India · Oral & IV · Heart Failure · Oedema · Acute Pulmonary Oedema · Paediatric · Lasix · Frusemide · Frusenex
📋 U&E (K⁺, Na⁺, Cr) weekly when stable
📋 Daily weight — target 0.5–1 kg/day loss
⚠️ Hypokalaemia → digoxin toxicity risk
⚠️ Hyponatraemia → confusion/seizures
⚠️ Dehydration / pre-renal AKI
✅ Potassium replacement often needed
✅ Add spironolactone to reduce K⁺ loss
Furosemide (frusemide, Lasix) is a loop diuretic and one of the most widely used drugs in Indian internal medicine, cardiology, and nephrology. It inhibits the Na⁺-K⁺-2Cl⁻ cotransporter in the thick ascending limb of the loop of Henle, producing powerful natriuresis and diuresis. It is first-line for oedema in heart failure, liver cirrhosis (often combined with spironolactone), and nephrotic syndrome, and the drug of choice for acute pulmonary oedema where its rapid IV action can be life-saving. Its important adverse effects — hypokalaemia, hyponatraemia, and volume depletion — require regular electrolyte monitoring.
Oral furosemide has approximately 50% bioavailability (highly variable: 10–100% depending on gut oedema and GI perfusion). The standard conversion is: 1 mg IV furosemide = 2 mg oral furosemide. So 40 mg IV = 80 mg oral. In decompensated heart failure with gut oedema, oral absorption is further impaired — IV furosemide is preferred for initial treatment. Once diuresis is established and the patient is clinically improving, convert to oral at double the IV dose.
IV furosemide is one of the cornerstones of acute pulmonary oedema (APO) management. Standard dose: 40–80 mg IV bolus for a furosemide-naïve patient; 1–1.5× the usual daily oral dose for a patient already on furosemide (e.g. if on 80 mg oral daily → give 80–120 mg IV). Onset of diuresis within 5–15 minutes; venodilatory effect (preload reduction) occurs even faster. Give alongside high-flow oxygen, sitting position, and consider IV nitrates (GTN) or IV morphine (with caution). Monitor urine output hourly and electrolytes 4–6 hours after initial dose.
Diuretic resistance occurs when adequate doses of furosemide fail to produce sufficient diuresis. Causes in India: reduced oral absorption (gut oedema — switch to IV), neurohormonal activation (add spironolactone), hypoalbuminaemia (furosemide binds albumin for delivery to renal tubule — treat hypoalbuminaemia), NSAIDs (reduce renal prostaglandins — stop if possible), and inadequate sodium restriction. Strategies: switch to IV, add metolazone or hydrochlorothiazide (sequential nephron blockade), increase frequency to BD, or continuous furosemide infusion in ICU (2.5–5 mg/hour).