Lab Testing "Ammonia"

[rpooo]

Since not all persons with cirrhosis are affected by elevated ammonia levels what’s the point in the test? Some persons are greatly affected with slightly elevated ammonia levels while others with experience no symptoms of hepatic encephalopathy with high ammonia levels or vice versa. Seeming that the test is irrelevant or at least this is the way of thinking by my hepatologist during my most recent visit to the transplant center in my area.

So why do we even talk about it?

My thinking is the test is relevant since it is a toxic chemical traveling through the blood stream and treatment for high ammonia levels is pertinent at some point whether HE is present or not.

Though not everyone is affected by HE I am not so lucky. My labs have included this test for the last three years and I know what level is normal for me.

Well just thinking "out-loud" wondering if these point are worth mentioning. Any thoughts are appreciated.

Randy

[Dee1956]

An NG tube? yuck!

[Dee1956]

So glad you explained, I was wondering......
I take lactulose as a preventative.  A doctor on here a couple of years ago recommended it.
Hector always has the very best answers
Dee

[rpooo]

Hector thank you so much for your terrific elaborate answer. I guess I should trust they are doing their best for me. I am always skeptical when starting out with a new doctor and this was only my second visit. I'm still getting use to the transplant center Vs. private practice doctors where being skeptical is in many cases important.

I accidently clicked best answer for Dee while looking this over. Ha ha I'm confident with a bit of research Dee would have done a great job also :)

Randy

[HectorSF]

The ammonia test is but one tool of many for assessment of hepatic encephalopathy (HE). A patient's history of liver disease (cirrhosis and portal hypertension) is the best indicator that a patient may have had an HE episode.

Most ammonia is produced in the intestine during the breakdown of nitrogenous compounds. Which is why patients with overt HE are advised to avoid red meats which during digestion create a lot of ammonia.  Other sources of serum ammonia are the kidneys and skeletal muscle. Normally, ammonia is metabolized by the liver. When the liver function is impaired, shunting of blood around the liver, and increased muscle wasting all lead to increased serum ammonia levels in cirrhotic patients.

But ammonia isn't the only toxin involved in HE. Certain amino acids and manganese are also involved and perhaps others.

So an ammonia blood result doesn't necessarily corresponding with HE or the degree of HE but is is a very convenient and easy test to perform to confirm HE. Ammonia is obviously much easier to measure than neurological function. Cognitive performance tests are complex and expensive tests to measure impairment of brain function and there still isn't an agreed upon standard at this time. Of course this assumes the patient in not in a stupor or coma and can take a test. So there is no way for an ER doctor to now what happened to the patient unless it is known that the patient has cirrhosis/portal hypertension and a history of at least Minimal HE.

For all patients hospitalized where episodic HE is suspected it is vital to search for the factor(s) that triggered the HE episode. A complete blood count, electrolyte levels, and renal function are looked at. If the patient is conscious they are asked if they used opiates or sedatives. An NG tube in the stomach and a stool sample will be taken to look for gastrointestinal bleeding from varices. Also dehydration. constipation and infections are also a common cause of a serious HE episode.

Cheers!
Hector