To prevent hypokalemia
and metabolic alkalosis, analdosteroneantagonist or potassium-sparing drug should be used
concomitantly with torsemide.

Ototoxicity
Tinnitus and hearing loss (usually reversible) have been observed after rapid intravenous injection of
other loop diuretics and have also been observed after oral Torsemide. It is not certain that these events
were attributable to torsemide . Ototoxicity has also been seen in animal studies when very high plasma
levels of torsemide were induced. Administered intravenously, torsemide should be injected slowly over
2 minutes, and single doses should not exceed 200 mg.

Volume and Electrolyte Depletion
Patients receiving diuretics should be observed for clinical evidence of electrolyteim balance,
hypovolemia, orprerenal azotemia . Symptoms of these disturbances may include one or more of the
following: dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains
or cramps, muscular fatigue , hypotension , oliguria, tachycardia, nausea, and vomiting. Excessive
diuresis may cause dehydration, blood-volume reduction , and possibly thrombosis and embolism,
especially in elderly patients. In patients who develop fluid and electrolyte imbalances, hypovolemia,
orprerenal azotemia, the observed laboratory changes may include hyper-orhypon atremia, hyper -or
hypochloremia, hyper- or hypokalemia, acid-base abnormalities, and increased blood urea nitrogen
(BUN). If any of these occur, to rsemide should be discontinued until the situation is corrected; torsemide
may be restarted at a lower dose.
In controlled studies in the United States, torsemide was administered to hypertensive patients at doses
o f 5 mg or 10 mg daily. Afte r 6 weeks at these doses, the mean decrease in serum potassium was
approximately 0.1 mEq/L. The percentage of patients who had a serum potassium level below 3.5 m Eq/L
at any time during the studies was essentially the same in patients who received torsemide ( 1.5%) as in
those who received placebo (3%) . In patients followed for 1 year, there was no further change in mean
serum potassium levels. In patients with congestive heart failure, hepatic cirrhosis, orrena l disease
treated with torsemide at doses higher than those studied in United States a ntihypertensive trials,
hypokalemia was observed with greater frequency, in a dose-related manner.
In patients with cardiovascular disease, especially those receiving digitalis glycosides, diuretic-induced
hypokelemia may be a risk factor for the development of arrhythmias. The risk of hypokalemia is
greatest in patients with cirrhosis of the liver, in patients experiencing a brisk diuresis, inpatients who
are receiving inadequate oral intake of electrolytes, and in patients receiving concomitant therapy with
corticosteroids or ACTH.
Periodic monitoring of serum potassium and other electrolytes is advised in patients treated with
torsemide.