Nursing care
Ammonia Level: reading the number and acting on it
Written and reviewed by Dana Whitfield, RN, MSN · 4 min read · Updated September 2026
Short answer
A raised serum ammonia usually reflects hepatic failure and correlates loosely with the degree of encephalopathy. It does not confirm or exclude encephalopathy on its own, since clinical grading matters more. Treatment is lactulose titrated to two or three soft stools a day, never titrated to chase a target ammonia value.
Why this value is ordered
Ammonia is drawn when a patient with known or suspected liver disease develops confusion, asterixis, or a falling level of consciousness. The liver normally converts ammonia, a byproduct of protein breakdown by gut bacteria, into urea for renal excretion. When hepatocytes fail or blood bypasses the liver through portosystemic shunting, ammonia accumulates and crosses into the brain.
It is also checked in patients with cirrhosis who present atypically, in anyone with unexplained altered mental status and risk factors for liver disease, and sometimes in suspected inborn errors of urea metabolism in younger patients. It is not a routine admission blood test and ordering it without a clinical reason to suspect hepatic encephalopathy adds little.
Interpreting the number in context
Normal venous ammonia sits roughly between 15 and 45 micromol/L, though reference ranges vary by lab and assay. The number matters far less than the trend and the patient in front of you. A level of 90 in an alert, oriented patient is less urgent than a level of 60 in someone who cannot name the month.
This is the detail worth remembering for practice: ammonia correlates with encephalopathy imperfectly. Some patients with grade 3 encephalopathy have near-normal levels; some with mildly raised levels are lucid. Grade the patient clinically, using the West Haven criteria or your unit's equivalent, and use the ammonia level as supporting evidence, not as the diagnosis itself.
Critical values and what to do
There is no single agreed critical threshold the way there is for potassium or glucose, but a sharply rising ammonia alongside a deteriorating Glasgow Coma Scale is an emergency. Falling level of consciousness with a compromised airway takes priority over the lab value. Protect the airway, position the patient to reduce aspiration risk, and escalate.
Report a marked rise to the prescriber promptly, along with the neuro exam that goes with it. Check for precipitants: gastrointestinal bleeding, constipation, infection, a new sedative or opioid, hypokalemia, or dehydration. Correcting the trigger often does more for the ammonia than any single dose of medication.
Related tests read alongside it
Liver function tests, albumin, and prothrombin time or INR describe how the liver itself is failing. A basic metabolic panel checks for hypokalemia and alkalosis, both of which raise renal ammonia production and worsen encephalopathy. A complete blood count screens for infection or occult bleeding, either of which can precipitate a hepatic encephalopathy episode.
In a patient not known to have liver disease, a raised ammonia with normal liver enzymes should prompt a look at medication history, particularly valproic acid, and consideration of a urea cycle disorder. Stool for occult blood is worth checking too, since a gastrointestinal bleed delivers a large protein load to the gut and can tip a compensated cirrhotic into overt encephalopathy.
Nursing implications
Lactulose is the mainstay, and the target is stool frequency, not a number on a lab slip. Titrate the dose to produce two to three soft, formed bowel movements a day. Too little and ammonia-producing bacteria keep working; too much causes watery diarrhea, dehydration, and electrolyte loss that can itself worsen encephalopathy.
Document mental status at every assessment using a consistent scale so trends are visible across shifts, not just the isolated ammonia value. Watch for asterixis, track intake and output, and hold sedatives where possible since they mask the neuro exam you need. Rifaximin is often added for patients who do not respond adequately to lactulose alone, and protein restriction is no longer standard practice for most patients since adequate nutrition supports recovery better than restriction does.
What patients ask about it
Patients and families often ask why the level does not match how confused the patient seems, or why a normal result does not rule out the diagnosis. Explain that ammonia is one piece of evidence among several, and that the exam in front of them tells the fuller story.
They also ask why lactulose makes them go to the toilet so often, and whether that is a side effect to worry about. It is not a side effect; it is the mechanism. The medication works by flushing ammonia-producing bacteria and their byproducts out through the bowel, and the stool count is exactly how you know it is working.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our gastrointestinal practice questions are the closest set to what this page covers.
Common questions
What is a normal ammonia level?
Roughly 15 to 45 micromol/L in venous blood, though the exact range depends on the lab and assay used. Always check the reference range printed on the result rather than a remembered number.
Does ammonia level correlate with hepatic encephalopathy severity?
Only loosely. Some patients with severe encephalopathy have near-normal ammonia, and some with high levels are clinically well. Grade encephalopathy by clinical exam and use the ammonia trend as supporting information.
How do you titrate lactulose?
To two or three soft, formed bowel movements a day, adjusting the dose up or down based on stool count and consistency, not the ammonia number. Watch for dehydration and hypokalemia if stooling becomes excessive.
Why would ammonia be high with normal liver function tests?
Consider medications, particularly valproic acid, gastrointestinal bleeding, severe constipation, or a urea cycle disorder, especially if the patient has no known liver disease. A raised ammonia is not always hepatic in origin.
Should protein intake be restricted in hepatic encephalopathy?
No, not routinely. Current practice favors adequate protein intake to support recovery and prevent muscle wasting, with restriction reserved for rare, treatment-resistant cases and only under specialist guidance.