AMS in the ICU and ammonia levels

[Ronin786]

In our ICU, any patient without an obvious cause of AMS gets their ammonia level drawn. It usually comes back slightly elevated and they end up getting some lactulose.

I've searched around regarding this and couldn't really find any sort of basis for it. I understand the pathophysiology of hyperammonemia and hepatic encephalopathy, but in the absence of acute or chronic liver failure or any overt urea cycle disorder, is there really any utility in checking ammonia levels? Especially given the poor correlation between an elevated level and the severity of encephalopathy. Also is this commonplace in other ICUs?

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[deleted171991]

Desperate times call for desperate measures.

Ammonia is useless, it's just one small part of the clinical picture. One can have high ammonia and no HE and the opposite. The dynamic doesn't matter either. The reason seems to be:
1. we don't really know the pathogenesis of HE
2. ammonia levels depend on phlebotomy techniques
3. ammonia is somewhat filtered by the blood-brain barrier, so the relationship with HE and AMS is non-linear.

I haven't worked in an ICU for a while, but yours is not the only one still anchored in the last century. Do they also restrict protein intake?

 

[fakin' the funk]

In our ICU, any patient without an obvious cause of AMS gets their ammonia level drawn... in the absence of acute or chronic liver failure or any overt urea cycle disorder, is there really any utility in checking ammonia levels?

While I'm tempted to answer emphatically NO, this is a patient population as you said "with AMS but without an obvious cause."

I think if you have AMS without an obvious cause after initial H+P, labs, etc., looking for long-shots or zebras is reasonable.

 

[seinfeld]

Best answer is because there is nothing else to go on.

It always annoys me when GI docs order it because it doesn't correlate with the degree of encephalopathy. Some Hepatologists actually debate whether lactulose is EBM, its not the silver bullet many believe it is. In the true HE population the lactulose is titrated to BM's and MS, not the ammonia level.

Next time you have a cirrhotic who is not altered order an ammonia level, order enough of them and youll see the number is meaningless

 

[Nash]

In our ICU, any patient without an obvious cause of AMS gets their ammonia level drawn. It usually comes back slightly elevated and they end up getting some lactulose.

I've searched around regarding this and couldn't really find any sort of basis for it. I understand the pathophysiology of hyperammonemia and hepatic encephalopathy, but in the absence of acute or chronic liver failure or any overt urea cycle disorder, is there really any utility in checking ammonia levels? Especially given the poor correlation between an elevated level and the severity of encephalopathy. Also is this commonplace in other ICUs?

I'm a pulmonary/CCM fellow, and I run in to this issue quite frequently. I would echo much of what has already been said in this thread. Ammonia levels can provide prognostic information in patients with acute liver failure, but I don't routinely check it in encephalopathic patients with known chronic liver disease. As Seinfeld mentioned, patient's with known or suspected cirrhosis and apparent encephalopathy get managed much the same way regardless of their ammonio levels.

I just reread the OP again and realized he was asking about the utility of checking an ammonia level in patients with unexplained AMS and no evidence of acute/chronic liver failure or a known urea cycle disorder. I don't think checking an ammonia level would be terribly useful in this setting. Obviously there are a number of other things that can cause hyperammonemia (GI bleeds, TPN, porto-systemic shunts, valproic acid therapy, salicylate overdose, etc.), but most of these conditions should be apparent. As a side note, I recently took care of a 21 y/o male post-bone marrow transplant patient who developed severe, refractory hyperammonemia (levels >700) related to his chemo regimen. We did trend his ammonio levels, but he was also being treated with IV arginine, hypertonic saline, CRRT, etc. That's obviously a different scenario than the OP referenced.

 

[MikeMerk-MtS]

Just like throwing a hail mary, I guess. But sometimes that's what you need!

 

[Ronin786]

I'm a pulmonary/CCM fellow, and I run in to this issue quite frequently. I would echo much of what has already been said in this thread. Ammonia levels can provide prognostic information in patients with acute liver failure, but I don't routinely check it in encephalopathic patients with known chronic liver disease. As Seinfeld mentioned, patient's with known or suspected cirrhosis and apparent encephalopathy get managed much the same way regardless of their ammonio levels.

I just reread the OP again and realized he was asking about the utility of checking an ammonia level in patients with unexplained AMS and no evidence of acute/chronic liver failure or a known urea cycle disorder. I don't think checking an ammonia level would be terribly useful in this setting. Obviously there are a number of other things that can cause hyperammonemia (GI bleeds, TPN, porto-systemic shunts, valproic acid therapy, salicylate overdose, etc.), but most of these conditions should be apparent. As a side note, I recently took care of a 21 y/o male post-bone marrow transplant patient who developed severe, refractory hyperammonemia (levels >700) related to his chemo regimen. We did trend his ammonio levels, but he was also being treated with IV arginine, hypertonic saline, CRRT, etc. That's obviously a different scenario than the OP referenced.

Thanks for all the replies. My issue was that somebody with a GI bleed might have an elevated ammonia level, but without any renal or liver dysfunction they should still be able to clear that ammonia. Granted most patients in the ICU setting have either or both of those, but in somebody who doesn't, does an elevated ammonia mean anything? Or is it possible to overwhelm the capacity of clearance so much so that mental status is affected?