In patients with severe symptoms of urinary retention (because of bladder emptying disorders, prostatic hyperplasia, urethral narrowing), the administration of furosemide can cause acute urinary retention related to increased production and retention of urine. Increases in blood glucose and alterations in glucose tolerance tests (with abnormalities of the fasting and 2-hour postprandial sugar) have been observed, and rarely, precipitation of diabetes mellitus has been reported. ![]() Digitalis therapy may exaggerate metabolic effects of hypokalemia, especially myocardial effects.Īll patients receiving furosemide therapy should be observed for these signs or symptoms of fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia or hypocalcemia): dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Hypokalemia may develop with furosemide, especially with brisk diuresis, inadequate oral electrolyte intake, when cirrhosis is present, or during concomitant use of corticosteroids, ACTH, licorice in large amounts, or prolonged use of laxatives. As with any effective diuretic, electrolyte depletion may occur during furosemide therapy, especially in patients receiving higher doses and a restricted salt intake. If the physician elects to use high dose parenteral therapy, controlled intravenous infusion is advisable (for adults, an infusion rate not exceeding 4 mg furosemide per minute has been used) (see PRECAUTIONS: Drug Interactions).Įxcessive diuresis may cause dehydration and blood volume reduction with circulatory collapse and possibly vascular thrombosis and embolism, particularly in elderly patients. Reports usually indicate that furosemide ototoxicity is associated with rapid injection, severe renal impairment, the use of higher than recommended doses, hypoproteinemia or concomitant therapy with aminoglycoside antibiotics, ethacrynic acid, or other ototoxic drugs. If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, furosemide should be discontinued.Ĭases of tinnitus and reversible or irreversible hearing impairment and deafness have been reported. Supplemental potassium chloride and, if required, an aldosterone antagonist are helpful in preventing hypokalemia and metabolic alkalosis. Sudden alterations of fluid and electrolyte balance in patients with cirrhosis may precipitate hepatic coma therefore, strict observation is necessary during the period of diuresis. In hepatic coma and in states of electrolyte depletion, therapy should not be instituted until the basic condition is improved. In patients with hepatic cirrhosis and ascites, furosemide therapy is best initiated in the hospital. There are no significant differences between the two oral formulations in the amount of unchanged drug excreted in urine. Significantly more furosemide is excreted in urine following the IV injection than after the tablet or oral solution. The terminal half-life of furosemide is approximately 2 hours. Peak plasma concentrations increase with increasing dose but times-to-peak do not differ among doses. Although furosemide is more rapidly absorbed from the oral solution (50 minutes) than from the tablet (87 minutes), peak plasma levels and area under the plasma concentration-time curves do not differ significantly. In fasted normal men, the mean bioavailability of furosemide from furosemide tablets and furosemide oral solution is 64% and 60%, respectively, of that from an intravenous injection of the drug. The duration of diuretic effect is 6 to 8 hours. ![]() The peak effect occurs within the first or second hour. The onset of diuresis following oral administration is within 1 hour. The unbound fraction averages 2.3 to 4.1% at therapeutic concentrations. ![]() Plasma concentrations ranging from 1 to 400 mcg/mL are 91 to 99% bound in healthy individuals. Furosemide is extensively bound to plasma proteins, mainly to albumin. Recent evidence suggests that furosemide glucuronide is the only or at least the major biotransformation product of furosemide in man. The action on the distal tubule is independent of any inhibitory effect on carbonic anhydrase and aldosterone. The high degree of efficacy is largely due to the unique site of action. It has been demonstrated that furosemide inhibits primarily the absorption of sodium and chloride not only in the proximal and distal tubules but also in the loop of Henle. Investigations into the mode of action of furosemide have utilized micropuncture studies in rats, stop flow experiments in dogs and various clearance studies in both humans and experimental animals.
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