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Torsemide (Torsemide) - Warnings and Precautions

 
 



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, 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. 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 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.

PRECAUTIONS

Laboratory Values
Potassium
See WARNINGS.

Calcium
Single doses of torsemide increased the urinary excretion of calcium by normal subjects, but serum
calcium levels were slightly increased in 4 to 6 week hypertension trials. In a long-term study of patients
with congestive heart failure, the average 1 year change in serum calcium was a decrease of 0.1 mgJdL
(0.02 mmoI/L). Among 426 patients treated with torsemide for an average o f 11 months, hypocalcemia
was not reported as an adverse event.

Magnesium
Single doses of torsemide caused healthy volunteers to increase the ir urinary excretion of magnesium,
but serum magnesium levels were slightly increased in 4 to 6 week hypertension trials. In long-term
hypertension studies, the average 1 year change in serum magnesium was an increase of 0.03 mgJdL
(0.01 mmoI/L). Among 426 patients treated with torsemide for an average of 11 months, one case of
hypomagnesemia (1.3 m gJdL [0.53 mmol/LJ) was reported as an adverse event.
In a tong- term clinical study of torsemide in patients with congestive heart failure, the estimated
annual change in serum magnesium was an increase of 0.2 mg/dL (0.08 mmoI/L), but these data are
confounded by the fact that many of these patients received magnesium supplements. In a 4 week
study in which magnesium supplementation was not given, the rate of occurrence of serum magnesium
levels below 1.7 mg/dL (0.7 mmol/L) was 60/0 a nd 9% in the groups receiving 5 mg a nd 10 mg of
torsemide, respectively.

Blood Urea Nitrogen (BUN), C reatinin e a nd Uric Acid
Torsemide produces small dose-related increases in each of these laboratory values. In hypertensive
patients who received 10 mg o f torsemide daily for 6 weeks, the mean increase in blood urea nitrogen
was 1.8 mg/dL (0.6 mmoI/L), the mean increase in serum creatinine was 0.05 mg/dL (4 mmol/ L), and
the mean increase in serum uric acid was 1.2 mg/dL (70 mmoI/L). Little further change occurred with
long-term treatment, and all changes reversed when treatment was discontinued.
Symptomatic gout has been reported in patients receiving torsemide, but its incidence has been similar
to that seen in patients receiving placebo.

Glucose
Hypertensive patients who received 10 m g of daily torsemide experienced a mean increase in serum
glucose concentration o f 5.5 mg/dL (0.3 mmol/L) after 6 weeks of therapy, with a further increase of
1.8mg/dL (0.1 mmol/L) during the subsequent year. In long-term studies in diabetics, mean fasting
glucose values were not significantly changed from baseline. Cases of hyperglycemia have been
reported but are uncommon.

Serum Lipids
In the controlled short-term hypertension studies in the United States, daily doses of 5 mg, 10 mg, and
20 mg of torsemide were associated with increases in total plasma cholesterol of 4, 4, and 8 mg/dL (0.1
to 0.2 mmoI/L), respectively. The changes subsided during chronic therapy.
In the same short- term hypertension studies, daily doses of 5 mg, 10 m g and 20 mg of torsemide were
associated with mean increases in plasma triglycerides of 16, 13, and 71 mg/dL (0. 15 to 0.8 mmoI/L),
respectively.
In long-term studies of 5 mg to 20 mg of torsemide daily, no clinically significant differences from
baseline lipid values were observed after 1 year of therapy.

Other
In long-term studies in hypertensive patients, torsemide has been associated with small mean
decreases in hemoglobin, hematocrit, and erythrocyte count and small mean increases in white blood
cell count, platelet count, and serum alkaline phosphatase. Although statistically significant, all of these
changes were medically inconsequential. No significant trends have been observed in any liver enzyme
tests other than alkaline phosphatase.

Page last updated: 2012-02-14

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