Kimberly A. Brown, MD, reviews classifying the severity of HE and defines covert vs overt HE.
Arun B. Jesudian, MD: When we classify hepatic encephalopathy [HE], there are a number of ways to do it. For example, there is type A, B, and C. Type A happens in acute liver failure, B is related to vascular malformations like portosystemic shunts, and C is in cirrhosis, which is what we spend the vast majority of our time dealing with. Within type C hepatic encephalopathy, how do you grade the severity, and could you draw the distinction for us between covert and overt hepatic encephalopathy?
Kimberly A. Brown, MD: That’s a great question. When I came up in training, the word covert never entered my vocabulary. It was all overt. It was something that you and I as clinicians could identify in a patient. We’ve used historically the West Haven criteria, grades 1, 2, 3, and 4, where 1 is very subtle and 4 is coma. Then we grade at 2 and 3 in between. We have always tested for asterixis or flapping tremor, but that’s often a moderate to late sign. In somebody with coma you can’t test for that, so I’ll test for hyper-reflexive indices at the wrist or ankle.
But the covert, that’s a really interesting concept. That’s the one by definition you and I can’t tell the patient has just by talking with them. There are some tests [Jasmohan] Bajaj, [MD,] has developed to try to identify those patients, but the testing is somewhat challenging to do in a typical clinic visit. So I think for the most part, we’re looking for the overt in the primary care arena. And subtle changes in the first stage can be even just the family members noticing that personality changes have happened with the patient.
Arun B. Jesudian, MD: Yes. I often ask, if there is a caregiver in the room, what they think about the patient’s mental status, especially in terms of forgetfulness, or confusion, or irritability. Some of those psychiatric adverse effects or mood issues might become apparent to a spouse or a child and not necessarily to the patient themselves who is impaired.
In terms of classification, we can also talk about hepatic encephalopathy as being episodic, or recurrent, or refractory, and then we can further talk about episodes as being either spontaneous or precipitated. Could you give us an idea of, if an episode was precipitated, what sort of other issues going on in that patient might have precipitated an episode of HE?
Kimberly A. Brown, MD: In my practice, and it’s probably very similar in your practice as well, new medications, particularly those that affect the brain function: sedatives, sleeping pills, and narcotics. I think patients’ brains in the setting of cirrhosis are much more sensitive to those effects than perhaps someone in the absence of liver disease would have. But other things include dehydration. Most of our patients are on water pills, so dehydration can occur. If they become sick and have nausea or vomiting, they can become dehydrated while they’re still taking their water pills. Also, too much lactulose. Patients might be having a lot of stools and they’re losing fluid in that way. One of the most common things we see is infection. Even minor infections will precipitate an event. Oftentimes urinary tract infections, ascites peritonitis, almost any other infection will do it as well. Then other things we talk about, too much protein in the diet, I think that’s a myth, don’t you?
Arun B. Jesudian, MD: I do. I agree with you.
Kimberly A. Brown, MD: I was taught as a fellow that we should limit protein in our patients with advanced liver disease. In fact, that’s wrong. We know that we now have to feed these patients because most of them are malnourished. I think that’s one of myths we have out in the community, that we should be restricting protein, when in fact we should be giving it.
Transcript edited for clarity