FUROSAN

Furosemide is a potent loop diuretic that acts on the kidneys to ultimately increase water loss from the body.

It is an anthranilic acid derivative.

Furosemide is used for edema secondary to various clinical conditions, such as congestive heart failure exacerbation, liver failure, renal failure, and high blood pressure.

It mainly works by inhibiting electrolyte reabsorption from the kidneys and enhancing the excretion of water from the body.

Furosemide has a fast onset and short duration of action and has been used safely and effectively in both pediatric and adult patients.

The use of furosemide is particularly beneficial in clinical settings that require a drug with a higher diuretic potential.

In addition to oral formulations, the solution for intravenous and intramuscular administration is also available, which is typically limited to patients who are unable to take oral medication or for patients in emergency clinical situations.

Furosemide is indicated for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome, in adults and pediatric patients. 9, 14 Oral furosemide is indicated alone for the management of mild to moderate hypertension or severe hypertension in combination with other antihypertensive medications.

Intravenous furosemide is indicated as adjunctive therapy in acute pulmonary edema when a rapid onset of diuresis is desired.

Subcutaneous furosemide is indicated for the treatment of congestion due to fluid overload in adults with NYHA Class II/III chronic heart failure.

This drug formulation is not indicated for emergency situations or in patients with acute pulmonary edema.

Subcutaneous furosemide is also indicated for the treatment of edema in pediatric patients weighing 43 kg and above.

Furosemide manages hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome.

Furosemide is a potent loop diuretic that works to increase the excretion of Na+ and water by the kidneys by inhibiting their reabsorption from the proximal and distal tubules, as well as the loop of Henle.

It works directly acts on the cells of the nephron and indirectly modifies the content of the renal filtrate.

Ultimately, furosemide increases the urine output by the kidney.

Protein-bound furosemide is delivered to its site of action in the kidneys and secreted via active secretion by nonspecific organic transporters expressed at the luminal site of action. 4, 9 Following oral administration, the onset of the diuretic effect is about and 1.5 hours 9, and the peak effect is reached within the first 2 hours.

The duration of effect following oral administration is about 4-6 hours but may last up to 8 hours.

Following intravenous administration, the onset of effect is within 5 minutes, and the peak effect is reached within 30 minutes.

The duration of action following intravenous administration is approximately 2 hours.

Following intramuscular administration, the onset of action is somewhat delayed.

Following oral administration, furosemide is absorbed from the gastrointestinal tract.

It displays variable bioavailability from oral dosage forms, ranging from 10-90%.

The oral bioavailability of furosemide from oral tablets or oral solution is about 64% and 60%, respectively, of that from an intravenous injection of the drug.

The volume of distribution following intravenous administration of 40 mg furosemide were 0.181 L/kg in healthy subjects and 0.140 L/kg in patients with heart failure.

The metabolism of furosemide occurs mainly in the kidneys and the liver, to a smaller extent.

The kidneys are responsible for about 85% of total furosemide total clearance, where about 40% involves biotransformation.

Two major metabolites of furosemide are furosemide glucuronide, which is pharmacologically active, and saluamine (CSA) or 4-chloro-5-sulfamoylanthranilic acid.

Hover over products below to view reaction partners Furosemide 4-chloro-5-sulfamoylanthranilic acid Furosemide glucuronide.

The kidneys are responsible for 85% of total furosemide total clearance, where about 43% of the drug undergoes renal excretion.

Significantly more furosemide is excreted in urine following the Intravenous. injection than after the tablet or oral solution.

Approximately 50% of the furosemide load is excreted unchanged in urine, and the rest is metabolized into glucuronide in the kidney.

The half-life from the dose of 40 mg furosemide was 4 hours following oral administration and 4.5 hours following intravenous administration.

The terminal half-life of furosemide is approximately 2 hours following parenteral administration.

The terminal half-life may be increased up to 24 hours in patients with severe renal failure.

Following intravenous administration of 400 mg furosemide, the plasma clearance was 1.23 mL/kg/min in patients with heart failure and 2.34 mL/kg/min in healthy subjects, respectively.

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Clinical consequences from overdose depend on the extent of electrolyte and fluid loss and include dehydration, blood volume reduction, hypotension, electrolyte imbalance, hypokalemia, hypochloremic alkalosis, 9 hemoconcentration, cardiac arrhythmias (including A-V block and ventricular fibrillation).

Symptoms of overdose include acute renal failure, thrombosis, delirious states, flaccid paralysis, apathy and confusion.

In cirrhotic patients, overdosage might precipitate hepatic coma.

In rats, the oral LD 50, intraperitoneal LD 50, and subcutaneous LD is 2600 mg/kg, 800 mg/kg, and 4600 mg/kg, respectively.

Lowest published toxic dose (TDLo) in a female is 6250 μg/kg.

Furosemide is a potent diuretic which, if given in excessive amounts, can lead to a profound diuresis with water and electrolyte depletion.

Therefore, careful medical supervision is required and dose and dose schedule must be adjusted to the individual patient's needs See DOSAGE AND ADMINISTRATION.

Furosemide tablets are contraindicated in patients with anuria and in patients with a history of hypersensitivity to furosemide.

Therapy should be individualized according to patient response to gain maximal therapeutic response and to determine the minimal dose needed to maintain that response.

The usual initial dose of furosemide tablets is to 80 mg given as a single dose.

Ordinarily a prompt diuresis ensues.

If needed, the same dose can be administered to 8 hours later or the dose may be increased.

The dose may be raised by 20 or 40 mg and given not sooner than to 8 hours after the previous dose until the desired diuretic effect has been obtained.

The individually determined single dose should then be given once or twice daily (e.g., at 8 am and 2 pm).

The dose of furosemide tablets may be carefully titrated up to 600 mg/day in patients with clinically severe edematous states.

Edema may be most efficiently and safely mobilized by giving furosemide tablets on to 4 consecutive days each week.

When doses exceeding 80 mg/day are given for prolonged periods, careful clinical observation and laboratory monitoring are particularly advisable.

In general, dose selection for the elderly patient should be cautious, usually starting at the low end of the dosing range.

The usual initial dose of oral furosemide in pediatric patients is 2 mg/kg body weight, given as a single dose.

If the diuretic response is not satisfactory after the initial dose, dosage may be increased by 1 or 2 mg/kg no sooner than to 8 hours after the previous dose.

Doses greater than 6 mg/kg body weight are not recommended.

For maintenance therapy in pediatric patients, the dose should be adjusted to the minimum effective level.

Therapy should be individualized according to the patient's response to gain maximal therapeutic response and to determine the minimal dose needed to maintain the therapeutic response.

The usual initial dose of furosemide tablets for hypertension is 80 mg, usually divided into 40 mg twice a day. Dosage should then be adjusted according to response.

If response is not satisfactory, add other antihypertensive agents.

Changes in blood pressure must be carefully monitored when furosemide tablets are used with other antihypertensive drugs, especially during initial therapy.

To prevent excessive drop in blood pressure, the dosage of other agents should be reduced by at least 50 percent when furosemide tablets are added to the regimen.

As the blood pressure falls under the potentiating effect of furosemide tablets, a further reduction in dosage or even discontinuation of other antihypertensive drugs may be necessary.

In general, dose selection and dose adjustment for the elderly patient should be cautious, usually starting at the low end of the dosing range.

Store at 20° to 25°C (68° to 77°F) .

Protect from light.

Dispense in well-closed, light-resistant containers.

Exposure to light might cause a slight discoloration.

Discolored tablets should not be dispensed.

Store at 20° to 25°C (68° to 77°F) .

Protect from light.

Dispense in well-closed, light-resistant containers.

Exposure to light might cause a slight discoloration.

Discolored tablets should not be dispensed.

Furosemide has been shown to cause unexplained maternal deaths and abortions in rabbits at and 8 times the maximal recommended human dose.

There are no adequate and well-controlled studies in pregnant women.

Furosemide should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Treatment during pregnancy requires monitoring of fetal growth because of the potential for higher birth weights.

The effects of furosemide on embryonic and fetal development and on pregnant dams were studied in mice, rats and rabbits.

Furosemide caused unexplained maternal deaths and abortions in the rabbit at the lowest dose of 25 mg/kg (2 times the maximal recommended human dose of 600 mg/day).

In another study, a dose of 50 mg/kg (4 times the maximal recommended human dose of 600 mg/day) also caused maternal deaths and abortions when administered to rabbits between Days and 17 of gestation.

In a third study, none of the pregnant rabbits survived a dose of 100 mg/kg. Data from the above studies indicate fetal lethality that can precede maternal deaths.

The results of the mouse study and one of the three rabbit studies also showed an increased incidence and severity of hydronephrosis (distention of the renal pelvis and, in some cases, of the ureters) in fetuses derived from the treated dams as compared with the incidence in fetuses from the control group.

Because it appears in breast milk, caution should be exercised when furosemide is administered to a nursing mother.

Furosemide may inhibit lactation.

In premature infants furosemide may precipitate nephrocalcinosis/nephrolithiasis.

Nephrocalcinosis/nephrolithiasis has also been observed in children under 4 years of age with no history of prematurity who have been treated chronically with furosemide.

Monitor renal function, and renal ultrasonography should be considered, in pediatric patients receiving furosemide.

If furosemide is administered to premature infants during the first weeks of life, it may increase the risk of persistence of patent ductus arteriosus.

Furosemide binding to albumin may be reduced in elderly patients.

Furosemide is predominantly excreted unchanged in the urine.

The renal clearance of furosemide after intravenous administration in older healthy male subjects (60 to 70 years of age) is statistically significantly smaller than in younger healthy male subjects (20 to 35 years of age).

The initial diuretic effect of furosemide in older subjects is decreased relative to younger subjects.