Arun Jesudian, MD: Can you give us a sense of how you work up patients [with hepatic encephalopathy]? When they’re in front of you in the room or on a stretcher, generally speaking, what history, exam, and diagnostic testing do you do?

James Williams, DO, MS, FACEP: It might be helpful to use a quick case that comes to mind. In the emergency department, we have so many patients, typically 8 to 10 patients at a time. One typical scenario is that we’ll get called to a room for a potential code stroke, and somebody will go directly to the CT scan to evaluate these patients because the premise was a stroke due to an altered mental status. The evaluation has to be fairly quick because it’s time sensitive in any of the differentials. One was an 84-year-old obese man. He was obtunded, his blood pressure was normal, his respirations were OK, his heartbeat was 70 [beats per minute]…and his D-stick [blood glucose level] was 187 mg/dL. But because of the altered mental status, he came in as a code stroke. His vitals were stable when I examined him in the CT scan. He didn’t have any lateralized motor findings but clearly had difficulty with his cognition; he wasn’t following commands.

That makes me think that this isn’t necessarily a stroke, though it could be. The primarily evaluation is going to be any other history I can get from caregivers. That’s a huge thing: to find out, whether it’s the caregivers or EMS [emergency medical services], the patient’s baseline mental status. It’s challenging. Patients are living longer with comorbidities, and their baseline may not be what you and I consider normal; they have subtle changes. If we can get any finding of the patient’s baseline, then we can understand what the delta…is from what we’re seeing today.

Once we have that, that gives us our baseline. We’re going to do a complete evaluation. We’re going to get a full panel of labs to look for any dysrhythmias, ACS [acute coronary syndrome], or metabolic derangements, whether it’s DKA [diabetic ketoacidosis], hyperglycemia, hyponatremia. If there’s a GI [gastrointestinal] bleed, you have to consider whether they’re hypovolemic, whether they have sepsis. If we’re getting lactate [tests] and cultures, we have to think about toxic germs and whether they’re actively intoxicated, neoplasms, adrenal crisis, and medication noncompliance. Those are all things we’re evaluating. At the same time, we’re sustaining the patient to the extent they need it. Once some of the labs are back, we’ll address those points.

One thing I want to clarify, and I guess you agree , is that we don’t need a lab to diagnose a hepatic encephalopathy [HE]…. We’ll probably always get it, but that doesn’t have to be elevated to have a patient who has a hepatic encephalopathy. That’s a key thing for everybody to remember.

Arun Jesudian, MD: That’s a fantastic point that. Hepatic encephalopathy is a clinical diagnosis. For a patient at risk, I’ll often know if a patient has cirrhosis, but in your environment you might not. You always have it on your differential diagnosis. We’re looking for signs and symptoms of end-stage liver disease and cirrhosis in combination with altered mental status. We’re assessing things like how alert and oriented the patient is and whether they have asterixis—the flapping tremor that’s characteristic of overt hepatic encephalopathy—which can be helpful in making that diagnosis without the need for a serum ammonia blood test. Unfortunately, that’s an unreliable test.

In our patients with cirrhosis who have altered mental status, we never want to miss another cause. Some things that jumped out to me that we want to rule out are whether they’re thrombocytopenic and coagulopathic, because they can bleed into their brain. I imagine you’re often getting some brain imaging in the emergency department.

James Williams, DO, MS, FACEP: That’s an interesting point, less for medical but more for the logistical practice of medicine. We’re often guarded about utilization of resources, and we want to be prudent with that. You don’t want to get a CT scan on everybody. But clearly, it’s a consideration. These patients aren’t always mobile, and they’re at high risk of falls. That’s the second consideration: do they have intracranial hemorrhage in addition to or as a consequence of hepatic encephalopathy, thrombocytopenia, or coagulopathies? They have a brain bleed now.

Arun Jesudian, MD: Even seizures sometimes need to be ruled out. Infections can cause altered mental status on their own or can exacerbate hepatic encephalopathy. Medications, toxins, looking at a urine [toxicology screen], and taking a history all play a role in ruling out alternative causes of altered mental status and in assessing precipitating factors of HE if that’s truly the diagnosis.

Transcript Edited for Clarity