Formulary
Furosemide: Uses, Dosing, Side Effects and Indian Brand Names
Furosemide is the most potent commonly used diuretic, acting at the loop of Henle to block the NKCC2 transporter, used as first-line therapy for acute pulmonary oedema, decompensated heart failure, and refractory oedema.
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Furosemide: Uses, Dosing, Side Effects and Indian Brand Names
Furosemide is the most potent commonly used diuretic, acting at the loop of Henle to block the NKCC2 transporter, used as first-line therapy for acute pulmonary oedema, decompensated heart failure, and refractory oedema.
NEET PG High-Yield: NKCC2 inhibition at thick ascending limb. Most potent diuretic (25% of filtered Na reabsorbed here). Causes calciURIA (contrast with thiazides which cause calciuria retention / hypercalcaemia). Contraction alkalosis. Hypokalaemia precipitates digoxin toxicity. Ototoxicity with aminoglycosides. Sulfonamide cross-reactivity (structural). Variable oral bioavailability (~50%). Loop diuretics LOSE efficacy in hypoalbuminaemia (furosemide is protein-bound in tubular lumen).
Clinical overview
Furosemide is the most widely used loop diuretic and the cornerstone of acute fluid management in cardiology, nephrology, and critical care. Its potency derives from acting at the thick ascending limb of the loop of Henle, where 25% of filtered sodium is reabsorbed -- far more than the 5-8% at the distal tubule (thiazide site). Furosemide has a steep dose-response curve and a ceiling effect, and its bioavailability after oral administration is highly variable (10-100%, average ~50%). IV furosemide has nearly 100% bioavailability and onset within 5 minutes, making it the agent of choice in acute pulmonary oedema and decompensated heart failure. The venodilatory effect (mediated by prostaglandin release) provides symptomatic relief even before diuresis begins. Furosemide causes significant electrolyte disturbances: hypokalaemia, hyponatraemia, hypocalcaemia, hypomagnesaemia, and metabolic alkalosis (contraction alkalosis). Unlike thiazides, loop diuretics increase urinary calcium excretion (calciuresis), making them useful in acute hypercalcaemia but potentially harmful in osteoporosis. Ototoxicity occurs with high IV bolus doses or concurrent aminoglycosides, and is usually reversible. In India, furosemide is on the NLEM and is ubiquitous in both hospital and primary care settings, often overused in mild oedema where other agents would be more appropriate.
Pharmacological class
Furosemide belongs to the Loop Diuretics class. Inhibits the sodium-potassium-2 chloride cotransporter (NKCC2/Na+-K+-2Cl- symporter) in the thick ascending limb of the loop of Henle, blocking reabsorption of approximately 25% of filtered sodium. This is the most powerful site for diuresis because the thick ascending limb is responsible for generating the corticomedullary osmotic gradient. Also increases renal prostaglandin synthesis, contributing to renal vasodilation.
Indian brand names and formulations
Available as: Lasix (Sanofi), Frusenex (Glenmark), Frusemide (various generic), Furoped (Ipca).
Tablets: 20 mg, 40 mg, 80 mg. Injection: 10 mg/mL (2 mL ampoule = 20 mg). Oral solution: 10 mg/mL (paediatric).
Regulatory status
Furosemide is classified under Schedule H in India under the Drugs and Cosmetics Act, 1940. Prescription-only. Listed on NLEM. Available at Jan Aushadhi centres.
Indications
- Acute pulmonary oedema
- Decompensated heart failure (fluid overload)
- Resistant hypertension (adjunct, not first-line)
- Acute and chronic renal failure (to maintain urine output)
- Acute hypercalcaemia (with saline rehydration)
- Ascites in liver cirrhosis (with spironolactone)
- Cerebral oedema (adjunct)
Dosing
Oral: 20-80 mg once or twice daily; may increase by 20-40 mg every 6-8 hours as needed. IV: 20-40 mg bolus; in acute pulmonary oedema, may give up to 80-120 mg. Maximum recommended: 600 mg/day (higher doses used in severe renal failure). IV infusion: 5-40 mg/hour for refractory cases. IV bolus should not exceed 4 mg/min (ototoxicity risk).
Contraindications
- Anuria unresponsive to a test dose of furosemide
- Severe hyponatraemia or hypokalaemia (correct first)
- Hepatic encephalopathy (may worsen due to alkalosis and hypokalaemia)
- Hypersensitivity to sulphonamides (structural cross-reactivity, though clinically rare)
Adverse effects
- Hypokalaemia (most clinically significant -- can precipitate digoxin toxicity and arrhythmias)
- Hyponatraemia
- Metabolic alkalosis (contraction alkalosis from loss of H+ and Cl-)
- Hypocalcaemia (unlike thiazides which cause hypercalcaemia)
- Hypomagnesaemia
- Ototoxicity (dose-related, usually with rapid IV bolus >4 mg/min; potentiated by aminoglycosides)
- Hyperuricaemia and gout (competes with uric acid for secretion in proximal tubule)
- Hyperglycaemia (less than thiazides)
Drug interactions
- Aminoglycosides (gentamicin, amikacin): additive ototoxicity and nephrotoxicity
- Digoxin: furosemide-induced hypokalaemia potentiates digoxin toxicity
- ACE inhibitors: first-dose hypotension; withhold furosemide 2-3 days before starting ACEI, or start at low ACEI dose
- NSAIDs: reduce diuretic efficacy (prostaglandin inhibition reduces renal blood flow)
- Lithium: reduced lithium clearance, risk of toxicity
- Cisplatin: additive nephrotoxicity and ototoxicity
Pregnancy and lactation
Category C. Crosses the placenta. May cause foetal electrolyte disturbances. Use only when oedema is causing maternal morbidity. Not routinely used for gestational oedema.
Exam-style clinical scenario
A patient with known heart failure presents to the emergency department with acute dyspnoea, orthopnoea, bilateral crackles, and SpO2 88%. CXR shows bilateral pulmonary oedema. What is the first-line drug? IV furosemide 40-80 mg -- provides immediate venodilation (preload reduction) followed by diuresis within 5 minutes.
Cost in India
Rs 5-15 for a strip of 10 tablets (40 mg). IV ampoules: Rs 5-10 per 20 mg/2 mL ampoule.
Clinical governance
Author: MedNext Editorial Team. Clinical reviewer: Awaiting clinical review. Jurisdiction: India (Drugs and Cosmetics Act, 1940). Sources: CIMS India, Indian Pharmacopoeia. Publication state: Awaiting clinical review. Correction: Report errors at support@mednext.academy.
Frequently Asked Questions
Why does furosemide cause hypocalcaemia while thiazides cause hypercalcaemia?
In the thick ascending limb, the NKCC2 transporter creates a lumen-positive electrical potential that drives paracellular calcium and magnesium reabsorption. Furosemide blocks NKCC2, abolishing this potential, and calcium is lost in the urine. Thiazides act at the distal convoluted tubule where they block the Na-Cl cotransporter; the resulting decreased intracellular sodium enhances basolateral Na+/Ca2+ exchange, increasing calcium reabsorption from the lumen.
Why is IV furosemide given slowly?
Rapid IV bolus (>4 mg/min) increases the risk of ototoxicity. Furosemide inhibits the Na-K-2Cl cotransporter in the stria vascularis of the cochlea (same NKCC1 transporter family), disrupting endolymph ion composition. Slow infusion achieves the same diuresis with lower peak drug levels in the cochlea. This risk is additive with aminoglycosides.
What is diuretic resistance and how is it managed?
Diuretic resistance occurs when increasing doses fail to produce adequate diuresis. Causes include poor oral absorption (switch to IV), post-diuretic sodium retention (give twice daily or continuous infusion), distal nephron hypertrophy (add a thiazide for sequential nephron blockade -- metolazone + furosemide), hypoalbuminaemia (furosemide is protein-bound in the tubular lumen), and NSAID use. Sequential nephron blockade is a high-yield NEET PG concept.
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