Furosemide is a very commonly used loop diuretic in current clinical practice. Ototoxicity is a significant side effect which may be transient or permanent. Investigations into the mechanisms of furosemide ototoxicity have used pharmacologic, neurophysiologic, and morphologic methods, but the exact mode of production of ototoxicity is unknown. Aminoglycoside antibiotics potentiate furosemide ototoxicity, but noise trauma apparently does not. Methods of avoiding ototoxicity are suggested including slow continuous infusion rather than bolus injection, use of divided oral dose regimens, and the measurement of blood levels to avoid exceeding 50 mcg/ml of furosemide. If a diuretic response cannot be obtained using the above measures, the substitution of another diuretic such as bumetanide is suggested to maintain the therapeutic response and minimize the ototoxicity.