Secondary prevention in cirrhosis

Today’s topic we picked from many candidates. My team worked 24 hours and we had 8 admissions. I asked the team (who are reading this blog) which topic today’s entry should stress. We chose the use of medications to prevent or treat complications of cirrhosis.

We discussed four conditions: (1) ascites; (2) variceal bleeding; (3) encephalopathy; and (4) spontaneous bacterial peritonitis. This entry represents my opinions – I encourage additions or disagreements from readers.

1. Ascites – ascites represents the combination of portal hypertension and decreased synthetic function. The patients develop decreased effective intravascular volume and subsequently secondary hyperaldosteronism.

My approach – I was taught many years ago to measure urine sodium and potassium. Patients with secondary hyperaldosteronism have a low urine sodium and high urine potassium. Other authors have suggests calculating the transtubular potassium gradient, but I have used the simpler technique successfully for over 30 years.

Once I document secondary hyperaldosteronism I start spironolactone. I usually start with 100 mg once daily. I then check the urine sodium and potassium again. If the urine sodium is now greater than the urine potassium, I can start a loop diuretic (usually furosemide 40 mg.) If not, I will double the spironolactone dose to 200 mg. In cirrhosis one can go as high as 450 mg daily.

Many patients will need daily diuretics for cirrhosis.

Caution - remember that we use much lower doses for heart failure – 25 mg daily.

2. Variceal bleeding – this represents another complication due to portal hypertension. Non-selective beta blockers can decrease the probability of variceal bleeding. I reserve beta blockers for patients who have had a bleed and have at least moderate varices on visualization. I prefer nadolol (start with 20 mg and titrate to a pulse around 60) because it works as a once daily drug.

3. Encephalopathy – while experts still debate the etiology of encephalopathy, we use serum ammonia levels as a surrogate for the neurotoxin. Our first line treatment and prophylaxis remains lactulose (although some argue against it.) Lactulose works by acidifying the stool, those trapping NH3 to NH4+. Our goal is 3 stools daily – titrate the lactulose dose to achieve this. The package insert suggests pH testing of the stool, but I have never seen this done.

When lactulose does not work, we add antibiotics. 30 years ago we used oral neomycin, a poorly absorbed aminoglycoside. The theory is that antibiotics change the bacterial flora, decreased toxin production. Other antibiotics used in 2008 include metronidazole, vancomycin, or rifaximin. I usually use metronidazole in the hospital when lactulose alone is not clearing the encephalopathy. I do continue the lactulose.

For outpatients I suggest using the number connection test to diagnosis subtle encephalopathy. This link goes to a drug company sponsored site – but I really like the test anyway -PSE-Test

4. Spontaneous bacterial peritonitis – most experts recommend antibiotics to prevent SBP I check each year with Sanford to find the currently accepted regimen. Currently I have used either weekly ciprofloxacin or 5 times a week trimethoprim-sulfamethoxazole.

Our discussion did not include other preventive measures like protein restriction and sodium restriction. Today we discussed cirrhosis 101. Perhaps later this week we will get to cirrhosis 201.

I hope this overview is helpful.