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Mr. Choudhury, a 45-year-old patient of cirrhosis of liver with oedema, attended hospital for his treatment. Both loop diuretics and thiazide diuretics failed to control oedema when used individually. (a) Explain why these two diuretics failed to respond. Which diuretic is to be used in this case and why? (b) Can acetazolamide be used in this case? Justify. (c) What adverse effects the patient may develop if your choice of diuretic is continued for prolonged period in this patient? (d) Why is the diuretic effect of furosemide blunted by indomethacin? ((2+2)+2+2+2=10

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cirrhosis ascites diuretics

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cirrhosis ascites spironolactone acetazolamide contraindicated hepatic encephalopathy furosemide indomethacin prostaglandins guideline

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https://pmc.ncbi.nlm.nih.gov/articles/PMC7788190

(a) Why did loop and thiazide diuretics fail? Which drug should be used?

In cirrhosis, splanchnic vasodilatation reduces effective arterial blood volume. This activates the renin-angiotensin-aldosterone system, producing secondary hyperaldosteronism.
  • Loop diuretics and thiazides increase sodium delivery to the distal nephron.
  • The excess aldosterone then causes marked sodium reabsorption in the late distal tubule and collecting duct, offsetting their natriuretic effect.
  • Cirrhosis also increases proximal tubular sodium reabsorption, reducing sodium delivery to the sites at which these drugs act.
Use spironolactone, an aldosterone receptor antagonist. It directly counters secondary hyperaldosteronism at the collecting duct, promotes sodium loss, and conserves potassium. It is therefore the preferred diuretic for cirrhotic ascites and oedema. In clinically significant or resistant fluid retention, it is commonly combined with furosemide. Current ascites guidance supports spironolactone as first-line treatment and use of a spironolactone-furosemide combination when faster or greater diuresis is needed, as summarized in these ascites guidelines.

(b) Can acetazolamide be used?

No. Acetazolamide should not be used in cirrhosis.
It inhibits carbonic anhydrase and decreases ammonium ion formation and urinary ammonia trapping. This can increase systemic ammonia and may precipitate hepatic encephalopathy in a patient with impaired hepatic ammonia detoxification. It is also a relatively weak diuretic and is unsuitable for this indication. Hepatic impairment is a listed contraindication because of this encephalopathy risk, according to this clinical drug reference.

(c) Adverse effects of prolonged spironolactone treatment

Important adverse effects include:
  1. Hyperkalaemia, which may cause dangerous cardiac arrhythmias.
  2. Endocrine or antiandrogenic effects, especially in men:
    • Gynaecomastia and breast tenderness
    • Impotence and decreased libido
  3. Menstrual irregularities in women.
  4. Hyponatraemia, dehydration, hypotension, and renal dysfunction can occur with excessive diuresis.

(d) Why does indomethacin blunt the action of furosemide?

Furosemide partly depends on increased renal prostaglandin synthesis, particularly PGE₂ and PGI₂, which dilate renal vessels, help maintain renal blood flow and GFR, suppress tubular sodium reabsorption, and augment natriuresis.
Indomethacin inhibits cyclo-oxygenase, thereby reducing renal prostaglandin synthesis. Consequently:
  • renal blood flow and GFR may decrease,
  • renin release is reduced,
  • sodium retention increases, and
  • the natriuretic and diuretic response to furosemide is diminished.
This interaction is particularly important in cirrhosis, where renal perfusion is already vulnerable.

Furosemide is used in acute pulmonary oedema with left ventricular failure

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acute pulmonary edema furosemide

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acute pulmonary edema furosemide venodilation preload guideline

Furosemide is used in acute pulmonary oedema due to left ventricular failure because it provides rapid relief by two mechanisms:
  1. Immediate effect after IV administration: venodilatation
    It dilates systemic veins before appreciable diuresis occurs. This decreases venous return to the heart, thereby reducing preload, pulmonary capillary wedge pressure, and pulmonary congestion.
  2. Subsequent diuretic effect
    By blocking the Na⁺-K⁺-2Cl⁻ cotransporter in the thick ascending limb of the loop of Henle, it produces powerful natriuresis and diuresis. This reduces circulating blood volume, preload, and pulmonary oedema.
Thus, IV furosemide rapidly lowers raised pulmonary venous pressure and removes excess fluid, improving dyspnoea and oxygenation. Textbook sources describe its acute preload-reducing venodilator action and its role in acute pulmonary oedema.
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