Furosemide is a potent loop diuretic that has been in clinical use since the early 1960s. It remains one of the most widely prescribed diuretics worldwide due to its rapid onset, strong natriuretic effect, and versatility across multiple conditions. Its mechanism of action involves inhibition of the sodium-potassium-chloride (Na+/K+/2Cl−) co-transporter in the thick ascending limb of the loop of Henle. By blocking this transporter, furosemide significantly reduces sodium and chloride reabsorption, leading to increased urine output and reduction of fluid overload. This pharmacologic action helps relieve symptoms of heart failure, liver disease, renal disease, and hypertension where excess fluid retention plays a central role.
Unlike thiazide diuretics, which act on the distal convoluted tubule, furosemide’s action in the loop of Henle enables a much more pronounced diuresis. This makes it especially valuable in acute and severe cases of oedema, including pulmonary oedema, where rapid fluid removal is critical to patient survival. Its oral bioavailability is variable (40–70%), but it can also be administered intravenously for immediate effect, an important feature in emergency settings.
In addition to its diuretic effect, furosemide causes venodilation shortly after IV administration, which can reduce pulmonary congestion even before diuresis occurs. This vasodilatory effect is thought to be mediated through prostaglandin release. Although beneficial, furosemide is also associated with risks such as electrolyte imbalances (notably hypokalaemia, hyponatraemia, and hypomagnesaemia), dehydration, hypotension, and kidney injury if overused or used in vulnerable patients.
Furosemide is listed on the World Health Organization’s Model List of Essential Medicines and remains a mainstay in guideline-directed therapy for heart failure and other fluid overload states. Its low cost, efficacy, and multiple administration routes contribute to its widespread use across healthcare systems globally.
Furosemide therapy is highly individualised depending on the severity of fluid overload, kidney function, and concurrent medications. Patients should not alter their dose without consulting their healthcare provider.
Close monitoring mitigates most risks. Patients are often advised to maintain dietary potassium intake or receive supplements.
Patients should be counselled about recognising warning signs such as dizziness, palpitations, or reduced urine output.
Patients should avoid over-the-counter NSAIDs unless cleared by their clinician. A full list of medications and supplements should always be provided to healthcare providers.
Overdose: Causes profound diuresis, severe dehydration, electrolyte imbalance, and potential kidney failure. Treatment is supportive with fluid and electrolyte replacement, close monitoring, and sometimes hospitalisation.
Accidental double dose: May lead to transient increased urination and mild dizziness; usually not life-threatening but consult a clinician if symptoms persist.
Missed dose: Take when remembered unless it is close to the next scheduled dose. Do not double up. Maintaining a dosing schedule is important to control fluid overload.
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