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WARNINGS 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, an aldosterone antagonist 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. Volume and Electrolyte Depletion Patients receiving diuretics should be observed for clinical evidence of electrolyte imbalance, hypovolemia, or prerenal 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, or prerenal azotemia, the observed laboratory changes may include hyper- or hyponatremia, hyper- or hypochloremia, hyper- or hypokalemia, acid-base abnormalities, and increased blood urea nitrogen (BUN). If any of these occur, torsemide 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 of 5 mg or 10 mg daily. After 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 mEq/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, or renal disease treated with torsemide at doses higher than those studied in United States antihypertensive trials, hypokalemia was observed with greater frequency, in a dose-related manner. In patients with cardiovascular disease, especially those receiving digitalis glycosides, diuretic-induced hypokalemia 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, in patients 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.
ADVERSE REACTIONS At the time of approval, torsemide had been evaluated for safety in approxi‑mately 4000 subjects: over 800 of these subjects received torsemide for at least 6 months, and over 380 were treated for more than 1 year. Among these subjects were 564 who received torsemide during United States-based trials in which 274 other subjects received placebo. The reported side effects of torsemide were generally transient, and there was no relationship between side effects and age, sex, race, or duration of therapy. Discontinuation of therapy due to side effects occurred in 3.5% of United States patients treated with torsemide and in 4.4% of patients treat‑ed with placebo. In studies conducted in the United States and Europe, dis‑continuation rates due to side effects were 3.0% (38/1250) with torsemide and 3.4% (13/380) with furosemide in patients with congestive heart failure, 2.0% (8/409) with torsemide and 4.8% (11/230) with furosemide in patients with renal insufficiency, and 7.6% (13/170) with torsemide and 0% (0/33) with furosemide in patients with cirrhosis. The most common reasons for discontinuation of therapy with torsemide were (in descending order of frequency) dizziness, headache, nausea, weakness, vomiting, hyperglycemia, excessive urination, hyperuricemia, hypokalemia, excessive thirst, hypovolemia, impotence, esophageal hemor‑rhage, and dyspepsia. Dropout rates for these adverse events ranged from 0.1% to 0.5%. The side effects considered possibly or probably related to study drug that occurred in United States placebo-controlled trials in more than 1% of patients treated with torsemide are shown in Table 1. Table 1 - Reactions Possibly or Probably Drug-Related United States Placebo-Controlled Studies Incidence (Percentages of Patients) Torsemide Placebo (N=564) (N=274) Headache 7.3 9.1 Excessive Urination 6.7 2.2 Dizziness 3.2 4.0 Rhinitis 2.8 2.2 Asthenia 2.0 1.5 Diarrhea 2.0 1.1 ECG Abnormality 2.0 0.4 Cough Increase 2.0 1.5 Constipation 1.8 0.7 Nausea 1.8 0.4 Arthralgia 1.8 0.7 Dyspepsia 1.6 0.7 Sore Throat 1.6 0.7 Myalgia 1.6 1.5 Chest Pain 1.2 0.4 Insomnia 1.2 1.8 Edema 1.1 1.1 Nervousness 1.1 0.4 The daily doses of torsemide used in these trials ranged from 1.25 mg to 20 mg, with most patients receiving 5 mg to 10 mg; the duration of treatment ranged from 1 to 52 days, with a median of 41 days. Of the side effects listed in the table, only “excessive urination” occurred significantly more frequently in patients treated with torsemide than in patients treated with placebo. In the placebo-controlled hypertension studies whose design allowed side-effect rates to be attributed to dose, excessive urination was reported by 1% of patients receiving placebo, 4% of those treated with 5 mg of daily torsemide, and 15% of those treated with 10 mg. The complaint of excessive urination was generally not reported as an adverse event among patients who received torsemide for cardiac, renal, or hepatic failure. Serious adverse events reported in the clinical studies for which a drug relationship could not be excluded were atrial fibrillation, chest pain, diar‑rhea, digitalis intoxication, gastrointestinal hemorrhage, hyperglycemia, hyperuricemia, hypokalemia, hypotension, hypovolemia, shunt thrombosis, rash, rectal bleeding, syncope, and ventricular tachycardia. Angioedema has been reported in a patient exposed to torsemide who was later found to be allergic to sulfa drugs. Of the adverse reactions during placebo-controlled trials listed without taking into account assessment of relatedness to drug therapy, arthritis and various other nonspecific musculoskeletal problems were more frequently reported in association with torsemide than with placebo, even though gout was somewhat more frequently associated with placebo. These reactions did not increase in frequency or severity with the dose of torsemide. One patient in the group treated with torsemide withdrew due to myalgia, and one in the placebo group withdrew due to gout. Hypokalemia: See WARNINGS .