Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/869
| Predicate | Object |
|---|---|
| rdf:type | |
| rdfs:label |
Furosemide (Injection, Solution)
|
| dailymed-instance:dosage |
Adults Parenteral
therapy with Furosemide Injection, USP should be used only in patients unable
to take oral medication or in emergency situations and should be replaced
with oral therapy as soon as practical. Edema The usual initial dose of furosemide is
20 to 40 mg given as a single dose injected intramuscularly or intravenously.
The intravenous dose should be given slowly (1 to 2 minutes). Ordinarily a
prompt diuresis ensues. If needed, another dose may be administered in the
same manner 2 hours later or the dose may be increased. The dose may be raised
by 20 mg and given not sooner than 2 hours after the previous dose until
the desired diuretic effect has been obtained. This individually determined
single dose should then be given once or twice daily. Therapy
should be individualized according to patient response to gain maximal therapeutic
response and to determine the minimal dose needed to maintain that response.
Close medical supervision is necessary. If the physician
elects to use high dose parenteral therapy, add the Furosemide Injection to
either Sodium Chloride Injection, USP, Lactated Ringer's Injection,
USP, or Dextrose (5%) Injection, USP after pH has been adjusted to above 5.5,
and administer as a controlled intravenous infusion at a rate not greater
than 4 mg/min. Furosemide Injection is a buffered alkaline solution with a
pH of about 9 and drug may precipitate at pH values below 7. Care must be
taken to ensure that the pH of the prepared infusion solution is in the weakly
alkaline to neutral range. Acid solutions, including other parenteral medications
(e.g., labetalol, ciprofloxacin, amrinone, milrinone) must not be administered
concurrently in the same infusion because they may cause precipitation of
the furosemide. In addition, furosemide injection should not be added to a
running intravenous line containing any of these acidic products. Acute Pulmonary Edema The
usual initial dose of furosemide is 40 mg injected slowly intravenously (over
1 to 2 minutes). If a satisfactory response does not occur within 1 hour,
the dose may be increased to 80 mg injected slowly intravenously (over 1 to
2 minutes). If necessary, additional therapy (e.g.,
digitalis, oxygen) may be administered concomitantly. Pediatric Patients Parenteral
therapy should be used only in patients unable to take oral medication or
in emergency situations and should be replaced with oral therapy as soon as
practical. The usual initial dose of Furosemide (intravenously
or intramuscularly) in pediatric patients is 1 mg/kg body weight and
should be given slowly under close medical supervision. If the diuretic response
to the initial dose is not satisfactory, dosage may be increased by 1 mg/kg
not sooner than 2 hours after the previous dose, until the desired diuretic
effect has been obtained. Doses greater than 6 mg/kg body weight are not recommended. Literature
reports suggest that the maximum dose for premature infants should not exceed
1 mg/kg/day (see WARNINGS, Pediatric Use). Furosemide
Injection should be inspected visually for particulate matter and discoloration
prior to administration whenever solution and container permit. Do not use
if solution is discolored. To prevent needle-stick
injuries, needles should not be recapped, purposely bent, or broken by hand.
|
| dailymed-instance:descripti... |
Furosemide Injection, USP is a sterile solution intended
for intramuscular or intravenous administration. Each mL contains furosemide
10 mg and sodium chloride sufficient to render solution isotonic in water
for injection. Contains sodium hydroxide and may contain hydrochloric acid
for pH adjustment. pH 9.0 (8.0 to 9.3). Furosemide
is a diuretic which is an anthranilic acid derivative, chemically identified
as 4-chloro-N-furfuryl-5-sulfamoylanthranilic
acid. Furosemide is a white to off-white odorless crystalline
powder. It is practically insoluble in water, sparingly soluble in alcohol,
freely soluble in dilute alkali solutions and insoluble in dilute acids. It
has the following structural formula: Molecular
formula: CHCl NOS Molecular
weight: 330.75 The plastic syringe is molded from a
specially formulated polypropylene. Water permeates from inside the container
at an extremely slow rate which will have an insignificant effect on solution
concentration over the expected shelf life. Solutions
in contact with the plastic container may leach out certain chemical components
from the plastic in very small amounts; however, biological testing was supportive
of the safety of the syringe material. Contains no preservative.
|
| dailymed-instance:clinicalP... |
Investigations into the mode of action of furosemide have
utilized micropuncture studies in rats, stop flow experiments in dogs and
various clearance studies in both humans and experimental animals. It
has been demonstrated that furosemide inhibits primarily the reabsorption
of sodium and chloride not only in the proximal and distal tubules but also
in the loop of Henle. The high degree of efficacy is largely due to this unique
site of action. The action on the distal tubule is independent of any inhibitory
effect on carbonic anhydrase and aldosterone. Recent
evidence suggests that furosemide glucuronide is the only or at least the
major biotransformation product of furosemide in man. Furosemide is extensively
bound to plasma proteins, mainly to albumin. Plasma concentrations ranging
from 1 to 400 mcg/mL are 91 to 99% bound in healthy individuals. The unbound
fraction averages 2.3 to 4.1% at therapeutic concentrations. The
onset of diuresis following intravenous administration is within 5 minutes
and somewhat later after intramuscular administration. The peak effect occurs
within the first half hour. The duration of diuretic effect is approximately
2 hours. In fasted normal men, the mean bioavailability
of furosemide from furosemide tablets and furosemide solution is approximately
60% of that from an intravenous injection of the drug. Although furosemide
is more rapidly absorbed from the oral solution than from the tablet, peak
plasma levels and area under the plasma concentration-time curves do not differ
significantly. Peak plasma concentrations increase with increasing dose but
times-to-peak do not differ among doses. The terminal half-life of furosemide
is approximately 2 hours. Significantly more furosemide
is excreted in urine following the I.V. injection than after the tablet or
oral solution. There are no significant differences between the two oral formulations
in the amount of unchanged drug excreted in urine.
|
| dailymed-instance:activeIng... | |
| dailymed-instance:contraind... |
Furosemide Injection is contraindicated in patients with
anuria and in patients with a history of hypersensitivity to furosemide.
|
| dailymed-instance:supply |
Furosemide Injection, USP 10 mg/mL is supplied as follows: Store at controlled room temperature 15��to 30��C
(59��to 86��F). [See USP.] Do
not use if solution is discolored or contains particulate. Protect from light. Do not remove from carton until ready
for use. Discard unused portion. HOSPIRA, INC., LAKE FOREST,
IL 60045 USA Abboject is a trademark of the
Abbott group of companies.
|
| dailymed-instance:genericDr... | |
| dailymed-instance:activeMoi... | |
| dailymed-instance:inactiveI... | |
| dailymed-instance:possibleD... | |
| dailymed-instance:precautio... |
General: Excessive diuresis may cause dehydration and blood volume
reduction with circulatory collapse and possibly vascular thrombosis and embolism,
particularly in elderly patients. As with any effective diuretic, electrolyte
depletion may occur during furosemide therapy, especially in patients receiving
higher doses and a restricted salt intake. Hypokalemia may develop with furosemide,
especially with brisk diuresis, inadequate oral electrolyte intake, when cirrhosis
is present, or during concomitant use of corticosteroids or ACTH. Digitalis
therapy may exaggerate metabolic effects of hypokalemia, especially myocardial
effects. All patients receiving furosemide therapy should
be observed for these signs or symptoms of fluid or electrolyte imbalance
(hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia, or hypocalcemia):
dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle
pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia,
or gastrointestinal disturbances such as nausea and vomiting. Increases
in blood glucose and alterations in glucose tolerance tests (with abnormalities
of the fasting and 2-hour postprandial sugar) have been observed, and rarely,
precipitation of diabetes mellitus has been reported. Asymptomatic
hyperuricemia can occur and gout may rarely be precipitated. Patients
allergic to sulfonamides may also be allergic to furosemide. The
possibility exists of exacerbation or activation of systemic lupus erythematosus. As
with many other drugs, patients should be observed regularly for the possible
occurrence of blood dyscrasias, liver or kidney damage, or other idiosyncratic
reactions.<br/>Information for Patients: Patients receiving furosemide should be advised that they
may experience symptoms from excessive fluid and/or electrolyte losses. The
postural hypotension that sometimes occurs can usually be managed by getting
up slowly. Potassium supplements and/or dietary measures may be needed to
control or avoid hypokalemia. Patients with diabetes
mellitus should be told that furosemide may increase blood glucose levels
and thereby affect urine glucose tests. The skin of some patients may be more
sensitive to the effects of sunlight while taking furosemide. Hypertensive
patients should avoid medications that may increase blood pressure, including
over-the-counter products for appetite suppression and cold symptoms.<br/>Laboratory Tests: Serum electrolytes (particularly potassium), CO,
creatinine and BUN should be determined frequently during the first few months
of furosemide therapy and periodically thereafter. Serum
and urine electrolyte determinations are particularly important when the patient
is vomiting profusely or receiving parenteral fluids. Abnormalities should
be corrected or the drug temporarily withdrawn. Other medications may also
influence serum electrolytes. Reversible elevations
of BUN may occur and are associated with dehydration, which should be avoided,
particularly in patients with renal insufficiency. Urine
and blood glucose should be checked periodically in diabetics receiving furosemide,
even in those suspected of latent diabetes. Furosemide
may lower serum levels of calcium (rarely cases of tetany have been reported)
and magnesium. Accordingly, serum levels of these electrolytes should be determined
periodically.<br/>Drug Interactions: Furosemide may increase the ototoxic potential of aminoglycoside
antibiotics, especially in the presence of impaired renal function. Except
in life-threatening situations, avoid this combination. Furosemide
should not be used concomitantly with ethacrynic acid because of the possibility
of ototoxicity. Patients receiving high doses of salicylates
concomitantly with furosemide, as in rheumatic disease, may experience salicylate
toxicity at lower doses because of competitive renal excretory sites. Furosemide
has a tendency to antagonize the skeletal muscle relaxing effect of tubocurarine
and may potentiate the action of succinylcholine. Lithium
generally should not be given with diuretics because they reduce lithium's
renal clearance and add a high risk of lithium toxicity. Furosemide
may add to or potentiate the therapeutic effect of other antihypertensive
drugs. Potentiation occurs with ganglionic or peripheral adrenergic blocking
drugs. Furosemide may decrease arterial responsiveness
to norepinephrine. However, norepinephrine may still be used effectively. One
study in six subjects demonstrated that the combination of furosemide and
acetylsalicylic acid temporarily reduced creatinine clearance in patients
with chronic renal insufficiency. There are case reports of patients who developed
increased BUN, serum creatinine and serum potassium levels, and weight gain
when furosemide was used in conjunction with NSAIDs. Literature
reports indicate that coadministration of indomethacin may reduce the natriuretic
and antihypertensive effects of furosemide in some patients by inhibiting
prostaglandin synthesis. Indomethacin may also affect plasma renin levels,
aldosterone excretion, and renin profile evaluation. Patients
receiving both indomethacin and furosemide should be observed closely to determine
if the desired diuretic and/or antihypertensive effect of furosemide is achieved.<br/>Carcinogenesis, Mutagenesis, Impairment of Fertility: Furosemide was tested for carcinogenicity by oral administration
in one strain of mice and one strain of rats. A small but significantly increased
incidence of mammary gland carcinomas occurred in female mice at a dose 17.5
times the maximum human dose of 600 mg. There were marginal increases in uncommon
tumors in male rats at a dose of 15 mg/kg (slightly greater than the maximum
human dose) but not at 30 mg/kg. Furosemide was devoid
of mutagenic activity in various strains of Salmonella
typhimurium when tested in the presence or absence of an in vitro metabolic activation system, and questionably
positive for gene mutation in mouse lymphoma cells in the presence of rat
liver S9 at the highest dose tested. Furosemide did not induce sister chromatid
exchangein human cells in vitro, but
other studies on chromosomal aberrations in human cells in
vitro gave conflicting results. In Chinese hamster cells it induced
chromosomal damage but was questionably positive for sister chromatid exchange.
Studies on the induction by furosemide of chromosomal aberrations in mice
were inconclusive. The urine of rats treated with this drug did not induce
gene conversion in Saccharomyces cerevisiae. Furosemide
produced no impairment of fertility in male or female rats, at 100 mg/kg/day
(the maximum effective diuretic dose in the rat and 8 times the maximal human
dose of 600 mg/day).<br/>Pregnancy: Teratogenic Effects: Pregnancy
Category C: Furosemide has been shown to cause unexplained maternal
deaths and abortions in rabbits at 2, 4, and 8 times the maximal recommended
human oral dose. There are no adequate and well-controlled studies in pregnant
women. Furosemide should be used during pregnancy only if the potential benefit
justifies the potential risk to the fetus. The effects
of furosemide on embryonic and fetal development and on pregnant dams were
studied in mice, rats and rabbits. Furosemide caused
unexplained maternal deaths and abortions in the rabbit at the lowest dose
of 25 mg/kg (2 times the maximal recommended human oral dose of 600 mg/day).
In another study, a dose of 50 mg/kg (4 times the maximal recommended human
oral dose of 600 mg/day) also caused maternal deaths and abortions when administered
to rabbits between Days 12 and 17 of gestation. In a third study, none of
the pregnant rabbits survived an oral dose of 100 mg/kg. Data from the above
studies indicate fetal lethality that can precede maternal deaths. The
results of the mouse study and one of the three rabbit studies also showed
an increased incidence and severity of hydronephrosis (distention of the renal
pelvis and, in some cases, of the ureters) in fetuses derived from treated
dams as compared with the incidence in fetuses from the control group.<br/>Nursing Mothers: Because it appears in breast milk, caution should be exercised
when furosemide is administered to a nursing mother.<br/>Pediatric Use: Renal calcifications (from barely visible on x-ray to staghorn)
have occurred in some severely premature infants treated with intravenous
furosemide for edema due to patent ductus arteriosus and hyaline membrane
disease. The concurrent use of chlorothiazide has been reported to decrease
hypercalciuria and dissolve some calculi.
|
| dailymed-instance:overdosag... |
The principal signs and symptoms of overdose with furosemide
are dehydration, blood volume reduction, hypotension, electrolyte imbalance,
hypokalemia and hypochloremic alkalosis, and are extensions of its diuretic
action. The acute toxicity of furosemide has been determined
in mice, rats and dogs. In all three, the oral LDexceeded 1000
mg/kg body weight, while the intravenous LDranged from 300 to
680 mg/kg. The acute intragastric toxicity in neonatal rats is 7 to 10
times that of adult rats. The concentration of furosemide
in biological fluids associated with toxicity or death is not known. Treatment
of overdosage is supportive and consists of replacement of excessive fluid
and electrolyte losses. Serum electrolytes, carbon dioxide level and blood
pressure should be determined frequently. Adequate drainage must be assured
in patients with urinary bladder outlet obstruction (such as prostatic hypertrophy). Hemodialysis
does not accelerate furosemide elimination.
|
| dailymed-instance:genericMe... |
Furosemide
|
| dailymed-instance:fullName |
Furosemide (Injection, Solution)
|
| dailymed-instance:adverseRe... |
Adverse reactions are categorized below by organ system and
listed by decreasing severity. Gastrointestinal
System Reactions (1) Pancreatitis (2) jaundice
(intrahepatic cholestatic jaundice) (3) anorexia (4) oral and gastric irritation
(5) cramping (6) diarrhea (7) constipation (8) nausea (9) vomiting. Systemic Hypersensitivity Reactions (1)
Systemic vasculitis (2) interstitial nephritis (3) necrotizing angiitis. Central Nervous System Reactions (1)
Tinnitus and hearing loss (2) paresthesias (3) vertigo (4) dizziness (5) headache
(6) blurred vision (7) xanthopsia. Hematologic
Reactions (1) Aplastic anemia (rare) (2) thrombocytopenia
(3) agranulocytosis (rare) (4) hemolytic anemia (5) leukopenia (6) anemia. Dermatologic-Hypersensitivity Reactions (1)
Exfoliative dermatitis (2) erythema multiforme (3) purpura (4) photosensitivity
(5) urticaria (6) rash (7) pruritus. Cardiovascular
Reaction Orthostatic hypotension may occur
and be aggravated by alcohol, barbiturates or narcotics. Other Reactions (1) Hyperglycemia
(2) glycosuria (3) hyperuricemia (4) muscle spasm (5) weakness (6) restlessness
(7) urinary bladder spasm (8) thrombophlebitis (9) transient injection site
pain following intramuscular injection (10) fever. Whenever
adverse reactions are moderate or severe, furosemide dosage should be reduced
or therapy withdrawn.
|
| dailymed-instance:warning |
In patients with hepatic cirrhosis and ascites, furosemide
therapy is best initiated in the hospital. In hepatic coma and in states of
electrolyte depletion, therapy should not be instituted until the basic condition
is improved. Sudden alterations of fluid and electrolyte balance in patients
with cirrhosis may precipitate hepatic coma; therefore, strict observation
is necessary during the period of diuresis. Supplemental potassium chloride
and, if required, an aldosterone antagonist are helpful in preventing hypokalemia
and metabolic alkalosis. If increasing azotemia and
oliguria occur during treatment of severe progressive renal disease, furosemide
should be discontinued. Cases of tinnitus and reversible
or irreversible hearing impairment have been reported. Usually, reports indicate
that furosemide ototoxicity is associated with rapid injection, severe renal
impairment, doses exceeding several times the usual recommended dose, or concomitant
therapy with aminoglycoside antibiotics, ethacrynic acid, or other ototoxic
drugs. If the physician elects to use high dose parenteral therapy, controlled
intravenous infusion is advisable (for adults, an infusion rate not exceeding
4 mg furosemide per minute has been used). Pediatric Use: In premature neonates with respiratory
distress syndrome, diuretic treatment with furosemide in the first few weeks
of life may increase the risk of persistent patent ductus arteriosus (PDA),
possibly through a prostaglandin-E-mediated process. Literature
reports indicate that premature infants with post conceptual age (gestational
plus postnatal) less than 31 weeks receiving doses exceeding 1 mg/kg/24 hours
may develop plasma levels which could be associated with potential toxic effects
including ototoxicity. Hearing loss in neonates has
been associated with the use of furosemide injection (see WARNINGS , above).
|
| dailymed-instance:indicatio... |
Parenteral therapy should be reserved for patients unable
to take oral medication or for patients in emergency clinical situations. Edema Furosemide is indicated
in adults and pediatric patients for the treatment of edema associated with
congestive heart failure, cirrhosis of the liver, and renal disease, including
the nephrotic syndrome. Furosemide is particularly useful when an agent with
greater diuretic potential is desired. Furosemide is
indicated as adjunctive therapy in acute pulmonary edema. The intravenous
administration of furosemide is indicated when a rapid onset of diuresis is
desired, e.g., in acute pulmonary edema. If gastrointestinal
absorption is impaired or oral medication is not practical for any reason,
furosemide is indicated by the intravenous or intramuscular route. Parenteral
use should be replaced with oral furosemide as soon as practical.
|
| dailymed-instance:represent... | |
| dailymed-instance:routeOfAd... | |
| dailymed-instance:name |
Furosemide
|