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Diuretic choice in decompensated liver disease

Posted Mar 31 2010 12:00am
Spironolactone has long been favored in the setting of decompensated liver disease; the effective control of “secondary aldosteronism” is usually given as the reason for this in textbooks. However, this is like saying you should open a new bank account as you’ll receive a nice pen. There are more rational reasons for choosing this agent:

Less renal dysfunction:
This complication of the management of edema in cirrhosis is frequently caused by over-aggressive diuresis, whereby ECF removed from the vascular space is not replaced from the interstitium quickly enough, resulting in renal ischemia.

The rate at which interstitial fluid may transfer to the vascular space is determined, in part, by the surface area of the local capillary network. As such, more than 3L of peripheral edema may be comfortably removed in a day (as in a typical dialysis session) whereas only ~0.5L of ascites can be safely removed (using diuretics) in 24 hours due to the sparse capillary monolayer of the abdominal wall available for fluid transfer. This explains why cirrhotic patients with both ascites and peripheral edema will often tolerate fairly aggressive diuresis up until the point that their peripheral edema has resolved, but quickly develop pre-renal failure thereafter.


Due to its distal site of action, spironolactone is the weakest diuretic. It is because of this that it has been the most successful choice in ascites, with most patients losing 0.5L/day on this agent, allowing systemic resorption of ascitic fluid to keep pace.



Less hypokalemia:
Hypokalemia can precipitate hepatic encephalopathy. During hypokalemia, K moves out of proximal tubular cells into the extracellular fluid, in exchange for H+ to maintain electroneutrality. The increased intracellular pH stimulates the tubular production of ammonia from the amino acid glutamine, resulting in encephalopathy.

Inhibition of effective mineralocorticoid excess
: Bile acids appear to contribute directly to sodium retention in cirrhosis by inhibiting 11 -hydroxy steroid dehydrogenase , allowing cortisol to activate mineralocorticoid receptors, much like in liquorice toxicity . Theorectically, spironolactone directly inhibits this process.

As a final aside, avoid acetazolamide (Diamox) in patients with cirrhosis. Renal ammonia excretion requires protonation of NH3 in the proximal tubule, an event that depends entirely upon bicarbonate resorption. Inhibition of this process with Diamox will also precipitate encephalopathy.
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