Furosemide 20mg/2ml Solution for infusion/injection ampoules (10mg/ml)

Furosemide 10 mg/ml solution for injection/infusion is indicated when no adequate diuresis is achieved with oral administration of furosemide or when oral use is not possible:

• oedemas and/or ascites secondary to cardiac or hepatic disorders

• oedemas secondary to renal disorders

• pulmonary oedema (e.g. in acute heart failure)

• hypertensive crisis (in addition to other therapeutic measures)

The dosage should be individually established, mainly depending on the success of therapy. The lowest dose at which the desired effect is obtained should always be used.

Posology

Adults

Oedemas and/or ascites secondary to cardiac or hepatic disorders

Initial dose 2-4 ml (equivalent to 20-40 mg furosemide) IV. For oedemas that are difficult to mobilise, this dose can be repeated at appropriate intervals until the onset of diuresis.

Oedemas secondary to renal disorders

Initial dose 2-4 ml (equivalent to 20-40 mg furosemide) IV. For oedemas that are difficult to mobilise, this dose can be repeated at appropriate intervals until the onset of diuresis.

In nephrotic syndrome, the dose must be cautiously determined due to the risk of an increase in adverse reactions.

Pulmonary oedema (e.g. in acute heart failure)

Use in conjunction with other therapeutic measures. Initial dose 2-4 ml (equivalent to 20-40 mg furosemide) IV.

If there is still no increase in diuresis, repeat after 30-60 minutes, if necessary at twice the dose.

Hypertensive crisis

The dose is 2-4 ml (equivalent to 20-40 mg furosemide) in addition to other therapeutic measures.

In adults, the maximum daily dose of furosemide should not exceed 1500 mg.

Paediatric population

Infants and children under 15 years should be given furosemide via the parenteral route only as an exception in threatening situations. The mean daily dose is 0.5 mg furosemide/kg body weight. Exceptionally, up to 1 mg furosemide/kg body weight can be injected IV.

Elderly

The recommended initial dose is 20 mg daily, increasing gradually until the required response is achieved.

Renal impairment

In patients with advanced renal failure (serum creatinine > 442 micromol/l [> 5 mg/dl]), the injection/infusion rate should not exceed 0.25 ml solution per minute (equivalent to 2.5 mg furosemide per minute).

Method of administration

Intravenous or intramuscular administration.

As a rule, Furosemide 10 mg/ml solution for injection/infusion is administered intravenously. In exceptional cases where neither oral nor intravenous administration is possible, Furosemide 10 mg/ml solution for injection/infusion can be administered intramuscularly, but not in acute situations (e.g. not in pulmonary oedema) and not at higher doses.

Parenteral administration of furosemide is indicated only in cases where oral administration is not feasible or not efficient (e.g. in patients with poor intestinal absorption) or when a quick effect is required.

In order to achieve optimum efficacy and suppress counter-regulation, a continuous furosemide infusion should be preferred to the repeated injections.

Parenteral use of furosemide, as soon as treatment permits, should be switched to oral administration.

With intravenous use, furosemide should be injected slowly. The injection rate of 0.4 ml solution for injection (equivalent to 4 mg furosemide) per minute must not be exceeded.

In cases where a dose increase to 25 ml is required (equivalent to 250 mg furosemide), this dose should be administered via a syringe pump. If necessary, the solution can be diluted (see section 6.6).

Furosemide 10 mg/ml solution for injection/infusion must not be given with other medicinal products in a mixed syringe.

Care must be taken to ensure that the pH of in-use solution is in the weakly alkaline to neutral range (pH not lower than 7). Acid solutions must not be used, as the active substance may precipitate.

Duration of use

The duration of use depends on the nature and severity of the disease.

• Hypersensitivity to furosemide, sulfonamides (possible cross-allergy with furosemide) or to any of the excipients listed in section 6.1

• Renal failure with anuria not responding to furosemide therapy.

• Coma and hepatic precoma associated with hepatic encephalopathy

• Severe hypokalaemia (see section 4.8).

• Severe hyponatraemia

• Hypovolaemia or dehydration

• Breast feeding

Particularly careful monitoring is required in the following cases:

• hypotension

• manifest or latent diabetes mellitus (regular glycaemic monitoring necessary)

• gout (regular monitoring of serum uric acid)

• urinary obstruction (e.g. in prostatic hypertrophy, hydronephrosis, ureteric stenosis)

• hypoproteinaemia, e.g. in nephrotic syndrome (careful titration of the dosage)

• hepatorenal syndrome (rapidly progressing renal failure combined with severe hepatic disease, e.g. liver cirrhosis)

• patients who would be at particular risk from an unwanted severe hypotensive episode, e.g. patients with cerebrovascular ischaemia or coronary heart disease

• preterm infants (risk of developing nephrocalcinosis/nephrolithiasis; monitoring of renal function, renal ultrasound).

In preterm infants with respiratory distress syndrome, diuretic treatment with furosemide in the first weeks of life can increase the risk of patent ductus arteriosus.

Patients receiving treatment with furosemide may experience symptomatic hypotension with dizziness, fainting or loss of consciousness. This particularly applies to the elderly, patients concomitantly taking other medicinal products that can cause hypotension and patients with other disorders associated with a risk of hypotension.

In patients with micturition disorders (e.g. in prostatic hypertrophy), furosemide may only be used if free urinary flow is ensured, as any sudden diuresis can lead to urinary retention with overextension of the bladder.

Furosemide leads to increased excretion of sodium and chloride and, consequently, of water. Excretion of other electrolytes (particularly potassium, calcium and magnesium) is also increased. As disturbances in the fluid and electrolyte balance are frequently observed during therapy with furosemide as a result of increased electrolyte excretion, regular monitoring of serum electrolytes is indicated.

Especially during long-term therapy with furosemide, serum electrolytes (especially potassium, sodium, calcium), bicarbonate, creatinine, urea and uric acid, as well as blood sugar, should be regularly monitored.

Particularly close supervision is required in patients at high risk of developing electrolyte disturbances or in the event of more severe fluid loss (e.g. due to vomiting, diarrhoea or intensive sweating). Hypovolaemia or dehydration, as well as marked electrolyte disturbances or acid-base imbalances, must be corrected. This may necessitate temporary discontinuation of treatment with furosemide.

The possible development of electrolyte disturbances is influenced by underlying diseases (e.g. liver cirrhosis, heart failure), co-medication (see section 4.5) and diet.

The weight loss caused by increased urine excretion should not exceed 1 kg/day, irrespective of the degree of urine excretion.

In nephrotic syndrome, the dose must be cautiously determined due to the risk of an increase in adverse reactions.

Concomitant use with risperidone:

In placebo-controlled studies with risperidone in elderly patients with dementia, a higher incidence of mortality was observed in patients treated concomitantly with furosemide and risperidone (7.3%; mean age 89 years, age range 75 to 97 years) compared to patients who had received risperidone alone (3.1%; mean age 84 years, age range 70 to 96 years) or furosemide alone (4.1%; mean age 80 years, age range 67 to 90 years). Concomitant use of risperidone with other diuretics (mainly low-dose thiazide diuretics) was not associated with any similar findings.

No pathophysiological mechanism could be identified to explain this finding, and no consistent pattern for cause of death was established. Nevertheless, caution is indicated 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 in patients who had received other diuretics as concomitant treatment with risperidone. Regardless of treatment, dehydration was an overall risk factor for mortality and should therefore be avoided in elderly patients with dementia (see section 4.3).

There is a potential for exacerbation or activation of systemic lupus erythematosus.

The use of furosemide can lead to positive results in doping controls. In addition, abuse of furosemide as a doping agent can endanger health.

Excipients

This medicinal product contains less than 1 mmol (23 mg) sodium per ampoule, that is to say essentially 'sodium-free'.

Glucocorticoids, carbenoxolone, laxatives and liquorice

Concomitant use of furosemide and glucocorticoids, carbenoxolone or laxatives can lead to increased potassium losses with a risk for the development of hypokalaemia. In this respect, large amounts of liquorice act like carbenoxolone.

Non-steroidal anti-inflammatory drugs (NSAIDs) and high-dose salicylates

NSAIDs (e.g. indomethacin and acetylsalicylic acid) can attenuate the effect of furosemide. In patients developing hypovolaemia during furosemide therapy or presenting with dehydration, concomitant administration of NSAIDs can precipitate acute renal failure.

The toxicity of high-dose salicylates can be potentiated with concomitant use of furosemide.

Medicinal products that undergo considerable renal tubular secretion

Probenecid, methotrexate and other medicinal products that, like furosemide, undergo considerable renal tubular secretion can reduce the effect of furosemide.

Conversely, furosemide can reduce the renal elimination of probenecid, methotrexate. In high-dose treatment (especially if both the dose of furosemide and the other medicinal product are high), this can lead to elevated serum levels and a greater risk of adverse effects due to furosemide or the concomitant medication.

Phenytoin

Attenuation of the effect of furosemide has been described with concomitant administration of phenytoin.

Cardiac glycosides and medicinal products that may cause prolongation of the QT interval

In concomitant treatment with cardiac glycosides, it should be remembered that, if hypokalaemia and/or hypomagnesaemia develop during furosemide therapy, myocardial sensitivity to cardiac glycosides will be increased.

There is a greater risk of ventricular arrhythmias (including torsade de pointes) with concomitant use of medicinal products that can cause long QT interval syndrome (e.g. terfenadine, some class I and III antiarrhythmic agents) and in the presence of electrolyte disturbances.

Nephrotoxic medicinal products

Furosemide can potentiate the harmful effects of nephrotoxic medicinal products (e.g. antibiotics such as aminoglycosides, cephalosporins, polymyxins).

Renal function may deteriorate in patients treated concomitantly with furosemide and high doses of certain cephalosporins.

If forced diuresis with furosemide is pursued during cisplatin treatment, furosemide may only be administered at low doses (e.g. 40 mg in patients with normal renal function) and if the fluid balance is positive. Otherwise, the nephrotoxicity of cisplatin may be enhanced.

Ototoxic medicinal products

The ototoxicity of aminoglycosides (e.g. kanamycin, gentamicin, tobramycin) and other ototoxic medicinal products may be increased with co-administration of furosemide. Any hearing disorders that occur may be irreversible. Concomitant use of the above-mentioned medicinal products should therefore be avoided.

The possibility of hearing damage must be taken into account with concomitant use of cisplatin and furosemide.

Lithium

Concomitant administration of furosemide and lithium leads to potentiation of the cardio- and neurotoxic effects of lithium, due to reduced lithium excretion. Therefore, careful monitoring of the lithium plasma level is recommended in patients receiving this combination.

Other antihypertensive medicinal products

If other antihypertensive agents, diuretics or medicinal products with a hypotensive potential are co-administered with furosemide, a relatively sharp decrease in blood pressure can be expected.

ACE inhibitors or angiotensin II receptor antagonists

Severe hypotensive episodes or even shock and worsening renal function (acute renal failure in individual cases) have been observed, particularly when an ACE inhibitor or angiotensin II receptor antagonist has been given for the first time, or for the first time at a higher dose. If possible, furosemide therapy should therefore be temporarily discontinued or, as a minimum, the dose should be reduced for 3 days before therapy with an ACE inhibitor or angiotensin II receptor antagonist is started or its dose increased.

Theophylline and curare-type muscle relaxants

The effect of theophylline or curare-type muscle relaxants may be potentiated by furosemide.

Antidiabetic medicinal products

The effect of antidiabetic agents may be attenuated with concomitant use of furosemide.

Sympathomimetics

The effect hypertensive sympathomimetics (e.g. epinephrine, norepinephrine) may be attenuated with concomitant use of furosemide.

Risperidone

Caution is indicated in patients treated with risperidone and the risks and benefits of such combination or co-treatment with furosemide or with other potent diuretics should be weighed up before deciding to treat (see section 4.4 regarding increased mortality in elderly patients with dementia concomitantly receiving risperidone).

Levothyroxine

High doses of furosemide may inhibit the binding of thyroid hormones to transport proteins. This may result in an initial transient increase in free thyroid hormones, followed overall by a decrease in total thyroid hormone levels. Thyroid hormone levels should be monitored.

Other interactions

Concomitant use of ciclosporin A and furosemide is associated with an increased risk of gouty arthritis as a result of hyperuricaemia caused by furosemide and impaired renal uric acid excretion caused by ciclosporin.

In patients at high risk of kidney damage due to radiocontrast media, worsening of renal function occurred more frequently with furosemide treatment after a radiocontrast examination than in risk patients who received only intravenous hydration prior to the contrast examination.

In isolated cases, after intravenous administration of furosemide, sensations of heat, sweating, restlessness, nausea, hypertension and tachycardia may occur within 24 hours after taking chloral hydrate. Concomitant use of furosemide and chloral hydrate should therefore be avoided.

Pregnancy

Furosemide should only be used in pregnancy for short periods and only after a particularly careful review of the indication for its use, as furosemide crosses the placental barrier.

Diuretics are not suitable for the routine treatment of hypertension and oedemas in pregnancy, as they impair placental perfusion and thus intrauterine growth.

If it is necessary to administer furosemide to pregnant women with heart failure or renal impairment, electrolytes and haematocrit, as well as foetal growth, must be closely monitored. Displacement of bilirubin from its albumin-binding sites and hence an increased risk of kernicterus in the presence of hyperbilirubinaemia has been discussed for furosemide.

Furosemide crosses the placenta and reaches 100% of maternal serum concentrations in umbilical cord blood. No malformations in humans have been reported to date, which might be associated with furosemide exposure. However, there is limited experience to allow a conclusive evaluation of any potential harmful effect on the embryo/foetus. Foetal urine production may be stimulated in utero. In the treatment of preterm infants with furosemide, urolithiasis has been observed to occur.

Breast-feeding

Furosemide is excreted in human milk and inhibits lactation. Women must therefore not be treated with furosemide if they are breast-feeding. If applicable, breast-feeding should be discontinued (see also section 4.3).

Fertility

No data are available.

Even when used as directed, this medicinal product can affect responsiveness to such an extent that the ability to drive, use machines or perform hazardous tasks may be impaired. This particularly applies at the start of treatment, when increasing the dose or switching medicinal products and in association with alcohol.

The following ratings are used for expressing the frequency of adverse reactions:

Very common (≥1/10)

Common (≥1/100 to <1/10)

Uncommon (≥1/1,000 to <1/100)

Rare (≥1/10,000 to <1/1,000)

Very rare (<1/10,000)

Not known (cannot be estimated from the available data)

The frequency ratings for adverse reactions are based on literature data and relate to studies in which a total of 1,387 patients were treated with various dosages of furosemide in various indications.

Blood and lymphatic system disorders

Common: haemoconcentration (if diuresis is excessive).

Uncommon: thrombocytopenia.

Rare: eosinophilia, leukopenia.

Very rare: haemolytic anaemia, aplastic anaemia, agranulocytosis.

Signs of agranulocytosis may include fever with chills, mucosal changes and sore throat.

Immune system disorders

Uncommon: allergic mucocutaneous reactions (see “Skin and subcutaneous tissue disorders”).

Rare: severe anaphylactic and anaphylactoid reactions such as anaphylactic shock (for treatment, see section 4.9). Initial signs of shock include skin reactions, such as flushing or urticaria, restlessness, headache, sweating, nausea, cyanosis.

Not known: exacerbation or activation of systemic lupus erythematosus.

Metabolism and nutrition disorders (see section 4.4)

Very common: electrolyte disturbances (including symptomatic), dehydration and hypovolaemia (especially in elderly patients), blood triglycerides increased.

Common: hyponatraemia and hypochloraemia (especially with restricted sodium chloride intake), hypokalaemia (especially with concomitant reduction of potassium intake and/or increased potassium losses, e.g. due to vomiting or chronic diarrhoea), blood cholesterol increased, blood uric acid increased and gout flare.

Uncommon: glucose tolerance decreased and hyperglycaemia. In patients with manifest diabetes mellitus, this can lead to a worsening of metabolic status. Latent diabetes mellitus may become manifest (see section 4.4).

Not known: hypocalcaemia, hypomagnesaemia, metabolic acidosis, pseudo-Bartter syndrome (associated with misuse and/or long-term use of furosemide).

Commonly observed symptoms of hyponatraemia are apathy, calf cramps, anorexia, asthenia, drowsiness, vomiting and confusional state.

Hypokalaemia can manifest as neuromuscular (muscle weakness, paraesthesia, paresis), intestinal (vomiting, constipation, meteorism), renal (polyuria, polydipsia) and cardiac symptoms (impulse formation and conduction disturbances). Severe potassium losses can lead to paralytic ileus or impaired consciousness and even coma.

Hypocalcaemia can induce tetany in rare cases.

As a result of hypomagnesaemia, tetany or occurrence of cardiac arrhythmias has been observed in rare cases.

Nervous system disorders

Common: hepatic encephalopathy in patients with hepatic impairment (see section 4.3).

Rare: paraesthesias.

Not known: dizziness, fainting and loss of consciousness, headache.

Ear and labyrinth disorders

Uncommon: hearing disorders, mostly reversible, especially in patients with renal impairment or hypoproteinaemia (e.g. in cases of nephrotic syndrome) and/or if intravenous injections are too rapid. Deafness (sometimes irreversible).

Rare: tinnitus.

Vascular disorders

Very common (with intravenous infusions): hypotension including orthostatic syndrome (see section 4.4).

Rare: vasculitis.

Not known: thrombosis (especially in elderly patients).

If diuresis is excessive, circulatory problems (including circulatory collapse) may occur, especially in elderly patients and children, which mainly manifest as headache, dizziness, visual disturbances, dry mouth and thirst, hypotension and orthostatic dysregulation.

Gastrointestinal disorders

Uncommon: nausea.

Rare: vomiting, diarrhoea.

Very rare: acute pancreatitis.

Hepatobiliary disorders

Very rare: intrahepatic cholestasis, transaminases increased.

Skin and subcutaneous tissue disorders

Uncommon: pruritus, urticaria, rashes, bullous dermatitis, erythema multiforme, pemphigoid, exfoliative dermatitis, purpura, photosensitivity.

Not known: Stevens-Johnson syndrome, toxic epidermal necrolysis, acute generalised exanthematous pustulosis (AGEP), drug rash with eosinophilia and systemic symptoms (DRESS), lichenoid reactions.

Musculoskeletal and connective tissue disorders

Not known: cases of rhabdomyolysis have been reported, often in association with severe hypokalaemia (see section 4.3).

Renal and urinary disorders

Very common: blood creatinine increased.

Common: urine volume increased.

Rare: tubulointerstitial nephritis.

Not known: urine sodium increased, urine chloride increased, blood urea increased, symptoms of urinary obstruction (e.g. in patients with prostatic hypertrophy, hydronephrosis, ureteric stenosis) and even urinary retention with secondary complications (see section 4.4), nephrocalcinosis and/or nephrolithiasis in preterm infants (see section 4.4), renal failure (see section 4.5).

Congenital, familial and genetic disorders

Not known: increased risk of patent ductus arteriosus when preterm infants are treated with furosemide in the first weeks of life.

General disorders and administration site conditions

Rare: fever.

Not known: after intramuscular injection, local reactions such as pain.

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.

a) Symptoms of overdose

The clinical picture in acute or chronic overdose depends on the extent of fluid and electrolyte loss. Overdose can lead to hypotension, orthostatic dysregulation, electrolyte disturbances (hypokalaemia, hyponatraemia, hypochloraemia) or alkalosis. In more severe cases of fluid depletion, marked hypovolaemia, dehydration, circulatory collapse and haemoconcentration with thrombotic tendency may occur. If fluid and electrolyte losses are rapid, delirious states may occur. In rare cases, anaphylactic shock (symptoms: sweating, nausea, cyanosis, severe hypotensive episode, impaired consciousness or even coma) may occur.

b) Therapeutic measures in case of overdose

In the event of overdose or signs of hypovolaemia (hypotension, orthostatic dysregulation), treatment with furosemide must be discontinued immediately.

In addition to monitoring vital parameters, the following must be repeatedly monitored and anomalies corrected as appropriate: fluid and electrolyte balance, acid-base balance, blood glucose and urinary substances.

In patients with micturition disorders (e.g. in patients with prostatic hypertrophy), free urinary flow must be ensured, as any sudden diuresis can lead to urinary retention with overextension of the bladder.

Treatment for hypovolaemia: volume replacement.

Treatment for hypokalaemia: potassium replacement.

Treatment for circulatory collapse: shock position, if necessary shock therapy.

Emergency measures for anaphylactic shock

At the first signs (e.g. cutaneous reactions such as urticaria or flushing, restlessness, headache, sweating, nausea, cyanosis):

• Stop the injection/infusion, maintain venous access

• In addition to standard emergency procedures, Trendelenburg position, maintenance of airway patency, oxygen administration

• If necessary, other measures must be implemented, including intensive care measures as appropriate (administration of epinephrine, volume replacements, glucocorticoids, etc.).

Pharmacotherapeutic group: high-ceiling diuretics, sulfonamides, plain,

ATC code: C03CA01

Furosemide is a potent, short- and fast-acting loop diuretic. By blocking the Na⁺/2Cl^-/K⁺ ion carrier, it inhibits the reabsorption of these ions in the ascending limb of the loop of Henle. Thus, fractional sodium excretion can amount to as much as 35% of sodium filtered by the glomeruli. As a result of increased sodium excretion, there is increased urine excretion and a rise in K⁺ secretion in the distal tubules as a secondary effect of osmotically-bound water. The elimination of Ca²⁺ and Mg²⁺ ions is also increased. In addition to loss of the aforementioned electrolytes, there may be decreased uric acid excretion and disturbances of the acid-base balance tending towards metabolic alkalosis.

Furosemide interrupts the tubuloglomerular feedback mechanism at the macula densa and hence there is no attenuation of saluretic activity.

Furosemide leads to dose-dependent stimulation of the renin-angiotensin aldosterone system.

In heart failure, furosemide leads to an acute reduction in cardiac preload due to dilation of the venous capacitance vessels. This early vascular effect appears to be mediated by prostaglandins and is dependent on adequate renal function with activation of the renin-angiotensin-aldosterone system and intact prostaglandin synthesis.

The hypotensive effect of furosemide is the result of increased sodium chloride excretion and decreased responsiveness of the vascular smooth muscles to vasoconstrictive stimuli, as well as a reduction in blood volume.

After intravenous administration of furosemide, onset of action can be expected within 2 to 15 minutes.

Plasma protein binding of furosemide is approximately 95%; in renal impairment, it may be reduced by as much as 10%. The relative volume of distribution is 0.2 l/kg body weight (in neonates, 0.8 l/kg body weight).

Furosemide undergoes only minor hepatic metabolism (approximately 10%) and is mainly excreted in unchanged form. Elimination takes place via the kidneys (two-thirds) and the bile and faeces (one-third).

In patients with normal renal function, the elimination half-life is approximately 1 hour; it can be prolonged to as much as 24 hours in cases of terminal renal failure.

Acute oral toxicity was low in all species tested. Chronic toxicity studies in rats and dogs led to changes in the kidneys (including fibrosis and calcification of the kidneys).

In vitro and in vivo genetic toxicology assays revealed no clinically relevant indications of any genotoxic potential for furosemide.

Long-term studies in rats and mice showed no indications of any tumorigenic potential.

In reproductive toxicology studies following administration of high doses, a reduced number of differentiated glomeruli and skeletal anomalies of the scapula, humerus and ribs (due to hypokalaemia) occurred in rat foetuses, as well as hydronephrosis in mouse and rabbit foetuses.

Sodium chloride

Sodium hydroxide (for pH adjustment)

Water for injections

Furosemide should not be mixed with strong acid solutions, such as solutions containing ascorbic acid, noradrenaline and adrenaline, due to the risk of precipitation. This medicinal product should not be mixed with other medicinal products except those mentioned in section 6.6.

24 months

After first opening:

The product should be used immediately.

After dilution:

Chemical and physical in-use stability has been demonstrated for 8 hours at 25°C when diluted with 0.9% Sodium chloride, 5% Glucose and Ringer Lactate.

From a microbiological point of view, the product should be used immediately. If not used immediately, in-use storage times and conditions prior to use are the responsibility of the user and would normally not be longer than 24 hours at 2 to 8°C, unless dilution has taken place in controlled and validated aseptic conditions.

This medicinal product does not require any special temperature storage conditions.

Keep the ampoules in the outer carton in order to protect from light.

For storage conditions of the diluted medicinal product, see section 6.3.

2 ml amber glass ampoules in a carton.

Pack sizes: 5 ampoules

For single use only.

The medicinal product should be used immediately after opening the ampoule. Any remaining contents after use should be discarded.

The medicinal product should be visually inspected prior to use. The medicinal product should not be used if there are any visible signs of deterioration (e.g. particles or discoloration).

Furosemide may be mixed with neutral, weak alkaline or acid solution, such as 0.9% sodium chloride, Ringer's lactate solution and glucose 5%.

Any unused medicinal product or waste material should be disposed of in accordance with local requirements.