FUROSEMIDE 50MG/ML ORAL SOLUTION

Active substance: FUROSEMIDE

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SUMMARY OF PRODUCT CHARACTERISTICS

1

NAME OF THE MEDICINAL PRODUCT
Furosemide 50 mg/5 ml Oral Solution

2.
QUALITATIVE AND QUANTITATIVE COMPOSITION
Each 5ml contains Furosemide 50 mg.
For excipients, see section 6.1.

3.

PHARMACEUTICAL FORM
Oral Solution
Clear, cherry flavoured, oral solution.

4.

CLINICAL PARTICULARS

4.1

Therapeutic Indications
Furosemide oral solution is indicated in all conditions requiring prompt
diuresis in patients who are unable to take solid dose forms. Indications,
include cardiac, pulmonary, hepatic and renal oedema, peripheral oedema due
to mechanical obstruction or venous insufficiency and hypertension.

4.2

Posology and method of administration
Furosemide 50mg/5ml has an exceptionally wide therapeutic range, the effect
being proportional to the dosage. Furosemide 50mg/5ml is best given as a
single dose either daily or on alternate days.
The usual initial daily dose is 40mg. This may require adjustment until the
effective dose is achieved as a maintenance dose. In mild cases, 20mg daily or
40mg on alternate days may be sufficient, whereas in cases of resistant
oedema, daily doses of 80mg and above may be used as one or two dose daily,
or intermittently. Severe cases may require gradual titration of the furosemide

dosage up to 600mg daily. The recommended maximum daily dose of
furosemide administration is 1500mg.
Elderly: The dosage recommendations for adults apply, but in the elderly,
furosemide is generally eliminated more slowly. Dosage should be titrated
until the required response is achieved.
Children: Oral doses for children range from 1 to 3 mg/Kg body weight daily
up to a maximum total dose of 40 mg/day.

4.3

Contraindications
Furosemide 50mg/5ml is contraindicated in patients with hypovolaemia or
dehydration, anuria or renal failure with anuria not responding to furosemide,
renal failure as a result of poisoning by nephrotoxic or hepatotoxic agents or
renal failure associated with hepatic coma, severe hypokalaemia, severe
hyponatraemia, pre-comatose and comatose states associated with hepatic
encephalopathy and breast feeding women.
Hypersensitivity to furosemide or any of the excipients of Furosemide
50mg/5ml. Patients allergic to sulphonamides may show cross-sensitivity to
furosemide.

4.4

Special warnings and precautions for use
Urinary output must be secured. Patients with partial obstruction of urinary
outflow, for example patients with prostatic hypertrophy or impairment of
micturition have an increased risk of developing acute retention and require
careful monitoring
Where indicated, steps should be taken to correct hypotension or
hypovolaemia before commencing therapy.
Particularly careful monitoring is necessary in:
• Patients with hypotension.
• Who are at risk from a pronounced fall in blood pressure.
• Where latent diabetes may become manifest or the insulin requirements of
diabetic patients may increase.
• With gout.
• With hepatorenal syndrome.
• With hypoproteinaemia e.g. associated with nephritic syndrome (the effect
of furosemide may be weakened and its ototoxicity potentiated). Cautious
dose titration is required.
• Premature
infants
(possible
development
of
nephrocalcinosis/nephrolithiasis; renal function must be monitored and
renal ultrasonography performed).
Caution should be observed in patients liable to electrolyte deficiency. 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. Hypovolaemia or dehydration as well as
any significant electrolyte and acid-base disturbances must be corrected. This
may require temporary discontinuation of furosemide.
This product contains liquid maltitol. Patients with a rare hereditary problem
of fructose intolerance should not take this medicine.

4.5
Interaction with other medicinal products and other forms of interaction
Antihypertensives – enhanced hypotensive effect possible with all types. Concurrent
use with ACEinhibitors can result in marked falls in blood pressure. Furosemide
should be stopped or the dose reduced before starting an ACE-inhibitor. There is a
risk of a first-dose effect with post-synaptic alphablockers eg prazosin.
Antipsychotics – furosemide-induced hypokalaemia increases the risk of cardiac
toxicity. Avoid concurrent use with pimozide. Increased risk of ventricular
arrhythmias with amisulpride or sertindole.
Enhanced hypotensive effect with phenothiazines.
Anti-arrhythmics (including amiodarone, disopyramide, flecanaide and sotalol) - risk
of cardiac toxicity (because of furosemide-induced hypokalaemia). The effects of
lidocaine, tocainide or mexiletine may be antagonised by furosemide.
Drugs associated with QT prolongation – cardiac toxicity may be increased by
furosemide-induced hypokalaemia and/or hypomagnesaemia
Cardiac glycosides – hypokalaemia and electrolyte disturbances (including
magnesium) increases the risk of cardiac toxicity
Vasodilators – enhanced hypotensive effect with moxisylyte (thymoxamine) or
hydralazine
Renin inhibitors – aliskiren reduces plasma concentrations of frurosemide
Nitrates – enhanced hypotensive effect
Lithium - Furosemide reduces lithium excretion with increased plasma lithium
concentrations (risk of toxicity). Avoid concomitant administration unless plasma
levels are monitored.
Chelating agents – sucralfate may decrease the gastro-intestinal absorption of
furosemide – the 2 drugs should be taken at least 2 hours apart
Lipid regulating drugs – Bile acid sequestrants (eg colestyramine: colestipol) –
reduced absorption of furosemide – administer 2 to 3 hours apart
NSAIDs – increased risk of nephrotoxicity (especially if there is hypovolaemia).
Indometacin and ketorolac may antagonise the effects of furosemide

Salicylates – effects may be potentiated by furosemide
Antibiotics – increased risk of ototoxicity with aminoglycosides, polymixins or
vancomycin. Increased risk of nephrotoxicity with aminoglycosides or cefaloridine.
Furosemide can decrease vancomycin serum levels after cardiac surgery
Antidepressants – enhanced hypotensive effect with MAOIs. Increased risk of
postural hypotension with TCAs (tricyclic antidepressants). Possible increased risk of
hypokalaemia with reboxetine.
Antidiabetics – hypoglycaemic effects antagonised by furosemide
Insulin - requirements may be increased (see section 4.4)
Antiepileptics – increased risk of hyponatraemia with carbamazepine. Diuretic effect
reduced by phenytoin. Barbiturates may decrease plasma concentrations of diuretics.
Possible increased risk of osteomalacia when diuretics combined with Phenobarbital
Antihistamines – hypokalaemia with increased risk of cardiac toxicity
Antifungals – increased risk of hypokalaemia with amphoterecin
Antivirals – plasma concentrations of diuretics may be increased by nelfinavir,
ritonavir or saquinavir
Anxiolytics and hypnotics – enhanced hypotensive effect.
CNS stimulants (drugs used for ADHD - atomoxetine) – hypokalaemia increases the
risk of ventricular arrhythmias
Corticosteroids – diuretic effect anatgonised (sodium retention) and increased risk of
hypokalaemia
Cytotoxics – increased risk of nephrotoxicity and ototoxicity with platinum
compounds.
Other diuretics – profound diuresis possible when furosemide given with metolazone.
Increased risk of hypokalaemia with thiazides.
Dopaminergics – enhanced hypotensive effect with levodopa.
Immunomodulators – enhanced hypotensive effect with aldesleukin. Increased risk of
nephrotoxicity (and possibly hypomagnesaemia) with ciclosporin. Increased risk of
hypokalaemia with tacrolimus.
Muscle relaxants – enhanced hypotensive effect with baclofen or tizanidine (see also
Anaesthetic agents below – curare )
Oestrogens and progestogens – diuretic effect antagonised
Prostaglandins – enhanced hypotensive effect with alprostadil

Sympathomimetics – increased risk of hypokalaemia with high doses of beta2
sympathomimetics (such as bambuterol, femoterol, salbutamol, salmeterol and
terbutaline)
Theophylline – enhanced hypotensive effect: increased risk of hypokalaemia
Probenecid – reduced renal clearance of furosemide and decreased diuretic effect.
Anaesthetic agents – general anaesthetic agents may enhance the hypotensive effects
of furosemide. The effects of curare may be enhanced by furosemide
Alcohol – enhanced hypotensive effect
Laxative abuse - increases the risk of potassium loss
Liquorice/carbenoxolone - excess intake may increase the risk of hypokalaemia
Potassium salts – increased risk of hyperkalaemia
Warfarin/clofibrate - competition with furosemide in binding to serum albumin –
possible significance in patients with low albumin levels (eg nephrotic syndrome).
Rapid/profound diuresis with dehydration may reduce antithrombotic effect of
warfarin

4.6

Fertility, pregnancy and lactation
Results of animal work, in general, show no hazardous effect of furosemide in
pregnancy. There is clinical evidence of safety of the drug in the third
trimester of human pregnancy; however, 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.
Furosemide passes into breast milk and may inhibit lactation. Women must
not breast-feed if they are being treated with furosemide.

4.7

Effects on ability to drive and use machines
Mental alertness may be reduced and the ability to drive or operate machinery
may be impaired.

4.8

Undesirable effects
Furosemide 50mg/5ml is generally well tolerated.

Eosinophilia is rare.
Occasionally, thrombocytopenia may occur. In rare cases, leucopenia and, in
isolated cases, agranulocytosis, aplastic anaemia or haemolytic anaemia may
develop.
Bone marrow depression has been reported as a rare complication and
necessitates withdrawal of treatment.
Rarely, paraesthesiae may occur.
Serum calcium levels may be reduced; in very rare cases tetany has been
observed. Nephrocalcinosis / nephrolithiasis has been reported in premature
infants.
Serum cholesterol and triglyceride levels may rise during furosemide
treatment. During long term therapy, they will usually return to normal within
six months.
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.
Hearing disorders and 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.
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.
In isolated cases, intrahepatic cholestasis, an increase in liver transaminases or
acute pancreatitis may develop.
The incidence of allergic reactions, such as skin rashes, photosensitivity,
vasculitis, fever, interstitial nephritis or shock, is very low, but when they
occur, treatment should be withdrawn. Skin and mucous membrane reactions
may occasionally occur, e.g. itching, urticaria, other rashes or bullous lesions,
erythema multiforme, exfoliative dermatitis, purpura.
As with other diuretics, electrolytes and water balance may be disturbed as a
result of diuresis after prolonged therapy. Furosemide leads to increased
excretion of sodium and chloride and consequently water. In addition,
excretion of other electrolytes (in particular potassium, calcium and
magnesium) is increased. 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. Warning signs of
electrolyte disturbances include increased thirst, headache, hypotension,
confusion, muscle cramps, tetany, muscle weakness, disorders of cardiac
rhythm and gastrointestinal symptoms. Pre-existing metabolic alkalosis (e.g.
in decompensated cirrhosis of the liver) may be aggravated by furosemide
treatment.
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.
Increased production of urine may provoke or aggravate complaints in patients
with an obstruction of urinary outflow. Thus, acute retention of urine with
possible secondary complications may occur for example, in patients with
bladder-emptying disorders, pro static hyperplasia or narrowing of the urethra.
If furosemide is administered to premature infants during the first weeks of
life, it may increase the risk of persistence of patent ductus arteriosus.
Severe anaphylactic or anaphylactoid reactions (e.g. with shock) occur rarely.
Side effects of a minor nature such as nausea, malaise or gastric upset
(vomiting or diarrhoea) may occur but are not usually severe enough to
necessitate withdrawal of treatment.
As with other diuretics, treatment with furosemide may lead to transitory
increases in blood creatinine and urea levels. Serum levels of uric acid may
increase and attacks of gout may occur.
4.9

Overdose
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.
Treatment should therefore be aimed at fluid replacement and correction of the
electrolyte imbalance. 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
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 designated to reduce
absorption (e.g. activated charcoal).

5.

PHARMACOLOGICAL PROPERTIES

5.1

Pharmacodynamic properties
Pharmacotherapeutic group:
High ceiling Diuretic Sulfonamide – CO3C 1 01
Furosemide is a potent loop diuretic which inhibits sodium and chloride
reabsorption at the Loop of Henlé. Furosemide acts at the luminal face of the
epithelial cells by inhibiting co-transport mechanisms for the entry of sodium
and chloride. Furosemide gains access to its site of action by being transported
through the secretory pathway for organic acids in the proximal tubule. It
reduces the renal excretion of uric acid. Furosemide causes an increased loss
of potassium in the urine and also increases the excretion of ammonia by the
kidney.

5.2

Pharmacokinetic properties
Furosemide is a weak carboxylic acid which exists mainly in the dissociated
form in the gastro-intestinal tract. Furosemide is rapidly but incompletely
absorbed (60-70%) on oral administration and its effect is largely over within
four hours. The optimal absorption site is the upper duodenum at pH 5.0. In
plasma, furosemide is extensively bound to proteins mainly albumin. The
unbound fraction in plasma averages 2 – 4% at therapeutic concentrations. The
volume of distribution ranges between 170 – 270 ml/Kg. The half life of the ß
phase ranges from 45 – 60 min.
Regardless of route of administration, 69-97% of activity from a radio-labelled
dose is excreted in the first 4 hours after the drug is given. Furosemide is
mainly eliminated via the kidneys (80-90%); a small fraction of the dose
undergoes biliary elimination and 10-15% of the activity can be recovered
from the faeces.

5.3

Preclinical safety data
Furosemide is a widely used diuretic which has been available for over thirty
years and its safety profile in man is well established.

6

PHARMACEUTICAL PARTICULARS

6.1

List of excipients

Ethanol, sodium hydroxide, cherry flavour (containing propylene glycol),
liquid maltitol, disodium hydrogen phosphate, citric acid monohydrate and
purified water.

6.2

Incompatibilities
None known

6.3

Shelf-life
18 months
3 months once opened

6.4

Special precautions for storage
Do not store above 25oC.

6.5

Nature and contents of container
Bottles: Amber (Type III) glass
Closures:
Polypropylene Child Resistant Closures (CRCs) with LDPE liners
Capacity: 150 ml

6.6

Instructions for use and handling
Not applicable.

7.

MARKETING AUTHORISATION HOLDER
Pinewood Laboratories Limited
Ballymacarbry
Clonmel
Co. Tipperary

Ireland

8.

MARKETING AUTHORISATION NUMBER(S)
PL 04917/0074

9

DATE OF FIRST AUTHORISATION/RENEWAL OF THE
AUTHORISATION
03/07/2006

10

DATE OF REVISION OF THE TEXT
13/09/2011

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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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