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FUROSEMIDE TABLETS 20 MG

Active substance(s): FUROSEMIDE / FUROSEMIDE / FUROSEMIDE

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SUMMARY OF PRODUCT CHARACTERISTICS

1

NAME OF THE MEDICINAL PRODUCT
Furosemide Tablets 20 mg

2

QUALITATIVE AND QUANTITATIVE COMPOSITION
Each tablet contains 20 mg of Furosemide.
For excipients, see 6.1.

3

PHARMACEUTICAL FORM
Tablet
White, round normal convex tablets engraved with company logo on one side and
A328 on the other side.

4

CLINICAL PARTICULARS

4.1

Therapeutic indications
Furosemide is a diuretic recommended for use in all indications where a prompt and
effective diuresis is required.
1) The treatment of oedema associated with congestive heart failure, cirrhosis of the
liver, renal disease including nephrotic syndrome and pulmonary oedema.
2) The treatment of peripheral oedema due to mechanical obstruction, venous
insufficiency, mild to moderate hypertension.

4.2

Posology and method of administration
Route of administration: Oral
Furosemide has a very wide therapeutic range, the effect being proportional to
dosage.
Furosemide is best given as a single dose either daily or on alternate days.
Adults and children over 12 years:

Oedema: Initially 40mg daily in the morning; ordinarily a prompt diuresis ensues and
the starting dose can then be maintained or even reduced. Diuresis lasts for
approximately four hours following administration and hence the time of
administration can be adjusted to suit the patient’s requirements. Maintenance dose is
20mg daily or 40mg on alternate days, increased in resistant oedema to 80mg daily.
Hypertension: 20-40mg twice daily; if 40mg twice daily does not lead to a clinically
satisfactory response, the addition of other antihypertensive agents, rather than an
increase in the dose of furosemide should be considered.
Children under 12 years:
1-3 mg/kg body weight daily. A more suitable dosage form should be used in this age
group.
Elderly:
In the elderly, furosemide is generally eliminated more slowly. Dosage should be
titrated until the required response is achieved.

4.3

Contraindications

Known hypersensitivity to furosemide, amiloride or any of the excipients of the
product.
Known hypersensitivity to sulphonamides and sulphonamide derivatives.
Anuria or renal failure with anuria not responding to furosemide.
Electrolyte deficiency.
Comatose or pre-comatose states associated with liver cirrhosis (see section 4.4);
Digitalis intoxication (see section 4.5).
Renal failure resulting from nephrotoxic and hepatotoxic agents.
Renal failure associated with hepatic coma.
Hypovolaemia and dehydration (with or without accompanying hypotension) (see
section 4.4)
Severe hypokalaemia: severe hyponatraemia (see section 4.4).
Impaired renal function with a creatinine clearance below 30ml/min per 1.73 m2
body surface area (see section 4.4).
Addison's disease (see section 4.4).
Children and adolescents under 18 years of age (safety in this age group has not yet

been established).

Porphyria
Concomitant potassium supplements or potassium sparing diuretics (see section
4.5).
Breast-feeding women (see section 4.6).

4.4

Special warnings and precautions for use

Patients with rare hereditary problems of galactose intolerance, the Lapp lactose
deficiency or glucose-galactose malabsorption should not take this medicine.
Conditions requiring correction before furosemide is started (see also section
4.3):


Hypotension and hypovolaemia



Severe electrolyte disturbances - particularly hypokalaemia, hyponatraemia
and acid-base disturbances.

Furosemide is not recommended:
• In patients at high risk for radiocontrast nephropathy - it should not be used
for diuresis as part of the preventative measures against radiocontrastinduced nephropathy.
Particular caution and/or dose reduction required:
• elderly patients (lower initial dose as particularly susceptible to side-effects see section 4.2).


patients with prostatic hypertrophy or impairment of micturition have an
increased risk of developing acute retention: consider lower dose.



closely monitor patients with partial occlusion of the urinary tract.



diabetes mellitus (latent diabetes may become overt: insulin requirements in
established diabetes may increase: stop furosemide before a glucose tolerance
test).
pregnancy (see section 4.6).
serum creatinine and uric acid/urea levels tend to rise during treatment with
furosemide and an acute attack of gout may occasionally be precipitated.
patients with hepatorenal syndrome
impaired hepatic function (see section 4.3 and below - monitoring required).
impaired renal function (see section 4.3 and below - monitoring required).
adrenal disease (see section 4.3 - contraindication in Addison's disease).
hypoproteinaemia e.g. nephrotic syndrome (effect of furosemide may be
impaired and its ototoxicity potentiated - cautious dose titration required).
















acute hypercalcaemia (dehydration results from vomiting and diuresis - correct
before giving furosemide). Treatment of hypercalcaemia with a high dose of
furosemide results in fluid and electrolyte depletion - meticulous fluid
replacement and correction of electrolyte required.
the dosage of concurrently administered cardiac glycosides or
antihypertensive agents may require adjustment.
patients who are at risk from a pronounced fall in blood pressure
premature infants (possible development nephrocalcinosis/nephrolithiasis;
renal function must be monitored and renal ultrasonography performed)
Symptomatic hypotension leading to dizziness, fainting or loss of
consciousness can occur in patients treated with furosemide, particularly in the
elderly, patients on other medications which can cause hypotension and
patients with other medical conditions that are risks for hypotension..

Avoidance with other medicines (see also section 4.5 for other interactions):
• concurrent NSAIDs should be avoided - if not possible diuretic effect of
furosemide may be attenuated.
• ACE-inhibitors & Angiotensin II receptor antagonists - severe hypotension
may occur - dose of furosemide should be reduced/stopped (3 days) before
starting or increasing the dose of these.
Laboratory monitoring requirements:
• Serum sodium
Particularly in the elderly or in patients liable to electrolyte deficiency.
• Serum potassium
The possibility of hypokalaemia should be taken into account, in particular in patients
with cirrhosis of the liver, those receiving concomitant treatment with corticosteroids,
those with an unbalanced diet and those who abuse laxatives. Regular monitoring of
plasma electrolytes, particularly sodium and potassium should be carried out and
electrolyte replacement therapy instituted accordingly, and if necessary treatment with
a potassium supplement, is recommended in all cases, but is essential at higher doses
and in patients with impaired renal function. It is especially important in the event of
concomitant treatment with digoxin, as potassium deficiency can trigger or exacerbate
the symptoms of digitalis intoxication (see section 4.5). Caution should be observed in
patients liable to electrolyte deficiency. During long-term or high dose therapy
potassium supplements are recommended.
Frequent checks of the serum potassium are necessary in patients with impaired renal
function and creatinine clearance below 60ml/min per 1.73m2 body surface area as
well as in cases where furosemide is taken in combination with certain other drugs
which may lead to an increase in potassium levels (see section 4.5 & refer to section
4.8 for details of electrolyte and metabolic abnormalities).
• Renal function
Marked diuresis can cause reversible impairment of kidney function in patients with
renal dysfunction. Frequent BUN determinations during the first few months of
therapy and periodically thereafter should be conducted. Long-term/high-dose BUN

should regularly be measured. Adequate fluid intake is necessary in such patients.
Serum creatinine and urea levels tend to rise during treatment
• Glucose
Adverse effect on carbohydrate metabolism - exacerbation of existing carbohydrate
intolerance or diabetes mellitus. Regular monitoring of blood glucose levels is
desirable.
• Other electrolytes
Patients with hepatic failure/alcoholic cirrhosis are particularly at risk of
hypomagnesia (as well as hypokalaemia). During long-term therapy (especially at
high doses) magnesium, calcium, chloride, bicarbonate and uric acid should be
regularly measured.
Clinical monitoring requirements:
Regular observations for possible occurrence of blood dyscrasias (If these occur, stop
Furosemide immediately), liver damage or idiosyncratic reactions are advisable.
Other alterations in lab values:
Serum cholesterol and triglyceride levels may rise during furosemide treatment but
will usually return to normal within six months of starting furosemide
Care needs to be taken when prescribing to patients with porphyria as furosemide
may induce acute porphyric crisis.
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 section 4.3 Contraindications).
4.5

Interaction with other medicinal products and other forms of interaction

General- The dosage of concurrently administered cardiac glycosides, diuretics,
anti-hypertensive agents, or other drug with blood-pressure-lowering potential may

require adjustment as a more pronounced fall in blood pressure must be anticipated
if given concomitantly with furosemide.
The toxic effects of nephrotoxic drugs may be increased by concomitant
administration of potent diuretics such as furosemide.
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).
Antihypertensives (ACE Inhibitors and Angiotensin-II Antagonists): concomitant
administration with furosemide can result in marked falls in blood pressure. This
enhancement may be extreme. The dose of furosemide should be reduced or the drug
stopped before initiating the ACE inhibitor or Angiotensin II receptor antagonists (see
section 4.4).
Antihypertensives: enhanced hypotensive effect; increased risk of first-dose
hypotensive effect of post synaptic alpha-blockers such as prazosin.
Alcohol: enhanced hypotensive effect when diuretics are given with alcohol.
Aminoglutethimide: increased risk of hyponatraemia with aminoglutethimide.
Antifungals/Amphotericin: there is an increased risk of hypokalaemia and
nephrotoxicity.
NSAIDs/Analgesics: there is an increased risk of nephrotoxicity of NSAIDs. Some
NSAIDs (Indometacin and ketorolac) and salicylates antagonise the diuretic effect
(avoid if possible; see section 4.4), and the effects of salicylates may be potentiated
by furosemide. Salicylic toxicity may be increased.
Anti-arrhythmics: the risk of cardiac toxicity of amiodarone, disopyramide,
flecainide, sotalol and quinidine may increase if furosemide induced hypokalaemia
occurs. The effects of lidocaine, tocainide or mexiletine may be antagonised by
furosemide.
Antibacterials: concomitant administration of loop diuretics may increase
ototoxicity of aminoglycosides, colistin, polymixins or vancomycin - only use
concurrently if compelling reasons. Loop diuretics may increase nephrotoxicity of
cephalosporins (including cefaloridine) or aminoglycosides. Impairment of renal
function may develop in patients receiving concurrent treatment with furosemide
and high doses of certain cephalosporins.
Furosemide can decrease vancomycin serum levels after cardiac surgery. Increased
risk of hyponatraemia with trimethoprim.
Antidepressants: there is an increased risk of postural hypotension with concomitant
administration of furosemide and tricyclic antidepressants. Concomitant
administration of loop diuretics with reboxetine may increase the risk of
hypokalaemia; there is an enhanced hypotensive effect with concomitant
administration with MAOIs.

Antidiabetics: the hypoglycaemic effect of antidiabetics is antagonised by loop
diuretics. (see section 4.4).
Anaesthetics, General: enhanced hypotensive effect when diuretics are given with
general anaesthetics. The effects of curare may be enhanced by furosemide.
Antiepileptics: effects of furosemide antagonised by phenytoin.
Carbamazepine: there is an increased risk of hyponatraemia.
Antihistamines - hypokalaemia with increased risk of cardiac toxicity.
Terfenidine: hypokalaemia or other electrolyte imbalance increases the risk of
ventricular arrhythmias
Anxiolytics and hypnotics- enhanced hypotensive effect. Chloral or triclofos may
displace thyroid hormone from binding site.
CNS stimulants (drugs used for ADHD) - hypokalaemia increases the risk of
ventricular arrhythmias.

Antipsychotics: Furosemide induced hypokalaemia increases the risk of cardiac
toxicity. Avoid concurrent use with pimozide or thioridazine, Increased risk of
ventricular arrhythmias with amisulpride or sertindole. Enhanced hypotensive effect
with phenothiazines.
When administering 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 section 4.4 Special
warnings and precautions for use regarding increased mortality in elderly patients
with dementia concomitantly receiving risperidone.
Beta-blockers: enhanced hypotensive effect.
Calcium-channel blockers: enhance hypotensive effect.
Cardiac glycosides: there is increased risk of cardiac toxicity if hypokalaemia and
electrolyte disturbances (including hypomagnesia) occurs with furosemide.
Drugs that prolong Q-T interval - increased risk of toxicity with furosemide-induced
electrolyte disturbances.
Renin inhibitors - aliskiren reduces plasma concentrations of furosemide.
Nitrates - enhanced hypotensive effect.
Corticosteroids e.g glucocorticoids: increased risk of hypokalaemia with loop
diuretics. Antagonism of diuretic effect (sodium retention).
Glychyrrizin (contained in liquorice) - may increase the risk of developing

hypokalaemia.
Cytotoxics: increased risk of nephrotoxicity and ototoxicity with platinum
compound/ cisplatin. 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.
Anti-metabolites - effects of furosemide may be reduced by methotrexate and
furosemide may reduce renal clearance of methotrexate.
Potassium salts - contraindicated - increased risk of hyperkalaemia (see section 4.3)
Dopaminergics - enhanced hypotensive effect with levodopa.
Immunomodulators - enhanced hypotensive effect with aldesleukin. Increased risk
of hyperkalaemia with ciclosprin and tacrolimus. Increased risk of gouty arthritis
with ciclosporin.
Diuretics: increased risk of hypokalaemia if acetazolamide, loop diuretics or
thiazides given together; profound diuresis possible if metolazone given with
furosemide. Contraindicated with potassium sparing diuretics (eg amiloride,
spironolactone) - increased risk of hyperkalaemia (see section 4.3).
Lithium: In common with other diuretics, serum lithium levels may be increased
when lithium is administered concomitantly with furosemide, resulting in in
increased lithium toxicity, including increased risk of cardiotoxic and neurotoxic
effects of lithium. Therefore, it is recommended that lithium levels are carefully
monitored and where necessary the lithium dosage is adjusted in patients receiving
this combination.
Chelating agents - sucralfate may decrease the gastro-intestinal absorption of
furosemide - the 2 drugs should be taken at least 2 hours apart.
Vasodilators- Moxisylyte (Thymoxamine) or hydralazine: enhance hypotensive
effect.
Muscle Relaxants: enhanced hypotensive effect with baclofen and tizanidine.
Increased effect of curare like muscle relaxants.
Oestrogens and Progestogens: oestrogens and combined oral contraceptives
antagonise diuretic effect, Progestogens (drospirenone) increased risk of
hyperkalaemia.
Prostaglandins - enhanced hypotensive effect with alprostadil.
Sympathomimetics: increased risk of hypokalaemia if loop diuretics given with high
doses of beta2 sympathomimetics (bambuterol, fenoterol, formoterol, ritodrine,
salbutamol, salmeterol and terbutaline).

Probenecid - effects of furosemide may be reduced by probenecid and furosemide
may reduce renal clearance of probenecid.
Theophylline: increased risk of hypokalaemia with loop diuretics. Enhanced
hypotensive effect.
Ulcer-healing drugs: increased risk of hypokalaemia if loop diuretics are given with
carbenoxolone. Carbenoxolone antagonises diuretic effect.
In cases of concomitant laxative abuse, the risk of an increased potassium loss should
be borne in mind.
4.6

Pregnancy and lactation

Pregnancy
Experimental work carried out on animals generally shows that furosemide has no
hazardous effects in pregnancy. There is no evidence of the safety of high doses of
furosemide in human pregnancy. However, there is clinical evidence of safety of the
drug in the third trimester of human pregnancy & furosemide has been given after the
first trimester of pregnancy for oedema, hypertension and toxaemia of pregnancy
without causing fetal or newborn adverse effects. Furosemide should be used in
pregnancy only if strictly indicated and for short term treatment.
Furosemide crosses the placental barrier and should not be given during pregnancy
unless there are compelling medical reasons. It should only be used for the
pathological causes of oedema which are not directly or indirectly linked to the
pregnancy. The treatment with diuretics of oedema and hypertension caused by
pregnancy is undesirable because placental perfusion can be reduced, so, if used,
monitoring of fetal growth is required.
Lactation (see section 4.3)
Furosemide is contraindicated as furosemide has an inhibiting effect on lactation and
may pass into the breast milk.

4.7

Effects on ability to drive and use machines
Reduced mental alertness, dizziness and blurred vision have been reported,
particularly at the start of treatment, with dose changes and in combination with
alcohol. Patients should be advised that if affected, they should not drive, operate
machinery or take part in activities where these effects could put themselves or others
at risk.

4.8

Undesirable effects

Undesirable effects can occur with the following frequencies: very common (>
1/10), common (> 1/100, < 1/10), uncommon (> 1/1,000, < 1/100), rare (> 1/10,000,
< 1/1,000) and very rare (< 1/10,000, including isolated reports).

Blood and lymphatic system disorders:
Uncommon: Thrombocytopenia
Rare:

eosinophilia

leukopenia

bone marrow depression (necessitates withdrawal of treatment). The
haemopoietic status should therefore be regularly monitored.
Very Rare:

aplastic anaemia or haemolytic anaemia

agranulocytosis
Nervous system disorders
Rare:

paraesthesia

hyperosmolar coma
Not known: dizziness, fainting or loss of consciousness caused by symptomatic
hypotension

Endocrine disorder
Glucose tolerance may decrease with furosemide. In patients with diabetes
mellitus this may lead to a deterioration of metabolic control; latent diabetes
mellitus may become manifest. Insulin requirements of diabetic patients may
increase.
Eye disorders
Uncommon: visual disturbance
Ear and labyrinth disorders
Uncommon: deafness (sometimes irreversible)
Hearing disorders, tinnitus, although usually transitory, may occur in rare cases,
particularly in patients with renal failure, hypoproteinaemia (e.g. in nephritic
syndrome) and/or when intravenous furosemide has been given too rapidly.
Cardiac disorders
Uncommon: cardiac arrhythmias
Furosemide may cause a reduction in blood pressure which, if pronounced may
cause signs and symptoms such as impairment of concentration and reactions, light
headedness, sensations of pressure in the head, headache, dizziness, drowsiness,
weakness, disorders of vision, dry mouth, orthostatic intolerance. The diuretic
effect of furosemide can result in hypovolaemia and dehydration, especially in the
elderly. There is an increased risk of thrombosis.
Hepatobiliary disorders

In isolated cases, intrahepatic cholestasis, an increase in liver transaminases or
acute pancreatitis may develop.
Hepatic encephalopathy in patients with hepatocellular insufficiency may occur
(see Section 4.3).
Vascular Disorder:
Rare: vasculitis
Skin and subcutaneous tissue disorders:
Uncommon: Photosensitivity
Rare:
Skin and mucous membrane reactions may occasionally occur, e.g. itching,
urticaria, other rashes or bullous lesions, fever, hypersensitivity to light, exudative
erythema multiforme (Lyell's syndrome and Stevens-Johnson syndrome), bullous
exanthema, various forms of dermatitis (including exfoliative dermatitis), purpura
and DRESS (Drug rash with eosinophilia and systemic symptoms).
Not known: AGEP (acute generalized exanthematous pustulosis).
When these occur, treatment with furosemide should be stopped.
Metabolism and nutrition disorders:
As with other diuretics, electrolytes and water balance may be disturbed as a result
of diuresis after prolonged therapy. This may cause symptoms such as
headache, hypotension or muscle cramps. Furosemide leads to increased
excretion of sodium and chloride and consequently increased excretion of water.
In addition, excretion of other electrolytes (in particular potassium, calcium and
magnesium) is increased.
Metabolic acidosis can also occur. The risk of this abnormality increases at higher
dosages and is influenced by the underlying disorder (e.g. cirrhosis of the liver,
heart failure), concomitant medication (see section 4.5) and diet. Pre-existing
metabolic alkalosis (e.g. in decompensated cirrhosis of the liver) may be
aggravated by furosemide treatment.
Symptomatic electrolyte disturbances and metabolic alkalosis may develop in the
form of a gradually increasing electrolyte deficit or e.g. where higher furosemide
doses are administered to patients with normal renal function, acute severe
electrolyte losses.
Symptoms of electrolyte imbalance depend on the type of disturbance:
Sodium deficiency can occur; this can manifest itself in the form of confusion,
muscle cramps, muscle weakness, loss of appetite, dizziness, drowsiness and
vomiting.
Potassium deficiency manifests itself in neuromuscular symptoms (muscular
weakness, paralysis), intestinal symptoms (vomiting, constipation, meterorism),

renal symptoms (polyuria) or cardiac symptoms. Severe potassium depletion can
result in paralytic ileus or confusion, which can result in coma.
Magnesium and calcium deficiency result very rarely in tetany and heart rhythm
disturbances.
Serum calcium levels may be reduced; in very rare cases tetany has been observed.
Nephrolithiasis/ Nephrocalcinosis has been reported in premature infants.
Serum cholesterol (reduction of serum HDL-cholesterol, elevation of serum LDLcholesterol) and triglyceride levels may rise during furosemide treatment. During
long term therapy they will usually return to normal within six months.
As with other diuretics, treatment with Furosemide may lead to transitory increase
in blood creatinine and urea levels. Serum levels of uric acid may increase and
attacks of gout may occur.
The diuretic action of furosemide may lead to or contribute to hypovolaemia and
dehydration, especially in elderly patients. Severe fluid depletion may lead to
haemoconcentration with a tendency for thromboses to develop.

General disorders and administration site conditions:
Uncommon: Fatigue
Rare:

severe anaphylactic or anaphylactoid reactions (e.g. with shock) occur
rarely.

fever

malaise

Gastrointestinal disorders:
Uncommon: dry mouth, thirst, nausea, bowel motility disturbances, vomiting,
diarrhoea, constipation.
Rare: Acute Pancreatitis
The gastro-intestinal disorders such as nausea or gastric upset (vomiting or
diarrhoea) and constipation are not usually severe enough to necessitate
withdrawal of treatment.
Renal and urinary disorders:
Uncommon:

serum creatinine and urea levels can be temporarily elevated during
treatment with furosemide.
Rare: interstitial nephritis, acute renal failure.

Increased urine production, urinary incontinence, can be caused or symptoms can
be exacerbated in patients with urinary tract obstruction. Acute urine retention,
possibly accompanied by complications, can occur for example in patients with
bladder disorders, prostatic hyperplasia or narrowing of the urethra.
Pregnancy, puerperium and perinatal conditions
In premature infants with respiratory distress syndrome, administration of
Furosemide Tablets in the initial weeks after birth entails an increased risk of a
persistent patent ductus arteriosus.
In premature infants, furosemide can be precipitated as nephrocalcinosis/kidney
stones.
Rare complications may include minor psychiatric disturbances.
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.

4.9

Overdose

Overdosage with furosemide results in dehydration, and electrolyte depletion due to
excessive diuresis.
Symptoms include dehydration, volume depletion, electrolyte depletion and
hypotension and cardiac toxicity due to excessive diuresis. In cirrhotic patients,
overdosage may precipitate hepatic coma. 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 due to
excessive diuresis. Symptoms of these disturbances include severe hypotension
(progressing to shock), acute renal failure, thrombosis, delirious states, flaccid
paralysis, apathy and confusion. High doses have the potential to cause transient
deafness and may precipitate gout (disturbed uric acid secretion).
Management
The benefit of gastric decontamination is uncertain. Consider activated charcoal
(50g for adults; 1g/kg for children) if an adult or child presents within 1 hour of
ingesting a toxic dose. Treatment should be aimed at fluid replacement and
correction of the electrolyte imbalance. The drug should be discontinued and
electrolyte and water replacement instituted immediately; adjustment should be on
the basis of careful monitoring.
• Observe for a minimum of 4 hours - monitor pulse and blood pressure.
• Treat hypotension and dehydration with appropriate IV fluids
• Monitor urinary output and serum electrolytes (including chloride and

bicarbonate). Correct electrolyte imbalances. Monitor 12 lead ECG in patients with
significant electrolyte disturbances

5

PHARMACOLOGICAL PROPERTIES

5.1

Pharmacodynamic properties
Pharmacotherapeutic group: High ceiling diuretics, sulphonamides, plain ATC
Code: CO3CA01
Furosemide is structurally related to thiazides, but its principal site of action is in the
ascending limb of the loop of henle. The loop diuretics like furosemide abolish the
concentration gradient which is produced by thiazides acting in the cortex, when the
fluid in the collecting tubules passes from the relatively hypotonic cortex, to the
relatively hypertonic medulla and becomes concentrated. Furosemide probably also
has effects along the entire nephron with the exception of the distal aldosteronesensitive portion. It has a steep dose-response curve and progressive increase of dose
causes progressive increase of urine production. Taken orally it acts within an hour
and diuresis lasts about six hours. Enormous urine volumes, e.g. 10 litres in 24 hours
can result and overdose can cause hypovolaemia and circulatory collapse. Given I.V.,
it acts within 30 minutes and can relieve acute pulmonary oedema, perhaps partially
due to a vasodilator action which precedes the diuresis. An important feature of
furosemide is its efficacy in the presence of glomerular filtration rates of 10ml/min or
less as in severe heart failure and renal failure where the other diuretics fail.

5.2

Pharmacokinetic properties
Furosemide is completely, but fairly rapidly, absorbed from the gastro-intestinal tract.
It has a biphasic half-life in the plasma with a terminal elimination phase up to 1.5
hours, but this rises to over 10 hours in renal failure. It is up to 99 per cent bound to
plasma proteins; and is mainly excreted in the urine, largely unchanged, but also in
the form of the glucuronide and free amine metabolites. Variable amounts are
excreted in the bile.
Furosemide crosses the placental barrier and is excreted in milk.

5.3

Preclinical safety data
There are no pre-clinical data of relevance to the prescriber that are additional to that
already included in other sections of the SPC.

6

PHARMACEUTICAL PARTICULARS

6.1

List of excipients
Lactose
Sodium starch glycollate
Magnesium stearate
Pregelatinised maize starch
Maize starch

6.2

Incompatibilities
None.

6.3

Shelf life

3 years for opaque plastic containers.
3 years for aluminium/opaque PVC blister packs.

6.4

Special precautions for storage
Store in the container provided. Do not store above 25°C.
Keep out of the reach and sight of children.

6.5

Nature and contents of container
Opaque plastic containers composed of polypropylene tubes and polyethylene
tamper-evident closures in pack sizes of 28, 30, 42, 50, 56, 60, 84, 90, 100, 112, 250,
500 and 1000 tablets.
High density polypropylene or polyethylene containers with a tamper evident or child
resistant tamper evident closure in pack sizes of 28, 30, 42, 50, 56, 60, 84, 90, 100,
112, 250, 500 and 1000 tablets.
Aluminium/PVC blister packs in pack sizes of 28, 30, 42, 56, 60, 84, 90 and 112
tablets.

6.6

Special precautions for disposal
None

7

MARKETING AUTHORISATION HOLDER
Crescent Pharma Limited
Units 3 & 4, Quidhampton Business Units
Polhampton Lane
Overton

Hants
RG25 3ED
United Kingdom

8

MARKETING AUTHORISATION NUMBER(S)
PL 20416/0078

9

DATE OF FIRST AUTHORISATION/RENEWAL OF THE
AUTHORISATION

17/10/1994 / 12/01/2004

10

DATE OF REVISION OF THE TEXT
07/10/2016

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Source: Medicines and Healthcare Products Regulatory Agency

Disclaimer: Every effort has been made to ensure that the information provided here is accurate, up-to-date and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. This information has been compiled for use by healthcare practitioners and consumers in the United States. The absence of a warning for a given drug or combination thereof in no way should be construed to indicate that the drug or combination is safe, effective or appropriate for any given patient. If you have questions about the substances you are taking, check with your doctor, nurse or pharmacist.

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