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Drug overview for LASIX ONYU (furosemide):
Generic name: FUROSEMIDE (fure-OH-se-mide)
Drug class: Diuretics
Therapeutic class: Cardiovascular Therapy Agents
Furosemide is a sulfonamide, loop-type diuretic and antihypertensive agent.
No enhanced Uses information available for this drug.
Generic name: FUROSEMIDE (fure-OH-se-mide)
Drug class: Diuretics
Therapeutic class: Cardiovascular Therapy Agents
Furosemide is a sulfonamide, loop-type diuretic and antihypertensive agent.
No enhanced Uses information available for this drug.
DRUG IMAGES
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The following indications for LASIX ONYU (furosemide) have been approved by the FDA:
Indications:
Peripheral edema due to chronic heart failure
Professional Synonyms:
Peripheral edema due to CHF
Peripheral edema due to congestive heart failure
Indications:
Peripheral edema due to chronic heart failure
Professional Synonyms:
Peripheral edema due to CHF
Peripheral edema due to congestive heart failure
The following dosing information is available for LASIX ONYU (furosemide):
Furosemide injection for IV or IM administration is available as the sodium salt; dosage is expressed in terms of furosemide. Furosemide dosage must be adjusted according to the patient's requirements and response.
The usual initial adult oral dose of furosemide for the management of edema is 20-80 mg given as a single dose, preferably in the morning. In adults who do not respond, the second and each succeeding oral dose may be increased in 20- to 40-mg increments every 6-8 hours until the desired diuretic response is obtained. The effective dose may be given once or twice daily thereafter, or, in some cases, by intermittent administration on 2-4 consecutive days each week.
Adult oral dosage of furosemide may be carefully titrated up to 600 mg daily in severely edematous patients.
For the management of fluid retention (e.g., edema) associated with heart failure, some experts recommend initiating furosemide at a low dosage (e.g., 20-40 mg once or twice daily) and increasing the dosage (maximum of 600 mg daily) until urine output increases and weight decreases, generally by 0.5-1 kg daily.
For infants and children, the usual initial oral dose of furosemide for the management of edema is 2 mg/kg administered as a single dose. If necessary, dosage may be increased in increments of 1 or 2 mg/kg every 6-8 hours to maximum individual doses of 6 mg/kg. For maintenance, the minimum effective dosage should be employed.
As a diuretic, the usual adult IM or IV dose is 20-40 mg given as a single injection. In adults who do not respond to the initial parenteral dose of furosemide, the second and each succeeding dose may be increased in 20-mg increments and given not more often than every 2 hours until the desired diuretic response is obtained. The effective single dose may then be given once or twice daily.
For the management of acute pulmonary edema in adults, 40 mg of furosemide may be slowly injected IV over 1-2 minutes. If the initial adult dose does not produce a satisfactory response within 1 hour, the dose may be increased to 80 mg IV given over 1-2 minutes.
For infants and children, the usual initial IV or IM dose of furosemide for the management of acute pulmonary edema or edema associated with heart failure or renal disease is 1 mg/kg. If necessary, the initial dose may be increased by 1 mg/kg no more often than every 2 hours until the desired effect has been obtained. Maximum individual parenteral doses recommended by the manufacturer for infants and children are 6 mg/kg.
For premature infants, the maximum parenteral dose should not exceed 1 mg/kg per day.
Furoscix(R): The single-use On-body Infusor with prefilled cartridge is pre-programmed to deliver a dosage of 30 mg of furosemide over the first hour, followed by 12.5 mg per hour for the subsequent 4 hours.
Lasix(R)ONYU:The Infusor with single-dose prefilled cartridge is pre-programmed to deliver a dosage of 30 mg of furosemide over the first hour, followed by 12.5 mg per hour for the subsequent 4 hours. The manufacturer states to administer once or twice daily as needed for edema.
Furosemide drug-device combinations for subcutaneous administration are not for chronic use and should be replaced with oral diuretics as soon as possible.
The usual initial adult oral dose of furosemide for the management of edema is 20-80 mg given as a single dose, preferably in the morning. In adults who do not respond, the second and each succeeding oral dose may be increased in 20- to 40-mg increments every 6-8 hours until the desired diuretic response is obtained. The effective dose may be given once or twice daily thereafter, or, in some cases, by intermittent administration on 2-4 consecutive days each week.
Adult oral dosage of furosemide may be carefully titrated up to 600 mg daily in severely edematous patients.
For the management of fluid retention (e.g., edema) associated with heart failure, some experts recommend initiating furosemide at a low dosage (e.g., 20-40 mg once or twice daily) and increasing the dosage (maximum of 600 mg daily) until urine output increases and weight decreases, generally by 0.5-1 kg daily.
For infants and children, the usual initial oral dose of furosemide for the management of edema is 2 mg/kg administered as a single dose. If necessary, dosage may be increased in increments of 1 or 2 mg/kg every 6-8 hours to maximum individual doses of 6 mg/kg. For maintenance, the minimum effective dosage should be employed.
As a diuretic, the usual adult IM or IV dose is 20-40 mg given as a single injection. In adults who do not respond to the initial parenteral dose of furosemide, the second and each succeeding dose may be increased in 20-mg increments and given not more often than every 2 hours until the desired diuretic response is obtained. The effective single dose may then be given once or twice daily.
For the management of acute pulmonary edema in adults, 40 mg of furosemide may be slowly injected IV over 1-2 minutes. If the initial adult dose does not produce a satisfactory response within 1 hour, the dose may be increased to 80 mg IV given over 1-2 minutes.
For infants and children, the usual initial IV or IM dose of furosemide for the management of acute pulmonary edema or edema associated with heart failure or renal disease is 1 mg/kg. If necessary, the initial dose may be increased by 1 mg/kg no more often than every 2 hours until the desired effect has been obtained. Maximum individual parenteral doses recommended by the manufacturer for infants and children are 6 mg/kg.
For premature infants, the maximum parenteral dose should not exceed 1 mg/kg per day.
Furoscix(R): The single-use On-body Infusor with prefilled cartridge is pre-programmed to deliver a dosage of 30 mg of furosemide over the first hour, followed by 12.5 mg per hour for the subsequent 4 hours.
Lasix(R)ONYU:The Infusor with single-dose prefilled cartridge is pre-programmed to deliver a dosage of 30 mg of furosemide over the first hour, followed by 12.5 mg per hour for the subsequent 4 hours. The manufacturer states to administer once or twice daily as needed for edema.
Furosemide drug-device combinations for subcutaneous administration are not for chronic use and should be replaced with oral diuretics as soon as possible.
Furosemide is administered orally (as tablets or oral solution); the drug can also be administered parenterally (by IM or IV injection, or by subcutaneous infusion using an infusor device). Furosemide 80 mg/mL injection (Furoscix(R)) is administered by subcutaneous infusion via a single-use On-body Infusor; the drug is contained in a prefilled cartridge that is designed to deliver 80 mg of furosemide in 10 mL solution over 5 hours. Furosemide 80 mg/2.67
mL injection (Lasix(R) ONYU) is administered by subcutaneous infusion via an Infusor; the drug is contained in a prefilled cartridge that is designed to deliver 80 mg of furosemide in 2.67 mL solution over 5 hours. The Infusor consists of a custom Reusable Unit that can be used for close to 50 treatments.
mL injection (Lasix(R) ONYU) is administered by subcutaneous infusion via an Infusor; the drug is contained in a prefilled cartridge that is designed to deliver 80 mg of furosemide in 2.67 mL solution over 5 hours. The Infusor consists of a custom Reusable Unit that can be used for close to 50 treatments.
| DRUG LABEL | DOSING TYPE | DOSING INSTRUCTIONS |
|---|---|---|
| LASIX ONYU 80 MG/2.67 ML KIT | Maintenance | Adults infuse 80 mg via on-body infusor over 5 hour(s) by subcutaneous route as directed per package instructions |
No generic dosing information available.
The following drug interaction information is available for LASIX ONYU (furosemide):
There are 2 contraindications.
These drug combinations generally should not be dispensed or administered to the same patient. A manufacturer label warning that indicates the contraindication warrants inclusion of a drug combination in this category, regardless of clinical evidence or lack of clinical evidence to support the contraindication.
| Drug Interaction | Drug Names |
|---|---|
| Ethacrynic Acid/Furosemide SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: The exact mechanism of the interaction is not well understood. CLINICAL EFFECTS: Concurrent use of furosemide and ethacrynic acid may increase the risk of ototoxicity.(1) PREDISPOSING FACTORS: Rapid intravenous injection, severe renal impairment, high doses exceeding the usual recommended dose, concomitant therapy with other drugs known to ototoxic. PATIENT MANAGEMENT: The US manufacturer of furosemide states that furosemide should not be used concurrently with ethacrynic acid.(1) DISCUSSION: Furosemide and ethacrynic acid have the potential to cause ototoxicity.(1,2) Deafness, tinnitus, and vertigo with a sense of fullness have occurred, most frequently in patients with severe renal impairment. The deafness usually has been reported as being transient in nature and of short duration (one to 24 hours) but in some patients the hearing loss has been permanent.(2) |
EDECRIN, ETHACRYNATE SODIUM, ETHACRYNIC ACID |
| Desmopressin/Loop Diuretics SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient. MECHANISM OF ACTION: Loop diuretics increase the risk of hyponatremia.(1-4) CLINICAL EFFECTS: Concurrent use of loop diuretics may increase the risk of hyponatremia with desmopressin.(1-4) PREDISPOSING FACTORS: Predisposing factors for hyponatremia include: polydipsia, renal impairment (eGFR < 50 ml/min/1.73m2), illnesses that can cause fluid/electrolyte imbalances, age >=65, medications that cause water retention and/or increase the risk of hyponatremia (carbamazepine, chlorpromazine, glucocorticoids, lamotrigine, NSAIDs, opioids, SSRIs, thiazide diuretics, and/or tricyclic antidepressants). PATIENT MANAGEMENT: The concurrent use of loop diuretics with desmopressin is contraindicated.(1-4) If concurrent use is deemed medically necessary, make sure serum sodium levels are normal before beginning therapy and consider using the desmopressin nasal 0.83 mcg dose. Consider measuring serum sodium levels more frequently than the recommended intervals of: within 7 days of concurrent therapy initiation, one month after concurrent therapy initiation and periodically during treatment. Counsel patients to report symptoms of hyponatremia, which may include: headache, nausea/vomiting, feeling restless, fatigue, drowsiness, dizziness, muscle cramps, changes in mental state (confusion, decreased awareness/alertness), seizures, coma, and trouble breathing. Counsel patients to limit the amount of fluids they drink in the evening and night-time and to stop taking desmopressin if they develop a stomach/intestinal virus with nausea/vomiting or any nose problems (blockage, stuffy/runny nose, drainage).(1) DISCUSSION: In clinical trials of desmopressin for the treatment of nocturia, 4 of 5 patients who developed severe hyponatremia (serum sodium <= 125 mmol/L) were taking systemic or inhaled glucocorticoids. Three of these patients were also taking NSAIDs and one was receiving a thiazide diuretic.(2) Drugs associated with hyponatremia may increase the risk, including loop diuretics, carbamazepine, chlorpromazine, glucocorticoids, lamotrigine, NSAIDs, opioids, SSRIs, thiazide diuretics, and/or tricyclic antidepressants.(1,3-4) |
DDAVP, DESMODA, DESMOPRESSIN ACETATE, NOCDURNA |
There are 3 severe interactions.
These drug interactions can produce serious consequences in most patients. Actions required for severe interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration scheduling, and providing additional patient monitoring. Review the full interaction monograph for more information.
| Drug Interaction | Drug Names |
|---|---|
| Lithium/Loop Diuretics SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Lithium is eliminated unchanged by the kidney; diuretic induced sodium elimination may lead to decreased renal clearance of lithium. CLINICAL EFFECTS: Lithium has a narrow therapeutic range; even modest, unintended increases in lithium concentration may result in lithium toxicity. Early symptoms of lithium toxicity may include: lethargy, muscle weakness or stiffness, new onset or coarsening of hand tremor, vomiting, diarrhea, confusion, ataxia, blurred vision, tinnitus and nystagmus. Severe toxicity may produce multiple organ dysfunction (e.g. seizures, coma, renal failure, cardiac arrhythmias, cardiovascular collapse) and may be fatal. PREDISPOSING FACTORS: Risk factors for lithium toxicity include: renal impairment or worsening of existing renal disease, dehydration, low sodium diet, and concomitant use of multiple medications which may impair renal elimination of lithium (e.g. ARBs, ACE Inhibitors, NSAIDs, diuretics). Patients who require higher therapeutic lithium levels to maintain symptom control are particularly susceptible to these factors. PATIENT MANAGEMENT: Monitor closely to decrease the risk for lithium toxicity. Evaluate renal function and most recent lithium levels. If renal function is not stable, it would be prudent to withhold combination therapy until renal function is stable. If a loop diuretic is started, or if the dose is increased in a patient stabilized on lithium therapy, consider empirically lowering the lithium dose, and recheck lithium levels 5 to 7 days after diuretic initiation. Adjust lithium or diuretic dose as required and continue frequent (e.g. weekly) monitoring of lithium until levels have stabilized. If lithium is to be started in a patient stabilized on a loop diuretic, consider starting with a lower lithium dose and titrate slowly as half-life may be prolonged. Monitor lithium concentrations until stabilized on the combination. Counsel patient to assure they know signs and symptoms of lithium toxicity and understand the importance of follow-up laboratory testing. DISCUSSION: The documentation for this interaction is conflicting. A large epidemiologic study in elderly bipolar patients and case reports describe interactions between lithium and furosemide or bumetanide which resulted in increased levels of lithium and lithium toxicity. Several studies in healthy subjects have found that furosemide had no effect on lithium clearance or lithium serum concentrations. Other studies performed to assess the accuracy of lithium clearance in assessing proximal tubular reabsorption found that furosemide and bumetanide increased lithium clearance. |
LITHIUM CARBONATE, LITHIUM CARBONATE ER, LITHIUM CITRATE, LITHIUM CITRATE TETRAHYDRATE, LITHOBID |
| Sodium Phosphate Bowel Cleanser/Diuretics SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Bowel cleansing with sodium phosphate causes dehydration, decreased intravascular volume and hyperphosphatemia, which increases phosphate levels in the renal tubules. Abnormally high levels of calcium and phosphate in the renal tubules may precipitate out, resulting in renal injury.(1) CLINICAL EFFECTS: Use of sodium phosphate for bowel cleansing in patients maintained on diuretics may increase the risk of acute phosphate nephropathy, which is an acute kidney injury associated with deposits of calcium phosphate crystal in the renal tubules that may result in permanent renal function impairment. Acute phosphate nephropathy presents as acute kidney injury with minimal proteinuria and a bland urine sediment.(2) Use of oral sodium phosphate products at laxative doses has not been associated with acute kidney injury.(3) PREDISPOSING FACTORS: Patients who may be at an increased risk of acute phosphate nephropathy include those who are over age 55; are hypovolemic or have decreased intravascular volume; have baseline kidney disease, bowel obstruction, or active colitis; and who are using medications that affect renal perfusion or function (such as diuretics, angiotensin converting enzyme (ACE) inhibitors, angiotension receptor blockers (ARBs) and possibly nonsteroidal anti-inflammatory drugs (NSAIDs).(2) PATIENT MANAGEMENT: If possible, use an alternative agent for bowel cleansing.(1) Use sodium phosphate products with caution in patients taking medications that affect kidney function or perfusion, such as diuretics. Obtain baseline and post-procedure labs (electrolytes, calcium, phosphate, BUN, creatinine, and [in smaller, frail individuals] glomerular filtration rate). Instruct patients to drink sufficient quantities of clear fluids before, during, and after bowel cleansing and to avoid other laxatives that contain sodium phosphate. Consider hospitalization and intravenous hydration during bowel cleansing to support frail patients who may be unable to drink an appropriate volume of fluid or who may be without assistance at home.(2) Use of an electrolyte solution for rehydration may decrease the risk of acute phosphate nephropathy.(4,5) DISCUSSION: Since May 2006, the FDA has received 20 reports of acute phosphate nephropathy associated with the use of Osmo Prep. Concomitant medications included ACE inhibitors or ARBs (11), diuretics (6), and NSAIDs (4).(2) In a retrospective review of colonoscopy patients, simultaneous use of ACE inhibitors or ARBs significantly increased the risk of acute kidney injury from oral sodium phosphate. Diuretic use was also a risk factor.(6) In a case series study of 21 cases of acute phosphate nephropathy in patients who had used oral sodium phosphate, 14 patients received an ACE inhibitor or ARB, 4 used a diuretic, and 3 used an NSAID.(7) Cases have also been reported with rectal products.(8) |
MB CAPS, SODIUM PHOSPHATE DIBASIC, URIMAR-T, URNEVA |
| Selected OAT1-OAT3 Substrates/Nitisinone SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction. MECHANISM OF ACTION: Nitisinone is an inhibitor of organic anion transporter 1 and 3 (OAT1/OAT3) which may inhibit the renal excretion of substrates of OAT1/OAT3.(1) CLINICAL EFFECTS: Administration of nitisinone with OAT1/OAT3 substrates may result in elevated levels of and toxicity of the substrates.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: The US manufacturer of nitisinone states concurrent use with OAT1/OAT3 substrates should be avoided.(1) DISCUSSION: Nitisinone increased the area-under-curve (AUC) and maximum concentration (Cmax) of furosemide, an OAT1/OAT3 substrate, by 72% and 12%, respectively.(1) OAT1/OAT3 substrates linked to this monograph include: adefovir, bumetanide, furosemide, tenofovir and vadadustat.(1-2) |
HARLIKU, NITISINONE, NITYR, ORFADIN |
There are 10 moderate interactions.
The clinician should assess the patient’s characteristics and take action as needed. Actions required for moderate interactions include, but are not limited to, discontinuing one or both agents, adjusting dosage, altering administration.
| Drug Interaction | Drug Names |
|---|---|
| Aminoglycosides/Loop Diuretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The coadministration of aminoglycosides and loop diuretics may result in additive or synergistic ototoxicity and/or nephrotoxicity. CLINICAL EFFECTS: The combination of an aminoglycoside and a loop diuretic may increase risk for serious nephrotoxicity or ototoxicity.(1,2) Vestibular or auditory ototoxicity may be permanent.(1,3) PREDISPOSING FACTORS: Preexisting renal impairment, extended duration of aminoglycoside therapy, greater than one aminoglycoside dose per day, rapid injection or high doses of loop diuretics, concomitant use of additional nephrotoxic agents such as iodinated contrast media or vancomycin, or sepsis appear to increase the risk for nephrotoxicity and ototoxicity.(1-6). Patients carrying certain variants in the MT-RNR1 gene (m.1555A>G, m.1095T>C, and m.1494C>T) are at increased risk of developing ototoxicity. An additional risk factor includes patients with a maternal relative known to have a clinically relevant MT-RNR1 variant. The risk of ototoxicity can occur at standard recommended doses of aminoglycosides.(7) PATIENT MANAGEMENT: Administer aminoglycoside dosage every 24 to > 48 hours based upon renal function and continue therapy for less than 4 to 7 days, whenever possible.(4,5) The recommended maximal infusion rate for high dose furosemide therapy is 4 mg/minute.(2) When concurrent therapy is necessary monitor renal, hearing, and vestibular function. Signs of vestibular dysfunction include loss of balance and/or the visual sensation that stationary objects are moving (oscillopsia). In hospitalized or bedbound patients these symptoms may not be noticed or may be ascribed to other etiologies.(3) DISCUSSION: Several studies and case reports have documented altered aminoglycoside levels, nephrotoxicity, and ototoxicity with concurrent therapy.(8-14) Otic aminoglycosides are included in this interaction because high aminoglycoside concentrations in the ear have been associated with an increased risk for hearing loss. |
AMIKACIN SULFATE, CORTISPORIN-TC, GENTAMICIN SULFATE, GENTAMICIN SULFATE IN NS, KANAMYCIN SULFATE, NEOMYCIN SULFATE, NEOMYCIN-POLYMYXIN-HC, NEOMYCIN-POLYMYXIN-HYDROCORT, STREPTOMYCIN SULFATE, TOBRAMYCIN, TOBRAMYCIN SULFATE, ZEMDRI |
| Digitalis Glycosides/Kaluretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Potassium-losing diuretics may result in potassium depletion which can predispose patients to digitalis toxicity. CLINICAL EFFECTS: May observe increased arrhythmias, resulting from an increase in the cardiac response to digitalis. Symptoms of digoxin toxicity can include anorexia, nausea, vomiting, headache, fatigue, malaise, drowsiness, generalized muscle weakness, disorientation, hallucinations, visual disturbances, and arrhythmias. PREDISPOSING FACTORS: Low body weight, advanced age, impaired renal function, hypokalemia, hypercalcemia, and/or hypomagnesemia may increase the risk of digoxin toxicity. PATIENT MANAGEMENT: Monitor serum potassium status and give potassium replacements as needed. DISCUSSION: This interaction is well documented. Most patients taking diuretics do not develop significant potassium depletion if they are on low doses of diuretics and have adequate potassium intake. |
DIGITEK, DIGOXIN, DIGOXIN MICRONIZED, LANOXIN, LANOXIN PEDIATRIC |
| NSAIDs; Salicylates/Loop Diuretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: During concurrent administration of a loop diuretic and a nonsteroidal anti-inflammatory drug (NSAID), patients may retain sodium as a result of NSAID-induced prostaglandin inhibition. CLINICAL EFFECTS: The pharmacological effects of loop diuretics may be decreased due to reduced antihypertensive and diuretic actions. Concurrent use of NSAIDs with loop diuretics and renin-angiotensin system (RAS) inhibitors may result in increased risk of acute kidney injury (AKI). PREDISPOSING FACTORS: Low water intake/dehydration, drug sensitivity, greater than 75 years of age, and renal impairment may increase an individuals susceptibility to AKI. PATIENT MANAGEMENT: Monitor patients for a decrease in the effects of the loop diuretic. It may be necessary to administer a higher dose of the diuretic or an alternative anti-inflammatory agent. Concurrent use of NSAIDs with loop diuretics and RAS inhibitors should be used with caution and monitored closely for signs of AKI. DISCUSSION: In a computational study, the risk of AKI using triple therapy with a diuretic, RAS inhibitor, and NSAID was assessed. The study found the following factors may increase an individual's susceptibility to AKI: low water intake, drug sensitivity, greater than 75 years of age, and renal impairment.(19,20) In an observational study, current use of a triple therapy with a diuretic, RAS inhibitor, and NSAID, was associated with an increased rate of acute kidney injury (rate ratio (RR) 1.31, 95% confidence interval (CI) 1.12-1.53). The highest risk of AKI associated with triple therapy were observed in the first 30 days of use (RR 1.82, CI 1.35-2.46). (21) Administration of indomethacin alone has been reported to decrease sodium excretion and increase blood pressure. In patients receiving a loop diuretic (e.g., bumetanide, furosemide), these effects interfere with clinical management. Several NSAIDs have been shown to interact with loop diuretics interfering with the pharmacological effects of the diuretic. In volunteers on sodium restricted diets, ibuprofen and indomethacin inhibited furosemide diuresis. |
ACETYL SALICYLIC ACID, ANAPROX DS, ARTHROTEC 50, ARTHROTEC 75, ASA-BUTALB-CAFFEINE-CODEINE, ASCOMP WITH CODEINE, ASPIRIN, BISMUTH SUBSALICYLATE, BROMFENAC SODIUM, BUTALBITAL-ASPIRIN-CAFFEINE, CALDOLOR, CAMBIA, CARISOPRODOL-ASPIRIN, CARISOPRODOL-ASPIRIN-CODEINE, CELEBREX, CELECOXIB, CHOLINE MAGNESIUM TRISALICYLAT, COMBOGESIC, COMBOGESIC IV, CONSENSI, COXANTO, DICLOFENAC, DICLOFENAC POTASSIUM, DICLOFENAC SODIUM, DICLOFENAC SODIUM ER, DICLOFENAC SODIUM MICRONIZED, DICLOFENAC SODIUM-MISOPROSTOL, DIFLUNISAL, DOLOBID, EC-NAPROSYN, ELYXYB, ETODOLAC, ETODOLAC ER, FELDENE, FENOPROFEN CALCIUM, FENOPRON, FLURBIPROFEN, HYDROCODONE-IBUPROFEN, IBU, IBUPAK, IBUPROFEN, IBUPROFEN LYSINE, IBUPROFEN-FAMOTIDINE, INDOCIN, INDOMETHACIN, INDOMETHACIN ER, INFLAMMACIN, INFLATHERM(DICLOFENAC-MENTHOL), KETOPROFEN, KETOPROFEN MICRONIZED, KETOROLAC TROMETHAMINE, LODINE, LOFENA, LURBIRO, MECLOFENAMATE SODIUM, MEFENAMIC ACID, MELOXICAM, NABUMETONE, NABUMETONE MICRONIZED, NALFON, NAPRELAN, NAPROSYN, NAPROTIN, NAPROXEN, NAPROXEN SODIUM, NAPROXEN SODIUM CR, NAPROXEN SODIUM ER, NAPROXEN-ESOMEPRAZOLE MAG, NEOPROFEN, NORGESIC, NORGESIC FORTE, ORPHENADRINE-ASPIRIN-CAFFEINE, ORPHENGESIC FORTE, ORUDIS, OXAPROZIN, PHENYL SALICYLATE, PHENYLBUTAZONE, PIROXICAM, RELAFEN DS, SALSALATE, SODIUM SALICYLATE, SULINDAC, SUMATRIPTAN SUCC-NAPROXEN SOD, SYMBRAVO, TOLECTIN 600, TOLMETIN SODIUM, TORONOVA II SUIK, TORONOVA SUIK, TRESNI, TREXIMET, VIVLODEX, VYSCOXA, XIFYRM, YOSPRALA, ZIPSOR, ZORVOLEX, ZYBIC |
| Tobramycin Inhalation/Selected Diuretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The combination may have additive or synergistic risks for ototoxicity and/or nephrotoxicity.(1,2) CLINICAL EFFECTS: Concurrent use may result in an increased risk of aminoglycoside toxicity.(1) PREDISPOSING FACTORS: Severe renal impairment, sepsis, or concomitant use of additional ototoxic or nephrotoxic agents may further increase the risk for toxicity. Patients carrying certain variants in the MT-RNR1 gene (m.1555A>G, m.1095T>C, and m.1494C>T) are at greatly increased risk of developing ototoxicity. An additional risk factor includes patients with a maternal relative known to have a clinically relevant MT-RNR1 variant. The risk of ototoxicity can occur at standard recommended doses of aminoglycosides.(3) PATIENT MANAGEMENT: Instruct patients to contact their provider for new onset or worsening tinnitus. Tinnitus may be a sentinel symptom of ototoxicity. In clinical trials of tobramycin inhalation 8 patients (3%) receiving tobramycin reported tinnitus while no patients in the placebo group reported this symptom.(1) For renally impaired patients receiving long term tobramycin inhalation therapy, consider measurement of serum tobramycin to assure low systemic levels. The manufacturer of tobramycin for inhalation states that the product should not be administered concurrently with ethacrynic acid, furosemide, intravenous mannitol, or urea.(1) DISCUSSION: Although systemic absorption of inhaled tobramycin is limited, the manufacturer states that because these diuretics may enhance the risk for aminoglycoside toxicity, they should not be administered concurrently with inhaled tobramycin.(1) |
BETHKIS, KITABIS PAK, TOBI, TOBI PODHALER, TOBRAMYCIN |
| ACE Inhibitors; ARBs/Loop Diuretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The exact mechanism is unknown. The initial hypotensive effect of the ACE inhibitors is mainly the result of suppression of the renin-angiotensin-aldosterone system. The ACE inhibitors inhibit the formation of angiotensin II and angiotensin II receptor antagonists block the action of angiotensin II, thereby lowering aldosterone levels with subsequent sodium and water depletion. Agents such as the loop diuretics that cause sodium and water loss may exaggerate the hypotensive state. CLINICAL EFFECTS: The addition of an ACE inhibitor to a patient receiving a loop diuretic may result in severe postural hypotension. This effect is transient and is not expected to occur during long-term dosing. Symptomatic hypotension may result in patients treated with loop diuretics who are started on an angiotensin II receptor antagonist. Concurrent use of a renin-angiotensin system (RAS) inhibitor with diuretics and NSAIDs may result in increased risk of acute kidney injury (AKI). PREDISPOSING FACTORS: Addition of an ACE inhibitor or an angiotensin II receptor antagonist to a patient already receiving a diuretic or who is sodium depleted. Low water intake/dehydration, drug sensitivity, greater than 75 years of age, and renal impairment may increase an individual's susceptibility to AKI. PATIENT MANAGEMENT: In patients without heart failure, it may be advisable to discontinue the diuretic, reduce the dose of the diuretic, or increase salt intake prior to the initiation of the ACE inhibitor. If hypotension occurs, place the patient in a supine position. Hypotension is most likely when the ACE inhibitor is initiated. However, if subsequent hypotension occurs, a dosage adjustment or discontinuation of one agent may be required. Intravascular volume depletion should be corrected in patients prior to the initiation of an angiotensin II receptor antagonist. Concurrent use of a RAS inhibitor with loop diuretics and NSAIDs should be used with caution and monitored closely for signs of AKI. DISCUSSION: In a computational study, the risk of AKI using triple therapy with a diuretic, renin-angiotensin system (RAS) inhibitor, and NSAID was assessed. The study found the following factors may increase an individual's susceptibility to AKI: low water intake, drug sensitivity, greater than 75 years of age, and renal impairment.(4,5) In an observational study, current use of a triple therapy with a diuretic, RAS inhibitor, and NSAID, was associated with an increased rate of acute kidney injury (rate ratio (RR) 1.31, 95% confidence interval (CI) 1.12-1.53). The highest risk of AKI associated with triple therapy were observed in the first 30 days of use (RR 1.82, CI 1.35-2.46). (6) Severe postural hypotension(1,2) and transient postural hypotension(3) has been reported in patients receiving concurrent captopril and furosemide. The effect is transient and may be more prevalent in patients who are sodium depleted.(8) Reversible renal failure(9) and decreased renal function(10) have been reported in patients receiving concurrent administration with enalapril and furosemide. In a study in which electrolytes were replaced with saline or Ringer's solution, no postural hypotension was noted; however, significant decreases in diastolic blood pressure occurred at three, four, and six hours after concurrent administration.(11) |
ALTACE, AMLODIPINE BESYLATE-BENAZEPRIL, AMLODIPINE-OLMESARTAN, AMLODIPINE-VALSARTAN, AMLODIPINE-VALSARTAN-HCTZ, ARBLI, ATACAND, ATACAND HCT, AVALIDE, AVAPRO, AZOR, BENAZEPRIL HCL, BENAZEPRIL-HYDROCHLOROTHIAZIDE, BENICAR, BENICAR HCT, CANDESARTAN CILEXETIL, CANDESARTAN-HYDROCHLOROTHIAZID, CAPTOPRIL, CAPTOPRIL-HYDROCHLOROTHIAZIDE, COZAAR, DIOVAN, DIOVAN HCT, EDARBI, EDARBYCLOR, ENALAPRIL MALEATE, ENALAPRIL-HYDROCHLOROTHIAZIDE, ENALAPRILAT, ENTRESTO, ENTRESTO SPRINKLE, EPANED, EPROSARTAN MESYLATE, EXFORGE, EXFORGE HCT, FILSPARI, FOSINOPRIL SODIUM, FOSINOPRIL-HYDROCHLOROTHIAZIDE, HYZAAR, IRBESARTAN, IRBESARTAN-HYDROCHLOROTHIAZIDE, LISINOPRIL, LISINOPRIL-HYDROCHLOROTHIAZIDE, LOSARTAN POTASSIUM, LOSARTAN-HYDROCHLOROTHIAZIDE, LOTENSIN, LOTENSIN HCT, LOTREL, MICARDIS, MICARDIS HCT, MOEXIPRIL HCL, OLMESARTAN MEDOXOMIL, OLMESARTAN-AMLODIPINE-HCTZ, OLMESARTAN-HYDROCHLOROTHIAZIDE, PERINDOPRIL ERBUMINE, PRESTALIA, QBRELIS, QUINAPRIL HCL, QUINAPRIL-HYDROCHLOROTHIAZIDE, RAMIPRIL, SACUBITRIL-VALSARTAN, TELMISARTAN, TELMISARTAN-AMLODIPINE, TELMISARTAN-HYDROCHLOROTHIAZID, TRANDOLAPRIL, TRANDOLAPRIL-VERAPAMIL ER, TRIBENZOR, VALSARTAN, VALSARTAN-HYDROCHLOROTHIAZIDE, VASERETIC, VASOTEC, ZESTORETIC, ZESTRIL |
| Furosemide/Aliskiren SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: The exact mechanism is unknown. CLINICAL EFFECTS: Concurrent use of aliskiren may decrease levels and effectiveness of furosemide.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Monitor patients receiving concurrent aliskiren and furosemide for decreased furosemide effects. The dose of furosemide may need to be adjusted if aliskiren is initiated or discontinued, or furosemide may need to be replaced with an alternative diuretic agent. DISCUSSION: Concurrent aliskiren decreased furosemide maximum concentration (Cmax) and area-under-curve (AUC) by 50% and 30%, respectively. There were no significant effects on aliskiren levels.(1) Concurrent aliskiren decreased furosemide Cmax and AUC by 27% and 17%, respectively and 24-hour urinary furosemide excretion was reduced by 29%. There were no significant effects on aliskiren levels.(2) |
ALISKIREN, TEKTURNA |
| Zoledronic Acid/Diuretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Concurrent use of zoledronic acid and a diuretic may have adverse effects on the renal system.(1,2) CLINICAL EFFECTS: Concurrent use of zoledronic acid and a diuretic may result in renal dysfunction. Deterioration in renal function, acute renal failure requiring dialysis, and death have been reported.(1) PREDISPOSING FACTORS: The interaction may be more likely in elderly patients, patients who are taking other drugs that impact renal function, patients with pre-existing renal compromise, and patients who are dehydrated.(1) PATIENT MANAGEMENT: Patients should be adequately hydrated with 500 ml (2 glasses of water) before and after zoledronic acid administration.(1) Creatinine clearance should be monitored before and after therapy and zoledronic acid should not be administered in patients with a creatinine clearance less than 35 ml/min.(1,3) DISCUSSION: Zoledronic acid has been associated with renal dysfunction, including deterioration in renal function, acute renal failure requiring dialysis, and death. Risk factors include advanced age, concomitant nephrotoxic agents, and dehydration.(1) The FDA has received 16 reports of fatal acute renal failure and 9 reports of renal injury requiring dialysis following the administration of Reclast (zoledronic acid).(3) |
RECLAST, ZOLEDRONIC ACID |
| SGLT2 Inhibitors/Loop Diuretics SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: SGLT2 inhibitors cause intravascular volume contraction through osmotic diuresis, which can result in hypotension in patients who are volume depleted from loop diuretic use.(1-7) CLINICAL EFFECTS: Concurrent use of SGLT2 inhibitors with loop diuretics may result in dehydration, hypotension, and acute renal failure.(1-8) PREDISPOSING FACTORS: This interaction may be more severe in patients who have a eGFR of less than 60 ml/min/1.73m2, are also taking ACE inhibitors or ARBs and/or NSAIDs, are on a low sodium diet, have low systolic blood pressure prior to initiating SGLT2 inhibitors, and/or are 65 years of age or older.(1-7) PATIENT MANAGEMENT: Before initiating SGLT2 inhibitors in patients maintained on loop diuretics, assess volume status and correct if needed and also assess renal function. Patients receiving concurrent therapy should be monitored for hypotension and acute renal failure.(1-8) DISCUSSION: In clinical trials of canagliflozin, volume depletion-related adverse effects were associated with the use of loop diuretics, moderate renal impairment (eGFR 30 ml/min/1.73m2 to less than 60 ml/min/1.73m2), and age 75 years and older. In a pool of eight Phase 3 clinical trials, 2.3% of all patients taking 100 mg of canagliflozin experienced at least one volume depletion-related event, compared to 3.2% of patients taking 100 mg of canagliflozin with a loop diuretic. 3.4% of all patients taking 300 mg of canagliflozin experienced at least one volume depletion-related event, compared to 8.8% of patients taking 300 mg of canagliflozin with a loop diuretic.(1,2) Cases of acute renal failure, most requiring hospitalization, have been reported in patients receiving canagliflozin and dapagliflozin. Twenty-six of 101 cases involved concurrent use of diuretics.(7) In a post-hoc analysis of the EMPEROR-Preserve trial, the combination of empagliflozin and diuretics was associated with a higher incidence of volume depletion events (HR 1.34; 95% CI, 1.13-1.59). The most commonly reported events were hypotension, syncope, and dehydration. Coadministration of diuretics and empagliflozin did not result in a difference in the incidence of acute renal failure, hyperkalemia, or adverse events leading to trial discontinuation (including fatal events) compared to empagliflozin alone. There was also no change in the benefit of empagliflozin for the primary end point of first hospitalization for heart failure or cardiovascular death.(8) |
BEXAGLIFLOZIN, BRENZAVVY, DAPAGLIFLOZIN, DAPAGLIFLOZIN-METFORMIN ER, FARXIGA, GLYXAMBI, INPEFA, INVOKAMET, INVOKAMET XR, INVOKANA, JARDIANCE, SEGLUROMET, STEGLATRO, STEGLUJAN, SYNJARDY, SYNJARDY XR, TRIJARDY XR, XIGDUO XR |
| Tizanidine/Selected Antihypertensives SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Tizanidine is an alpha-2 agonist. Concurrent use with antihypertensive agents may result in additive effects on blood pressure.(1) CLINICAL EFFECTS: Concurrent use of antihypertensives and tizanidine may result in hypotension.(1) PREDISPOSING FACTORS: None determined. PATIENT MANAGEMENT: Patients receiving concurrent therapy should be monitored for hypotension. The risk of hypotension may be decreased by careful titration of tizanidine dosages and monitoring for hypotension prior to dose advancement. Counsel patients about the risk of orthostatic hypotension.(1) DISCUSSION: Severe hypotension has been reported following the addition of tizanidine to existing lisinopril therapy.(2-4) |
ONTRALFY, TIZANIDINE HCL, ZANAFLEX |
| Apomorphine/Selected Antihypertensives and Vasodilators SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed. MECHANISM OF ACTION: Apomorphine causes dose-dependent decreases in blood pressure. Concurrent use with antihypertensive agents may result in additive effects on blood pressure.(1) CLINICAL EFFECTS: Concurrent use of antihypertensives and apomorphine may result in orthostatic hypotension with or without dizziness, nausea, or syncope.(1) PREDISPOSING FACTORS: The risk of orthostatic hypotension may be increased during dose escalation of apomorphine and in patients with renal or hepatic impairment.(1) PATIENT MANAGEMENT: Patients receiving concurrent therapy should be monitored for hypotension. Counsel patients about the risk of orthostatic hypotension.(1) DISCUSSION: Healthy volunteers who took sublingual nitroglycerin (0.4 mg) concomitantly with apomorphine experienced a mean largest decrease in supine systolic blood pressure (SBP) of 9.7 mm Hg and in supine diastolic blood pressure (DBP) of 9.3 mm Hg, and a mean largest decrease in standing SBP and DBP of 14.3 mm Hg and 13.5 mm Hg, respectively. The maximum decrease in SBP and DBP was 65 mm Hg and 43 mm Hg, respectively. When apomorphine was taken alone, the mean largest decrease in supine SBP and DBP was 6.1 mm Hg and 7.3 mm Hg, respectively, and in standing SBP and DBP was 6.7 mm Hg and 8.4 mm Hg, respectively.(1) |
APOKYN, APOMORPHINE HCL, ONAPGO |
The following contraindication information is available for LASIX ONYU (furosemide):
Drug contraindication overview.
*Anuria. *Hypersensitivity to furosemide or any component of the formulations.
*Anuria. *Hypersensitivity to furosemide or any component of the formulations.
There are 0 contraindications.
There are 12 severe contraindications.
Adequate patient monitoring is recommended for safer drug use.
| Severe List |
|---|
| Anuria |
| Azotemia |
| Hypocalcemia |
| Hypochloremia |
| Hypokalemia |
| Hypomagnesemia |
| Hyponatremia |
| Hypoproteinemia |
| Hypotension |
| Hypovolemia |
| Metabolic alkalosis |
| Pancreatitis |
There are 10 moderate contraindications.
Clinically significant contraindication, where the condition can be managed or treated before the drug may be given safely.
| Moderate List |
|---|
| Acute myocardial infarction |
| Benign prostatic hyperplasia |
| Bladder outflow obstruction |
| Cardiogenic shock |
| Diabetes mellitus |
| Gout |
| Hearing loss |
| Hyperuricemia |
| Orthostatic hypotension |
| Systemic lupus erythematosus |
The following adverse reaction information is available for LASIX ONYU (furosemide):
Adverse reaction overview.
Adverse effects associated with oral administration of furosemide (categorized by body system and listed in order of severity) are: GI system reactions (hepatic encephalopathy in patients with hepatocellular insufficiency, pancreatitis, jaundice (intrahepatic cholestatic jaundice), increased liver enzymes, anorexia, oral/gastric irritation, cramping, diarrhea, constipation, nausea, and vomiting); systemic hypersensitivity reactions (severe anaphylactic or anaphylactoid reactions, systemic vasculitis, interstitial nephritis, necrotizing angiitis); CNS reactions (tinnitus and hearing loss, paresthesias, vertigo, dizziness, headache, blurred vision, xanthopsia); hematologic reactions (aplastic anemia, thrombocytopenia, agranulocytosis, hemolytic anemia, leukopenia, anemia, eosinophilia); dermatologic-hypersensitivity reactions (toxic epidermal necrolysis, Stevens-Johnson Syndrome, erythema multiforme, drug rash with eosinophilia and systemic symptoms, acute generalized exanthematous pustulosis, exfoliative dermatitis, bullous pemphigoid, purpura, photosensitivity, rash, pruritus, urticaria); cardiovascular reactions (orthostatic hypotension, increase in serum cholesterol and triglycerides); and various other reactions (hyperglycemia, glycosuria, hyperuricemia, muscle spasm, weakness, restlessness, urinary bladder spasm, thrombophlebitis, fever). The most common adverse effects associated with intramuscular or IV administration of furosemide are related to fluid and electrolyte imbalance. Common adverse effects associated with subcutaneous administration of furosemide via infusors include administration site and skin reactions, including erythema, bruising, edema, and infusion site pain.
Adverse effects associated with oral administration of furosemide (categorized by body system and listed in order of severity) are: GI system reactions (hepatic encephalopathy in patients with hepatocellular insufficiency, pancreatitis, jaundice (intrahepatic cholestatic jaundice), increased liver enzymes, anorexia, oral/gastric irritation, cramping, diarrhea, constipation, nausea, and vomiting); systemic hypersensitivity reactions (severe anaphylactic or anaphylactoid reactions, systemic vasculitis, interstitial nephritis, necrotizing angiitis); CNS reactions (tinnitus and hearing loss, paresthesias, vertigo, dizziness, headache, blurred vision, xanthopsia); hematologic reactions (aplastic anemia, thrombocytopenia, agranulocytosis, hemolytic anemia, leukopenia, anemia, eosinophilia); dermatologic-hypersensitivity reactions (toxic epidermal necrolysis, Stevens-Johnson Syndrome, erythema multiforme, drug rash with eosinophilia and systemic symptoms, acute generalized exanthematous pustulosis, exfoliative dermatitis, bullous pemphigoid, purpura, photosensitivity, rash, pruritus, urticaria); cardiovascular reactions (orthostatic hypotension, increase in serum cholesterol and triglycerides); and various other reactions (hyperglycemia, glycosuria, hyperuricemia, muscle spasm, weakness, restlessness, urinary bladder spasm, thrombophlebitis, fever). The most common adverse effects associated with intramuscular or IV administration of furosemide are related to fluid and electrolyte imbalance. Common adverse effects associated with subcutaneous administration of furosemide via infusors include administration site and skin reactions, including erythema, bruising, edema, and infusion site pain.
There are 37 severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
| None. |
Hypocalcemia Hypokalemia Hypomagnesemia Hyponatremia |
| Rare/Very Rare |
|---|
|
Abnormal hepatic function tests Acute generalized exanthematous pustulosis Acute pancreatitis Agranulocytosis Allergic dermatitis Anaphylaxis Anemia Aplastic anemia Bullous pemphigoid Dehydration DRESS syndrome Eosinophilia Erythema multiforme Exfoliative dermatitis Hearing loss Hemolytic anemia Hypersensitivity angiitis Hypochloremic alkalosis Interstitial nephritis Jaundice Leukopenia Obstructive hyperbilirubinemia Ototoxicity Purpura Skin rash Stevens-johnson syndrome Systemic lupus erythematosus Thrombocytopenic disorder Thrombophlebitis Toxic epidermal necrolysis Urticaria Vasculitis Xanthopsia |
There are 34 less severe adverse reactions.
| More Frequent | Less Frequent |
|---|---|
|
Orthostatic hypotension |
Abdominal pain with cramps Anorexia Blurred vision Cramps Diarrhea Dizziness Drowsy Edema Headache disorder Injection site pain Muscle spasm Skin photosensitivity Xerostomia |
| Rare/Very Rare |
|---|
|
Accidental fall Constipation Fever Gastrointestinal irritation General weakness Glycosuria Hypercholesterolemia Hyperglycemia Hypertriglyceridemia Hyperuricemia Mouth irritation Muscle weakness Nausea Nervousness Paresthesia Pruritus of skin Tinnitus Ureteral spasm Vertigo Vomiting |
The following precautions are available for LASIX ONYU (furosemide):
Safety and efficacy of subcutaneous administration of furosemide via on-body infusor have not been established in pediatric patients. In premature neonates, diuretic therapy with furosemide during the first weeks of life may increase the risk of persistent patent ductus arteriosus (PDA). Hearing loss has been reported in neonates receiving furosemide.
Therefore, the manufacturer states that parenteral furosemide dosages should not exceed 1 mg/kg per 24 hours in premature neonates with <31 weeks postconception age (gestational age at birth plus postnatal age), because higher dosages may be associated with potentially toxic plasma concentrations of the drug. Furosemide may precipitate nephrocalcinosis/nephrolithiasis in premature neonates. Nephrocalcinosis/nephrolithiasis has also been observed in patients <=4 years of age with no history of prematurity receiving chronic treatment with furosemide. Monitor renal function and consider renal ultrasonography in pediatric patients receiving furosemide.
Contraindicated
Severe Precaution
Management or Monitoring Precaution
Therefore, the manufacturer states that parenteral furosemide dosages should not exceed 1 mg/kg per 24 hours in premature neonates with <31 weeks postconception age (gestational age at birth plus postnatal age), because higher dosages may be associated with potentially toxic plasma concentrations of the drug. Furosemide may precipitate nephrocalcinosis/nephrolithiasis in premature neonates. Nephrocalcinosis/nephrolithiasis has also been observed in patients <=4 years of age with no history of prematurity receiving chronic treatment with furosemide. Monitor renal function and consider renal ultrasonography in pediatric patients receiving furosemide.
Contraindicated
| None |
Severe Precaution
| None |
Management or Monitoring Precaution
| None |
Available data from published observational studies, case reports, and postmarketing reports over decades of use have not demonstrated a drug-associated risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes with furosemide use during pregnancy. However, untreated congestive heart failure and hepatic cirrhosis can lead to adverse outcomes in both the mother and fetus. In reproduction studies involving rabbits, administration of furosemide caused unexplained abortions and maternal and fetal deaths. In addition, an increased incidence of hydronephrosis occurred in fetuses of animals treated with the drug.
Furosemide is distributed into human milk; there are no data on the effects on the breast-fed infant or on milk production. Doses associated with clinically significant diuresis may impair milk production. The developmental and health benefits of breast-feeding should be considered along with the mother's clinical need for furosemide and any potential adverse effects on the breast-fed infant from furosemide or from the underlying maternal condition.
Clinical studies of furosemide did not include sufficient numbers of patients to determine whether those who were >=65 years of age responded differently from younger patients. Other reported clinical experience has not identified differences in response between geriatric and younger patients. In general, dose selection should be cautious in geriatric patients, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy in this population.
Binding of furosemide to albumin may be reduced in geriatric patients. Furosemide is predominantly excreted unchanged in the urine. Following IV administration, the renal clearance of furosemide is substantially smaller in older healthy male patients (60-70 years of age) compared to younger healthy male patients (20-35 years of age). The initial diuretic effect of furosemide is also generally decreased in geriatric patients relative to younger patients.
Binding of furosemide to albumin may be reduced in geriatric patients. Furosemide is predominantly excreted unchanged in the urine. Following IV administration, the renal clearance of furosemide is substantially smaller in older healthy male patients (60-70 years of age) compared to younger healthy male patients (20-35 years of age). The initial diuretic effect of furosemide is also generally decreased in geriatric patients relative to younger patients.
The following prioritized warning is available for LASIX ONYU (furosemide):
No warning message for this drug.
No warning message for this drug.
The following icd codes are available for LASIX ONYU (furosemide)'s list of indications:
| Peripheral edema due to chronic heart failure | |
| R60 | Edema, not elsewhere classified |
| R60.9 | Edema, unspecified |
Formulary Reference Tool