Hepatic edema is caused by decreased hepatic protein synthesis, a consequence of decompensated liver cirrhosis. Fluid accumulation occurs when there is an increase in hydrostatic pressure in the hepatic sinusoids and splanchnic capillaries, as well as low albumin. The first-line treatment for cirrhosis-related ascites is an aldosterone antagonist (spironolactone); however, in severe and recurring ascites, a combination of aldosterone antagonists and loop diuretics (torsemide, furosemide, and bumetanide) is preferable. Torsemide outperformed furosemide in terms of natriuretic and diuretic effects at an equivalent dose. Pharmacological features of torsemide, such as lesser hypokalemia effect, longer duration of action, higher bioavailability, and extended half-life, make it a better alternative than furosemide. In clinical studies, it is considered a safer and more acceptable choice with fewer complications.