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Indications/Uses
Fluid retention associated with chronic congestive cardiac failure (if diuretic treatment is required).
Fluid retention associated with acute congestive cardiac failure.
Fluid retention associated with chronic renal failure.
Maintenance of fluid excretion in acute renal failure, including that due to pregnancy or burns.
Fluid retention associated with nephrotic syndrome (if diuretic treatment is required).
Fluid retention associated with liver disease (if necessary to supplement treatment with aldosterone antagonists).
Hypertension.
Hypertensive crisis (as a supportive measure).
Support of forced diuresis.
Fluid retention associated with acute congestive cardiac failure.
Fluid retention associated with chronic renal failure.
Maintenance of fluid excretion in acute renal failure, including that due to pregnancy or burns.
Fluid retention associated with nephrotic syndrome (if diuretic treatment is required).
Fluid retention associated with liver disease (if necessary to supplement treatment with aldosterone antagonists).
Hypertension.
Hypertensive crisis (as a supportive measure).
Support of forced diuresis.
Dosage/Direction for Use
The dose used must be the lowest that is sufficient to achieve the desired effect.
Furosemide is given intravenously only when oral administration is not feasible or is ineffective (e.g. in impaired intestinal absorption) or if a rapid effect is required. If intravenous therapy is used, it is recommended that transfer to oral therapy be carried out as soon as possible.
In adults, the recommended maximum daily dose of furosemide for both oral and intravenous administration is 1500 mg.
The duration of treatment depends on the indication and is determined on an individual basis by the physician.
Injection: To achieve optimum efficacy and suppress counter-regulation, a continuous furosemide infusion is generally to be preferred to repeated bolus injections. Where continuous furosemide infusion is not feasible for follow-up treatment after one or several acute bolus doses, a follow-up regimen with low doses given at short intervals (approx. 4 hours) is to be preferred to a regimen with higher bolus doses at longer intervals.
Special Populations: Children: In children dosage is to be reduced in relation to body weight.
Tablet: In children, the recommended dose of furosemide for oral administration is 2 mg/kg body weight up to a maximum daily dose of 40 mg.
Injection: The recommended dose of furosemide for parenteral administration is 1 mg/kg body weight up to a maximum daily dose of 20 mg.
Adults: Hepatic impairment: Fluid retention associated with liver disease: Furosemide is used to supplement treatment with aldosterone antagonists in cases where these alone are not sufficient. In order to avoid complications such as orthostatic intolerance or electrolyte and acid-base imbalances, the dose must be carefully titrated so that the initial loss of fluid is gradual. For adults, this means a dose which leads to a loss of approx. 0.5 kg body weight per day.
Tablet: The recommended initial oral dose is 20 mg to 80 mg daily. This may be adjusted as necessary according to response. The daily dose may be given as a single dose or divided doses.
Injection: If intravenous treatment is absolutely necessary, the initial single dose is 20 mg to 40 mg.
Renal impairment: Fluid retention associated with chronic renal failure: The natriuretic response to furosemide depends on a number of factors, including severity of renal failure and the sodium balance, and, therefore, the effect of a dose cannot be accurately predicted. In patients with chronic renal failure, the dose must be carefully titrated so that the initial loss of fluid is gradual. For adults, this means a dose which leads to a loss of approx. 2 kg body weight (approx. 280 mmol Na+) per day.
Tablet: The recommended initial oral dose is 40 mg to 80 mg daily. This may be adjusted as necessary according to response. The total daily dose may be given as a single dose or two divided doses.
In dialysis patients, the usual oral maintenance dose is 250 mg to 1500 mg daily.
Injection: In intravenous treatment, the dose of furosemide may be determined by starting with a continuous intravenous infusion of 0.1 mg per minute and then gradually increasing the rate every half hour according to response.
Renal impairment: Maintenance of fluid excretion in acute renal failure: Hypovolaemia, hypotension, and significant electrolyte and acid-base imbalances must be corrected before starting furosemide. It is recommended that transfer from the intravenous to the oral route of administration is carried out as soon as possible.
Tablet: Renal impairment: Fluid retention associated with nephrotic syndrome: The recommended initial oral dose is 40 mg to 80 mg daily. This may be adjusted as necessary according to response. The total daily dose may be given as a single dose or several divided doses. See Precautions.
Fluid retention associated with chronic congestive cardiac failure: The recommended initial oral dose is 20 mg to 80 mg daily. This may be adjusted as necessary according to response. It is recommended that the daily dose is given as two or three divided doses.
Hypertension: Furosemide can be used alone or in combination with other antihypertensive agents.
The usual oral maintenance dose is 20 mg to 40 mg daily. In hypertension associated with chronic renal failure, higher doses may be required.
Injection: The recommended initial dose is 40 mg given as an intravenous injection. If this does not lead to the desired increase in fluid excretion, furosemide may be given as a continuous intravenous infusion, starting with a rate of 50 mg to 100 mg per hour.
Fluid retention associated with acute congestive cardiac failure: The recommended initial dose is 20 to 40 mg given as an intravenous bolus injection. The dose may be adjusted as necessary according to response.
Hypertensive crisis: The recommended initial dose of 20 mg to 40 mg is given as an intravenous bolus injection. This may be adjusted as necessary according to response.
Support of forced diuresis in poisoning: Furosemide is given intravenously in addition to infusions of electrolyte solutions. The dose is dependent on the response to furosemide. Fluid and electrolyte losses must be corrected before and during treatment.
In case of poisoning with acid or alkaline substances, elimination can be increased further by alkalization or acidification respectively, of the urine. The recommended initial dose is 20 mg to 40 mg given intravenously.
Administration: Tablet: It is recommended that Furosemide (Lasix) be taken on an empty stomach. Tablets are to be swallowed without chewing and with sufficient amounts of liquid.
Intravenous injection/infusion: Intravenous furosemide must be injected or infused slowly; a rate of 4 mg per minute must not be exceeded. In patients with severe impairment of renal function (serum creatinine >5 mg/dl), it is recommended that an infusion rate of 2.5 mg per minute is not exceeded.
Intramuscular injection: Intramuscular administration must be restricted to exceptional cases where neither oral nor intravenous administration is feasible. It must be noted that intramuscular injection is not suitable for the treatment of acute conditions such as pulmonary oedema.
Furosemide is given intravenously only when oral administration is not feasible or is ineffective (e.g. in impaired intestinal absorption) or if a rapid effect is required. If intravenous therapy is used, it is recommended that transfer to oral therapy be carried out as soon as possible.
In adults, the recommended maximum daily dose of furosemide for both oral and intravenous administration is 1500 mg.
The duration of treatment depends on the indication and is determined on an individual basis by the physician.
Injection: To achieve optimum efficacy and suppress counter-regulation, a continuous furosemide infusion is generally to be preferred to repeated bolus injections. Where continuous furosemide infusion is not feasible for follow-up treatment after one or several acute bolus doses, a follow-up regimen with low doses given at short intervals (approx. 4 hours) is to be preferred to a regimen with higher bolus doses at longer intervals.
Special Populations: Children: In children dosage is to be reduced in relation to body weight.
Tablet: In children, the recommended dose of furosemide for oral administration is 2 mg/kg body weight up to a maximum daily dose of 40 mg.
Injection: The recommended dose of furosemide for parenteral administration is 1 mg/kg body weight up to a maximum daily dose of 20 mg.
Adults: Hepatic impairment: Fluid retention associated with liver disease: Furosemide is used to supplement treatment with aldosterone antagonists in cases where these alone are not sufficient. In order to avoid complications such as orthostatic intolerance or electrolyte and acid-base imbalances, the dose must be carefully titrated so that the initial loss of fluid is gradual. For adults, this means a dose which leads to a loss of approx. 0.5 kg body weight per day.
Tablet: The recommended initial oral dose is 20 mg to 80 mg daily. This may be adjusted as necessary according to response. The daily dose may be given as a single dose or divided doses.
Injection: If intravenous treatment is absolutely necessary, the initial single dose is 20 mg to 40 mg.
Renal impairment: Fluid retention associated with chronic renal failure: The natriuretic response to furosemide depends on a number of factors, including severity of renal failure and the sodium balance, and, therefore, the effect of a dose cannot be accurately predicted. In patients with chronic renal failure, the dose must be carefully titrated so that the initial loss of fluid is gradual. For adults, this means a dose which leads to a loss of approx. 2 kg body weight (approx. 280 mmol Na+) per day.
Tablet: The recommended initial oral dose is 40 mg to 80 mg daily. This may be adjusted as necessary according to response. The total daily dose may be given as a single dose or two divided doses.
In dialysis patients, the usual oral maintenance dose is 250 mg to 1500 mg daily.
Injection: In intravenous treatment, the dose of furosemide may be determined by starting with a continuous intravenous infusion of 0.1 mg per minute and then gradually increasing the rate every half hour according to response.
Renal impairment: Maintenance of fluid excretion in acute renal failure: Hypovolaemia, hypotension, and significant electrolyte and acid-base imbalances must be corrected before starting furosemide. It is recommended that transfer from the intravenous to the oral route of administration is carried out as soon as possible.
Tablet: Renal impairment: Fluid retention associated with nephrotic syndrome: The recommended initial oral dose is 40 mg to 80 mg daily. This may be adjusted as necessary according to response. The total daily dose may be given as a single dose or several divided doses. See Precautions.
Fluid retention associated with chronic congestive cardiac failure: The recommended initial oral dose is 20 mg to 80 mg daily. This may be adjusted as necessary according to response. It is recommended that the daily dose is given as two or three divided doses.
Hypertension: Furosemide can be used alone or in combination with other antihypertensive agents.
The usual oral maintenance dose is 20 mg to 40 mg daily. In hypertension associated with chronic renal failure, higher doses may be required.
Injection: The recommended initial dose is 40 mg given as an intravenous injection. If this does not lead to the desired increase in fluid excretion, furosemide may be given as a continuous intravenous infusion, starting with a rate of 50 mg to 100 mg per hour.
Fluid retention associated with acute congestive cardiac failure: The recommended initial dose is 20 to 40 mg given as an intravenous bolus injection. The dose may be adjusted as necessary according to response.
Hypertensive crisis: The recommended initial dose of 20 mg to 40 mg is given as an intravenous bolus injection. This may be adjusted as necessary according to response.
Support of forced diuresis in poisoning: Furosemide is given intravenously in addition to infusions of electrolyte solutions. The dose is dependent on the response to furosemide. Fluid and electrolyte losses must be corrected before and during treatment.
In case of poisoning with acid or alkaline substances, elimination can be increased further by alkalization or acidification respectively, of the urine. The recommended initial dose is 20 mg to 40 mg given intravenously.
Administration: Tablet: It is recommended that Furosemide (Lasix) be taken on an empty stomach. Tablets are to be swallowed without chewing and with sufficient amounts of liquid.
Intravenous injection/infusion: Intravenous furosemide must be injected or infused slowly; a rate of 4 mg per minute must not be exceeded. In patients with severe impairment of renal function (serum creatinine >5 mg/dl), it is recommended that an infusion rate of 2.5 mg per minute is not exceeded.
Intramuscular injection: Intramuscular administration must be restricted to exceptional cases where neither oral nor intravenous administration is feasible. It must be noted that intramuscular injection is not suitable for the treatment of acute conditions such as pulmonary oedema.
Overdosage
Signs and Symptoms: The clinical picture in acute or chronic overdose depends primarily on the extent and consequences of electrolyte and fluid loss, e.g. hypovolaemia, dehydration, haemoconcentration, cardiac arrhythmias (including AV block and ventricular fibrillation). Symptoms of these disturbances include severe hypotension (progressing to shock), acute renal failure, thrombosis, delirious states, flaccid paralysis, apathy and confusion.
Management: No specific antidote to furosemide is known. If ingestion has only just taken place, attempts may be made to limit further systemic absorption of the active ingredient by measures such as gastric lavage or those designed to reduce absorption (e.g. activated charcoal).
Clinically relevant disturbances in electrolyte and fluid balance must be corrected. Together with the prevention and treatment of serious complications resulting from such disturbances and of other effects on the body, this corrective action may necessitate general and specific intensive medical monitoring and therapeutic measures.
Management: No specific antidote to furosemide is known. If ingestion has only just taken place, attempts may be made to limit further systemic absorption of the active ingredient by measures such as gastric lavage or those designed to reduce absorption (e.g. activated charcoal).
Clinically relevant disturbances in electrolyte and fluid balance must be corrected. Together with the prevention and treatment of serious complications resulting from such disturbances and of other effects on the body, this corrective action may necessitate general and specific intensive medical monitoring and therapeutic measures.
Administration
Tab: Should be taken on an empty stomach: Do not chew.
Contraindications
Furosemide (Lasix) must not be used: in patients with hypersensitivity to furosemide or any of the excipients of Furosemide (Lasix). Patients allergic to sulfonamides (e.g. sulfonamide antibiotics or sulfonylureas) may show cross-sensitivity to furosemide; in patients with hypovolaemia or dehydration; in patients with anuric renal failure not responding to furosemide; in patients with severe hypokalaemia (see Adverse Reactions); in patients with severe hyponatraemia; in patients with pre-comatose and comatose states associated with hepatic encephalopathy; in breast-feeding women.
Concerning use during pregnancy, see Use in Pregnancy & Lactation.
Concerning use during pregnancy, see Use in Pregnancy & Lactation.
Special Precautions
Urinary outflow must be secured.
In patients with a partial obstruction of urinary outflow (e.g. in patients with bladder-emptying disorders, prostatic hyperplasia or narrowing of the urethra), increased production of urine may provoke or aggravate complaints.
Thus, these patients require careful monitoring-especially during the initial stages of treatment.
Treatment with Furosemide (Lasix) necessitates regular medical supervision. Particularly careful monitoring is necessary: in patients with hypotension; in patients who would be at particular risk from a pronounced fall in blood pressure, e.g. patients with significant stenoses of the coronary arteries or of the blood vessels supplying the brain; in patients with latent or manifest diabetes mellitus; in patients with gout; in patients with hepatorenal syndrome, i.e. functional renal failure associated with severe liver disease; in patients with hypoproteinaemia, e.g. associated with nephrotic syndrome (the effect of furosemide may be weakened and its ototoxicity potentiated). Cautious dose titration is required; in premature infants (possible development nephrocalcinosis/nephrolithiasis; renal function must be monitored and renal ultrasonography performed).
Regular monitoring of serum sodium, potassium and creatinine is generally recommended during furosemide therapy; particularly close monitoring is required in patients at high risk of developing electrolyte imbalances or in case of significant additional fluid loss (e.g. due to vomiting, diarrhoea or intense sweating). Hypovolaemia or dehydration as well as any significant electrolyte and acid-base disturbances must be corrected. This may require temporary discontinuation of furosemide.
Concomitant use with risperidone: In risperidone placebo-controlled trials in elderly patients with dementia, a higher incidence of mortality was observed in patients treated with furosemide plus risperidone (7.3%; mean age 89 years, range 75-97 years) when compared to patients treated with risperidone alone (3.1%; mean age 84 years, range 70-96 years) or furosemide alone (4.1%; mean age 80 years, range 67-90 years).
Concomitant use of risperidone with other diuretics (mainly thiazide diuretics used in low dose) was not associated with similar findings.
No pathophysiological mechanism has been identified to explain this finding, and no consistent pattern for cause of death observed. Nevertheless, caution should be exercised and the risks and benefits of this combination or co-treatment with other potent diuretics should be considered prior to the decision to use. There was no increased incidence of mortality among patients taking other diuretics as concomitant treatment with risperidone. Irrespective of treatment, dehydration was an overall risk factor for mortality and should therefore be avoided in elderly patients with dementia (see Contraindications).
The possibility exists of exacerbation or activation of systemic lupus erythematosus.
Driving a Vehicle or Performing Other Hazardous Tasks: Some adverse effects (e.g. an undesirably pronounced fall in blood pressure) may impair the patient's ability to concentrate and react, and, therefore, constitute a risk in situations where these abilities are of special importance (e.g. operating a vehicle or machinery).
In patients with a partial obstruction of urinary outflow (e.g. in patients with bladder-emptying disorders, prostatic hyperplasia or narrowing of the urethra), increased production of urine may provoke or aggravate complaints.
Thus, these patients require careful monitoring-especially during the initial stages of treatment.
Treatment with Furosemide (Lasix) necessitates regular medical supervision. Particularly careful monitoring is necessary: in patients with hypotension; in patients who would be at particular risk from a pronounced fall in blood pressure, e.g. patients with significant stenoses of the coronary arteries or of the blood vessels supplying the brain; in patients with latent or manifest diabetes mellitus; in patients with gout; in patients with hepatorenal syndrome, i.e. functional renal failure associated with severe liver disease; in patients with hypoproteinaemia, e.g. associated with nephrotic syndrome (the effect of furosemide may be weakened and its ototoxicity potentiated). Cautious dose titration is required; in premature infants (possible development nephrocalcinosis/nephrolithiasis; renal function must be monitored and renal ultrasonography performed).
Regular monitoring of serum sodium, potassium and creatinine is generally recommended during furosemide therapy; particularly close monitoring is required in patients at high risk of developing electrolyte imbalances or in case of significant additional fluid loss (e.g. due to vomiting, diarrhoea or intense sweating). Hypovolaemia or dehydration as well as any significant electrolyte and acid-base disturbances must be corrected. This may require temporary discontinuation of furosemide.
Concomitant use with risperidone: In risperidone placebo-controlled trials in elderly patients with dementia, a higher incidence of mortality was observed in patients treated with furosemide plus risperidone (7.3%; mean age 89 years, range 75-97 years) when compared to patients treated with risperidone alone (3.1%; mean age 84 years, range 70-96 years) or furosemide alone (4.1%; mean age 80 years, range 67-90 years).
Concomitant use of risperidone with other diuretics (mainly thiazide diuretics used in low dose) was not associated with similar findings.
No pathophysiological mechanism has been identified to explain this finding, and no consistent pattern for cause of death observed. Nevertheless, caution should be exercised and the risks and benefits of this combination or co-treatment with other potent diuretics should be considered prior to the decision to use. There was no increased incidence of mortality among patients taking other diuretics as concomitant treatment with risperidone. Irrespective of treatment, dehydration was an overall risk factor for mortality and should therefore be avoided in elderly patients with dementia (see Contraindications).
The possibility exists of exacerbation or activation of systemic lupus erythematosus.
Driving a Vehicle or Performing Other Hazardous Tasks: Some adverse effects (e.g. an undesirably pronounced fall in blood pressure) may impair the patient's ability to concentrate and react, and, therefore, constitute a risk in situations where these abilities are of special importance (e.g. operating a vehicle or machinery).
Use In Pregnancy & Lactation
Pregnancy: Furosemide crosses the placental barrier. It must not be given during pregnancy unless there are compelling medical reasons. Treatment during pregnancy requires monitoring of foetal growth.
Lactation: Furosemide passes into breast milk and may inhibit lactation. Women must not breast-feed if they are treated with furosemide.
Lactation: Furosemide passes into breast milk and may inhibit lactation. Women must not breast-feed if they are treated with furosemide.
Adverse Reactions
The frequencies are derived from literature data referring to studies where furosemide is used in a total of 1387 patients, at any dose and in any indication. When the frequency category for the same ADR was different, the highest frequency category was selected.
The following CIOMS frequency rating is used, when applicable: Very common ≥10%; Common ≥1 and <10%; Uncommon ≥0.1 and <1%; Rare ≥0.01 and <0.1%; Very rare <0.01%, Not known (cannot be estimated from available data).
Metabolism and nutrition disorders (see Precautions): Very common: electrolyte disturbances (including symptomatic), dehydration and hypovolaemia especially in elderly patients, blood creatinine increased, blood triglyceride increased.
Common: hyponatremia, hypochloremia, hypokalaemia, blood cholesterol increased, blood uric acid increased and attacks of gout.
Uncommon: glucose tolerance impaired. Latent diabetes mellitus may become manifest. See Precautions.
Not known: hypocalcemia, hypomagnesemia, blood urea increased, metabolic alkalosis, Pseudo-Bartter syndrome in the context of misuse and/or long-term use of furosemide.
Vascular disorders: Very common (for intravenous infusion): Hypotension including orthostatic hypotension (see Precautions).
Rare: vasculitis.
Not known: thrombosis.
Renal and urinary disorders: Common: urine volume increased.
Rare: tubulointerstitial nephritis.
Not known: urine sodium increased, urine chloride increase, urine retention (in patients with a partial obstruction of urinary outflow, see Precautions), nephrocalcinosis/nephrolithiasis in premature infants (see Precautions), renal failure (see Interactions).
Gastrointestinal disorders: Uncommon: nausea.
Rare: vomiting, diarrhoea.
Very rare: pancreatitis acute.
Hepato-biliary disorders: Very rare: cholestasis, transaminases increased.
Ear and labyrinth disorders: Uncommon: hearing disorders although usually transitory, particularly in patients with renal failure, hypoproteinaemia (e.g. in nephrotic syndrome) and/or when intravenous furosemide has been given too rapidly. Cases of deafness, sometimes irreversible have been reported after oral or IV administration of furosemide.
Rare: tinnitus.
Skin and subcutaneous disorders: Uncommon: pruritus, urticaria, rashes, dermatitis bullous, erythema multiforme, pemphigoid, dermatitis exfoliative, purpura, photosensitivity reaction.
Not known: Stevens-Johnson syndrome, toxic epidermal necrolysis, AGEP (acute generalized exanthematous pustulosis) and DRESS (Drug Rash with Eosinophilia and Systemic Symptoms), lichenoid reactions.
Immune system disorders: Rare: severe anaphylactic or anaphylactoid reactions (e.g. with shock).
Not known: exacerbation or activation of systemic lupus erythematosus.
Nervous system disorders: Rare: paraesthesiae.
Common: hepatic encephalopathy in patients with hepatocellular insufficiency (see Contraindications).
Not known: dizziness, fainting or loss of consciousness, headache.
Blood and the lymphatic system disorders: Common: haemoconcentration.
Uncommon: thrombocytopenia.
Rare: leucopoenia, eosinophilia.
Very rare: agranulocytosis, aplastic anaemia or haemolytic anaemia.
Musculoskeletal and connective tissue disorders: Not known: cases of rhabdomyolysis have been reported, often in the context of severe hypokalaemia (see Contraindications).
Congenital and familial/genetic disorders: Not known: increased risk of persistence of patent ductus arteriosus when furosemide is administered to premature infants during the first weeks of life.
General disorders and administration site conditions: Not known: following intramuscular injection, local reactions such as pain.
Rare: fever.
The following CIOMS frequency rating is used, when applicable: Very common ≥10%; Common ≥1 and <10%; Uncommon ≥0.1 and <1%; Rare ≥0.01 and <0.1%; Very rare <0.01%, Not known (cannot be estimated from available data).
Metabolism and nutrition disorders (see Precautions): Very common: electrolyte disturbances (including symptomatic), dehydration and hypovolaemia especially in elderly patients, blood creatinine increased, blood triglyceride increased.
Common: hyponatremia, hypochloremia, hypokalaemia, blood cholesterol increased, blood uric acid increased and attacks of gout.
Uncommon: glucose tolerance impaired. Latent diabetes mellitus may become manifest. See Precautions.
Not known: hypocalcemia, hypomagnesemia, blood urea increased, metabolic alkalosis, Pseudo-Bartter syndrome in the context of misuse and/or long-term use of furosemide.
Vascular disorders: Very common (for intravenous infusion): Hypotension including orthostatic hypotension (see Precautions).
Rare: vasculitis.
Not known: thrombosis.
Renal and urinary disorders: Common: urine volume increased.
Rare: tubulointerstitial nephritis.
Not known: urine sodium increased, urine chloride increase, urine retention (in patients with a partial obstruction of urinary outflow, see Precautions), nephrocalcinosis/nephrolithiasis in premature infants (see Precautions), renal failure (see Interactions).
Gastrointestinal disorders: Uncommon: nausea.
Rare: vomiting, diarrhoea.
Very rare: pancreatitis acute.
Hepato-biliary disorders: Very rare: cholestasis, transaminases increased.
Ear and labyrinth disorders: Uncommon: hearing disorders although usually transitory, particularly in patients with renal failure, hypoproteinaemia (e.g. in nephrotic syndrome) and/or when intravenous furosemide has been given too rapidly. Cases of deafness, sometimes irreversible have been reported after oral or IV administration of furosemide.
Rare: tinnitus.
Skin and subcutaneous disorders: Uncommon: pruritus, urticaria, rashes, dermatitis bullous, erythema multiforme, pemphigoid, dermatitis exfoliative, purpura, photosensitivity reaction.
Not known: Stevens-Johnson syndrome, toxic epidermal necrolysis, AGEP (acute generalized exanthematous pustulosis) and DRESS (Drug Rash with Eosinophilia and Systemic Symptoms), lichenoid reactions.
Immune system disorders: Rare: severe anaphylactic or anaphylactoid reactions (e.g. with shock).
Not known: exacerbation or activation of systemic lupus erythematosus.
Nervous system disorders: Rare: paraesthesiae.
Common: hepatic encephalopathy in patients with hepatocellular insufficiency (see Contraindications).
Not known: dizziness, fainting or loss of consciousness, headache.
Blood and the lymphatic system disorders: Common: haemoconcentration.
Uncommon: thrombocytopenia.
Rare: leucopoenia, eosinophilia.
Very rare: agranulocytosis, aplastic anaemia or haemolytic anaemia.
Musculoskeletal and connective tissue disorders: Not known: cases of rhabdomyolysis have been reported, often in the context of severe hypokalaemia (see Contraindications).
Congenital and familial/genetic disorders: Not known: increased risk of persistence of patent ductus arteriosus when furosemide is administered to premature infants during the first weeks of life.
General disorders and administration site conditions: Not known: following intramuscular injection, local reactions such as pain.
Rare: fever.
Drug Interactions
Food: Whether and to what extent the absorption of furosemide is affected by taking it with food seems to depend on the pharmaceutical formulation. It is recommended that oral formulations of Furosemide (Lasix) be taken on an empty stomach.
Drug Interactions: Not recommended associations: In isolated cases intravenous administration of furosemide within 24 hours of taking chloral hydrate may lead to flushing, sweating attacks, restlessness, nausea, increase in blood pressure and tachycardia. Use of furosemide concomitantly with chloral hydrate is, therefore, not recommended.
Furosemide may potentiate the ototoxicity of aminoglycosides and other ototoxic drugs. Since this may lead to irreversible damage, these drugs must only be used with furosemide if there are compelling medical reasons.
Precautions for use: There is a risk of ototoxic effects if cisplatin and furosemide are given concomitantly. In addition, nephrotoxicity of cisplatin may be enhanced if furosemide is not given in low doses (e.g. 40 mg in patients with normal renal function) and with positive fluid balance when used to achieve forced diuresis during cisplatin treatment.
Oral furosemide and sucralfate must not be taken within 2 hours of each other because sucralfate decreases the absorption of furosemide from the intestine and so reduces its effect.
Furosemide decreases the excretion of lithium salts and may cause increased serum lithium levels, resulting in increased risk of lithium toxicity, including increased risk of cardiotoxic and neurotoxic effects of lithium. Therefore, it is recommended that lithium levels are carefully monitored in patients receiving this combination.
Patients who are receiving diuretics may suffer severe hypotension and deterioration in renal function, including cases of renal failure, especially when an angiotensin converting enzyme inhibitor (ACE inhibitor) or angiotensin II receptor antagonist is given for the first time or for the first time in an increased dose. Consideration must be given to interrupting the administration of furosemide temporarily or at least reducing the dose of furosemide for three days before starting treatment with, or increasing the dose of, an ACE inhibitor or angiotensin II receptor antagonist.
Risperidone: Caution should be exercised and the risks and benefits of the combination or co-treatment with furosemide or with other potent diuretics should be considered prior to the decision to use. See Precautions, regarding increased mortality in elderly patients with dementia concomitantly receiving risperidone.
Levothyroxine: High doses of furosemide may inhibit binding of thyroid hormones to carrier proteins and thereby lead to an initial transient increase in free thyroid hormones, followed by an overall decrease in total thyroid hormone levels. Thyroid hormone levels should be monitored.
Take into account: Concomitant administration of non-steroidal anti-inflammatory drugs including acetylsalicylic acid may reduce the effect of furosemide. In patients with dehydration or hypovolaemia, non-steroidal anti-inflammatory drugs may cause acute renal failure. Salicylate toxicity may be increased by furosemide.
Attenuation of the effect of furosemide may occur following concurrent administration of phenytoin.
Corticosteroids, carbenoxolone, liquorice in large amounts, and prolonged use of laxatives may increase the risk of developing hypokalaemia.
Some electrolyte disturbances (e.g. hypokalaemia, hypomagnesaemia) may increase the toxicity of certain other drugs (e.g. digitalis preparations and drugs inducing QT interval prolongation syndrome).
If antihypertensive agents, diuretics or other drugs with blood-pressure-lowering potential are given concomitantly with furosemide, a more pronounced fall in blood pressure must be anticipated.
Probenecid, methotrexate and other drugs which, like furosemide, undergo significant renal tubular secretion may reduce the effect of furosemide. Conversely, furosemide may decrease renal elimination of these drugs. In case of high-dose treatment (in particular, of both furosemide and the other drugs), this may lead to increased serum levels and an increased risk of adverse effects due to furosemide or the concomitant medication.
The effects of antidiabetic drugs and blood-pressure-increasing sympathomimetics (e.g. epinephrine, norepinephrine) may be reduced. The effects of curare-type muscle relaxants or of theophylline may be increased.
The harmful effects of nephrotoxic drugs on the kidney may be increased.
Impairment of renal function may develop in patients receiving concurrent treatment with furosemide and high doses of certain cephalosporins.
Concomitant use of cyclosporine A and furosemide is associated with increased risk of gouty arthritis secondary to furosemide-induced hyperuricaemia and cyclosporine impairment of renal urate excretion.
Patients who were at high risk for radiocontrast nephropathy treated with furosemide experienced a higher incidence of deterioration in renal function after receiving radiocontrast compared to high-risk patients who received only intravenous hydration prior to receiving radiocontrast.
Drug Interactions: Not recommended associations: In isolated cases intravenous administration of furosemide within 24 hours of taking chloral hydrate may lead to flushing, sweating attacks, restlessness, nausea, increase in blood pressure and tachycardia. Use of furosemide concomitantly with chloral hydrate is, therefore, not recommended.
Furosemide may potentiate the ototoxicity of aminoglycosides and other ototoxic drugs. Since this may lead to irreversible damage, these drugs must only be used with furosemide if there are compelling medical reasons.
Precautions for use: There is a risk of ototoxic effects if cisplatin and furosemide are given concomitantly. In addition, nephrotoxicity of cisplatin may be enhanced if furosemide is not given in low doses (e.g. 40 mg in patients with normal renal function) and with positive fluid balance when used to achieve forced diuresis during cisplatin treatment.
Oral furosemide and sucralfate must not be taken within 2 hours of each other because sucralfate decreases the absorption of furosemide from the intestine and so reduces its effect.
Furosemide decreases the excretion of lithium salts and may cause increased serum lithium levels, resulting in increased risk of lithium toxicity, including increased risk of cardiotoxic and neurotoxic effects of lithium. Therefore, it is recommended that lithium levels are carefully monitored in patients receiving this combination.
Patients who are receiving diuretics may suffer severe hypotension and deterioration in renal function, including cases of renal failure, especially when an angiotensin converting enzyme inhibitor (ACE inhibitor) or angiotensin II receptor antagonist is given for the first time or for the first time in an increased dose. Consideration must be given to interrupting the administration of furosemide temporarily or at least reducing the dose of furosemide for three days before starting treatment with, or increasing the dose of, an ACE inhibitor or angiotensin II receptor antagonist.
Risperidone: Caution should be exercised and the risks and benefits of the combination or co-treatment with furosemide or with other potent diuretics should be considered prior to the decision to use. See Precautions, regarding increased mortality in elderly patients with dementia concomitantly receiving risperidone.
Levothyroxine: High doses of furosemide may inhibit binding of thyroid hormones to carrier proteins and thereby lead to an initial transient increase in free thyroid hormones, followed by an overall decrease in total thyroid hormone levels. Thyroid hormone levels should be monitored.
Take into account: Concomitant administration of non-steroidal anti-inflammatory drugs including acetylsalicylic acid may reduce the effect of furosemide. In patients with dehydration or hypovolaemia, non-steroidal anti-inflammatory drugs may cause acute renal failure. Salicylate toxicity may be increased by furosemide.
Attenuation of the effect of furosemide may occur following concurrent administration of phenytoin.
Corticosteroids, carbenoxolone, liquorice in large amounts, and prolonged use of laxatives may increase the risk of developing hypokalaemia.
Some electrolyte disturbances (e.g. hypokalaemia, hypomagnesaemia) may increase the toxicity of certain other drugs (e.g. digitalis preparations and drugs inducing QT interval prolongation syndrome).
If antihypertensive agents, diuretics or other drugs with blood-pressure-lowering potential are given concomitantly with furosemide, a more pronounced fall in blood pressure must be anticipated.
Probenecid, methotrexate and other drugs which, like furosemide, undergo significant renal tubular secretion may reduce the effect of furosemide. Conversely, furosemide may decrease renal elimination of these drugs. In case of high-dose treatment (in particular, of both furosemide and the other drugs), this may lead to increased serum levels and an increased risk of adverse effects due to furosemide or the concomitant medication.
The effects of antidiabetic drugs and blood-pressure-increasing sympathomimetics (e.g. epinephrine, norepinephrine) may be reduced. The effects of curare-type muscle relaxants or of theophylline may be increased.
The harmful effects of nephrotoxic drugs on the kidney may be increased.
Impairment of renal function may develop in patients receiving concurrent treatment with furosemide and high doses of certain cephalosporins.
Concomitant use of cyclosporine A and furosemide is associated with increased risk of gouty arthritis secondary to furosemide-induced hyperuricaemia and cyclosporine impairment of renal urate excretion.
Patients who were at high risk for radiocontrast nephropathy treated with furosemide experienced a higher incidence of deterioration in renal function after receiving radiocontrast compared to high-risk patients who received only intravenous hydration prior to receiving radiocontrast.
Storage
Protect from light.
Tablet: Store at temperatures not exceeding 30°C.
Injection: Store below 30°C.
Tablet: Store at temperatures not exceeding 30°C.
Injection: Store below 30°C.
Action
Pharmacology: Pharmacodynamics: Mode of Action: Furosemide is a loop diuretic that produces a comparatively powerful and short-lived rapid-onset diuresis.
Furosemide blocks the Na+K+2Cl- co-transport system located in the luminal cell membrane of the thick ascending limb of the loop of Henle: the effectiveness of the saluretic action of furosemide, therefore, depends on the drug reaching the tubular lumen via an anion transport mechanism. The diuretic action results from inhibition of the reabsorption of sodium chloride in this segment of the loop of Henle. As a result, fractional sodium excretion may be as much as 35% of glomerular sodium filtration. The secondary effects of increased sodium excretion are increased urine excretion (due to osmotically bound water) and increased distal tubular potassium secretion. The excretion of calcium and magnesium ions is also increased.
Furosemide interrupts the tubulo-glomerular feedback mechanism in the macula densa, with the result that there is no attenuation of saluretic activity. Furosemide causes dose-dependent stimulation of the renin-angiotensin-aldosterone system.
In heart failure, furosemide produces an acute reduction in cardiac pre-load (by dilating the venous capacitance vessels). This early vascular effect appears to be prostaglandin-mediated and presupposes adequate renal function with activation of the renin-angiotensin system and intact prostaglandin synthesis. Moreover, because of its natriuretic effect, furosemide lowers vascular reactivity to catecholamines which is increased in hypertensive patients.
The antihypertensive effectiveness of furosemide is attributable to increased sodium excretion, reduced blood volume and reduced responsiveness of vascular smooth muscle to vasoconstrictor stimuli.
Pharmacodynamic Characteristics: The diuretic effect of furosemide occurs within 15 minutes of an intravenous dose and within 1 hour of an oral dose.
A dose-dependent increase in diuresis and natriuresis has been shown in healthy subjects receiving furosemide at doses of 10 mg to 100 mg. The duration of action is approx. 3 hours after an intravenous dose of furosemide 20 mg, 3 to 6 hours after an oral dose of 40 mg in healthy people.
In patients, the relationship between intratubular concentrations of unbound (free) furosemide (estimated using the rate of furosemide excretion in urine) and its natriuretic effect is in the shape of a sigmoid curve with a minimal effective excretion rate of furosemide of approx. 10 microgram per minute. Therefore, a continuous infusion of furosemide is more effective than repetitive bolus injections. Moreover, above a certain bolus dose of the drug there is no significant increase in effect. The effect of furosemide is reduced if there is lowered tubular secretion or intra-tubular albumin binding of the drug.
Pharmacokinetics: Absorption: Furosemide is rapidly absorbed from the gastrointestinal tract. The tmax is 1 to 1.5 hours for Furosemide (Lasix). The absorption of the drug shows large inter- and intra-individual variability.
The bioavailability of furosemide in healthy volunteers is approximately 50% to 70% for tablets and approximately 80% for the oral solution. In patients, the bioavailability of the drug is influenced by various factors including underlying diseases, and it may be reduced to 30% (e.g. in nephrotic syndrome).
Whether and to what extent the absorption of furosemide is affected by taking it with food seems to depend on the pharmaceutical formulation.
Distribution: The volume of distribution of furosemide is 0.1 to 0.2 litres per kg body weight. The volume of distribution may be higher depending on the underlying disease.
Metabolism: Furosemide is strongly (more than 98%) bound to plasma protein, mainly albumin.
Elimination: Furosemide is eliminated mainly as the unchanged drug, primarily by secretion into the proximal tubule.
After intravenous administration 60% to 70% of the furosemide dose is excreted in this way. A glucuronide metabolite of furosemide accounts for 10% to 20% of the substances recovered in the urine.
The remaining dose is excreted in the faeces, probably following biliary secretion.
The terminal half-life of furosemide after intravenous administration is approx. 1 to 1.5 hours.
Furosemide is excreted in breast milk. Furosemide passes the placental barrier and transfers to the foetus slowly. It is found in the foetus or newborn in the same concentrations as in the mother.
Special Populations: Elderly, congestive heart failure, severe hypertension: The elimination of furosemide is slowed down due to reduced renal function in patients with congestive heart failure, severe hypertension or in the elderly.
Paediatric patients: Depending on the maturity of the kidney, the elimination of furosemide may be slowed down. The metabolism of the drug is also reduced if the infant's glucuronisation capacity is impaired. The terminal half-life is below 12 hours in infants with a post-conceptional age of more than 33 weeks. In infants of 2 months and older, the terminal clearance is the same as in adults.
Hepatic impairment: In liver failure, the half-life of furosemide is increased by 30% to 90% mainly due to a larger volume of distribution. Additionally, in this patient group there is a wide variation in all pharmacokinetic parameters.
Renal impairment: In renal failure, the elimination of furosemide is slowed down and the half-life prolonged; the terminal half-life may be up to 24 hours in patients with severe renal failure.
In nephrotic syndrome the reduced plasma protein concentration leads to a higher concentration of unbound (free) furosemide. On the other hand, efficacy of furosemide is reduced in these patients due to binding to intratubular albumin and lowered tubular secretion.
Furosemide is poorly dialysable in patients undergoing haemodialysis, peritoneal dialysis and CAPD.
Toxicology: Non-Clinical Safety Data: Acute Toxicity: Studies conducted with oral and intravenous administration of furosemide in various rodent species and dogs revealed low acute toxicity. The oral LD50 of furosemide is between 1050 and 4600 mg/kg body weight in mice and rats, and 243 mg/kg body weight in guinea pigs. In dogs, the oral LD50 is approx. 2000 mg/kg body weight, and the i.v. LD50 is greater than 400 mg/kg body weight.
Chronic Toxicity: In rats and dogs after 6 and 12 months' administration, renal changes (including focal fibrosis, calcification) were encountered in the top dosage groups (10 to 20 times the therapeutic dose in humans).
Carcinogenicity: Furosemide in the approximate amount of 200 mg/kg body weight (14,000 ppm) daily was administered to female mice and rats over a 2 year period with their diet. An increased incidence of mammary adenocarcinoma was noted in the mice, but not in the rats. This dose is considerably greater than the therapeutic dose administered in human patients. Moreover, these tumours were morphologically identical to the spontaneously occurring tumours observed in 2% to 8% of control animals.
Thus, it appears unlikely that this incidence of tumours is relevant to the treatment of humans. Indeed, there is no evidence of increased incidence of human mammary adenocarcinoma following the use of furosemide. Based on epidemiological studies, a carcinogenicity classification for furosemide in humans is not possible.
In a carcinogenicity study, rats were administered furosemide in daily doses of 15 and 30 mg/kg body weight. Male rats in the 15 mg/kg-dose category, but not in the 30 mg/kg-dose category, showed a marginal increase in uncommon tumours. These findings are considered to be incidental. Nitrosamine-induced urinary bladder carcinogenesis in rats yielded no evidence to suggest that furosemide is a promoting factor.
Mutagenicity: In in vitro tests on bacteria and mammalian cells, both positive and negative results have been obtained.
Induction of gene and chromosome mutations, however, has been observed only where furosemide reached cytotoxic concentrations.
Teratogenicity: No relevant embryotoxic or teratogenic effects were revealed in various mammalian species including mouse, rat, cat, rabbit and dog after treatment with furosemide. Retarded renal maturation - a reduction in the number of differentiated glomeruli - has been described in the progeny of rats treated with 75 mg furosemide per kg body weight during days 7 to 11 and 14 to 18 of pregnancy.
Furosemide crosses the placental barrier and in umbilical cord blood it attains 100% of maternal serum concentrations. To date, no malformations have been detected in humans which might be linked with exposure to furosemide. However, sufficient experience has not been gained to permit a conclusive assessment of possible harmful effects on the embryo/foetus. Urine production in the foetus can be stimulated in utero.
Urolithiasis and nephrocalcinosis have been observed following treatment of premature infants with furosemide. No studies have been conducted to assess the effects on the infant of furosemide when ingested with the breast milk.
Impairment of Fertility: Furosemide did not impair fertility of male and female rats at daily doses of 90 mg/kg body weight and of male and female mice at daily doses of 200 mg/kg body weight orally.
Ototoxicity: Furosemide may interfere with transport processes in the stria vascularis of the internal ear, possibly leading to a - generally reversible - hearing disorder.
Furosemide blocks the Na+K+2Cl- co-transport system located in the luminal cell membrane of the thick ascending limb of the loop of Henle: the effectiveness of the saluretic action of furosemide, therefore, depends on the drug reaching the tubular lumen via an anion transport mechanism. The diuretic action results from inhibition of the reabsorption of sodium chloride in this segment of the loop of Henle. As a result, fractional sodium excretion may be as much as 35% of glomerular sodium filtration. The secondary effects of increased sodium excretion are increased urine excretion (due to osmotically bound water) and increased distal tubular potassium secretion. The excretion of calcium and magnesium ions is also increased.
Furosemide interrupts the tubulo-glomerular feedback mechanism in the macula densa, with the result that there is no attenuation of saluretic activity. Furosemide causes dose-dependent stimulation of the renin-angiotensin-aldosterone system.
In heart failure, furosemide produces an acute reduction in cardiac pre-load (by dilating the venous capacitance vessels). This early vascular effect appears to be prostaglandin-mediated and presupposes adequate renal function with activation of the renin-angiotensin system and intact prostaglandin synthesis. Moreover, because of its natriuretic effect, furosemide lowers vascular reactivity to catecholamines which is increased in hypertensive patients.
The antihypertensive effectiveness of furosemide is attributable to increased sodium excretion, reduced blood volume and reduced responsiveness of vascular smooth muscle to vasoconstrictor stimuli.
Pharmacodynamic Characteristics: The diuretic effect of furosemide occurs within 15 minutes of an intravenous dose and within 1 hour of an oral dose.
A dose-dependent increase in diuresis and natriuresis has been shown in healthy subjects receiving furosemide at doses of 10 mg to 100 mg. The duration of action is approx. 3 hours after an intravenous dose of furosemide 20 mg, 3 to 6 hours after an oral dose of 40 mg in healthy people.
In patients, the relationship between intratubular concentrations of unbound (free) furosemide (estimated using the rate of furosemide excretion in urine) and its natriuretic effect is in the shape of a sigmoid curve with a minimal effective excretion rate of furosemide of approx. 10 microgram per minute. Therefore, a continuous infusion of furosemide is more effective than repetitive bolus injections. Moreover, above a certain bolus dose of the drug there is no significant increase in effect. The effect of furosemide is reduced if there is lowered tubular secretion or intra-tubular albumin binding of the drug.
Pharmacokinetics: Absorption: Furosemide is rapidly absorbed from the gastrointestinal tract. The tmax is 1 to 1.5 hours for Furosemide (Lasix). The absorption of the drug shows large inter- and intra-individual variability.
The bioavailability of furosemide in healthy volunteers is approximately 50% to 70% for tablets and approximately 80% for the oral solution. In patients, the bioavailability of the drug is influenced by various factors including underlying diseases, and it may be reduced to 30% (e.g. in nephrotic syndrome).
Whether and to what extent the absorption of furosemide is affected by taking it with food seems to depend on the pharmaceutical formulation.
Distribution: The volume of distribution of furosemide is 0.1 to 0.2 litres per kg body weight. The volume of distribution may be higher depending on the underlying disease.
Metabolism: Furosemide is strongly (more than 98%) bound to plasma protein, mainly albumin.
Elimination: Furosemide is eliminated mainly as the unchanged drug, primarily by secretion into the proximal tubule.
After intravenous administration 60% to 70% of the furosemide dose is excreted in this way. A glucuronide metabolite of furosemide accounts for 10% to 20% of the substances recovered in the urine.
The remaining dose is excreted in the faeces, probably following biliary secretion.
The terminal half-life of furosemide after intravenous administration is approx. 1 to 1.5 hours.
Furosemide is excreted in breast milk. Furosemide passes the placental barrier and transfers to the foetus slowly. It is found in the foetus or newborn in the same concentrations as in the mother.
Special Populations: Elderly, congestive heart failure, severe hypertension: The elimination of furosemide is slowed down due to reduced renal function in patients with congestive heart failure, severe hypertension or in the elderly.
Paediatric patients: Depending on the maturity of the kidney, the elimination of furosemide may be slowed down. The metabolism of the drug is also reduced if the infant's glucuronisation capacity is impaired. The terminal half-life is below 12 hours in infants with a post-conceptional age of more than 33 weeks. In infants of 2 months and older, the terminal clearance is the same as in adults.
Hepatic impairment: In liver failure, the half-life of furosemide is increased by 30% to 90% mainly due to a larger volume of distribution. Additionally, in this patient group there is a wide variation in all pharmacokinetic parameters.
Renal impairment: In renal failure, the elimination of furosemide is slowed down and the half-life prolonged; the terminal half-life may be up to 24 hours in patients with severe renal failure.
In nephrotic syndrome the reduced plasma protein concentration leads to a higher concentration of unbound (free) furosemide. On the other hand, efficacy of furosemide is reduced in these patients due to binding to intratubular albumin and lowered tubular secretion.
Furosemide is poorly dialysable in patients undergoing haemodialysis, peritoneal dialysis and CAPD.
Toxicology: Non-Clinical Safety Data: Acute Toxicity: Studies conducted with oral and intravenous administration of furosemide in various rodent species and dogs revealed low acute toxicity. The oral LD50 of furosemide is between 1050 and 4600 mg/kg body weight in mice and rats, and 243 mg/kg body weight in guinea pigs. In dogs, the oral LD50 is approx. 2000 mg/kg body weight, and the i.v. LD50 is greater than 400 mg/kg body weight.
Chronic Toxicity: In rats and dogs after 6 and 12 months' administration, renal changes (including focal fibrosis, calcification) were encountered in the top dosage groups (10 to 20 times the therapeutic dose in humans).
Carcinogenicity: Furosemide in the approximate amount of 200 mg/kg body weight (14,000 ppm) daily was administered to female mice and rats over a 2 year period with their diet. An increased incidence of mammary adenocarcinoma was noted in the mice, but not in the rats. This dose is considerably greater than the therapeutic dose administered in human patients. Moreover, these tumours were morphologically identical to the spontaneously occurring tumours observed in 2% to 8% of control animals.
Thus, it appears unlikely that this incidence of tumours is relevant to the treatment of humans. Indeed, there is no evidence of increased incidence of human mammary adenocarcinoma following the use of furosemide. Based on epidemiological studies, a carcinogenicity classification for furosemide in humans is not possible.
In a carcinogenicity study, rats were administered furosemide in daily doses of 15 and 30 mg/kg body weight. Male rats in the 15 mg/kg-dose category, but not in the 30 mg/kg-dose category, showed a marginal increase in uncommon tumours. These findings are considered to be incidental. Nitrosamine-induced urinary bladder carcinogenesis in rats yielded no evidence to suggest that furosemide is a promoting factor.
Mutagenicity: In in vitro tests on bacteria and mammalian cells, both positive and negative results have been obtained.
Induction of gene and chromosome mutations, however, has been observed only where furosemide reached cytotoxic concentrations.
Teratogenicity: No relevant embryotoxic or teratogenic effects were revealed in various mammalian species including mouse, rat, cat, rabbit and dog after treatment with furosemide. Retarded renal maturation - a reduction in the number of differentiated glomeruli - has been described in the progeny of rats treated with 75 mg furosemide per kg body weight during days 7 to 11 and 14 to 18 of pregnancy.
Furosemide crosses the placental barrier and in umbilical cord blood it attains 100% of maternal serum concentrations. To date, no malformations have been detected in humans which might be linked with exposure to furosemide. However, sufficient experience has not been gained to permit a conclusive assessment of possible harmful effects on the embryo/foetus. Urine production in the foetus can be stimulated in utero.
Urolithiasis and nephrocalcinosis have been observed following treatment of premature infants with furosemide. No studies have been conducted to assess the effects on the infant of furosemide when ingested with the breast milk.
Impairment of Fertility: Furosemide did not impair fertility of male and female rats at daily doses of 90 mg/kg body weight and of male and female mice at daily doses of 200 mg/kg body weight orally.
Ototoxicity: Furosemide may interfere with transport processes in the stria vascularis of the internal ear, possibly leading to a - generally reversible - hearing disorder.
MedsGo Class
Diuretics
Features
Brand
Lasix
Full Details
Dosage Strength
40 mg
Drug Ingredients
- Furosemide
Drug Packaging
Tablet 100's
Generic Name
Furosemide
Dosage Form
Tablet
Registration Number
DR-1110
Drug Classification
Prescription Drug (RX)