Episode 129: Encephalopathic Disorders

All right, welcome to another episode of the Physician Assistant Exam Review Podcast. I’m so excited to have you here today because we’re moving on from cranial nerves, which is really my number one priority. My name is Brian Wallace. I’m the host and creator here at Physician Assistant Exam Review, and I am having an absolute blast. One of the main reasons is that I’m bringing on, like I told you before, coaches for the 33 Days program. And working with these people, even just a little bit, has been so much fun. They are energetic.

They are interested. They are dying to give back and help students who are struggling the way that they were and now have gone on to do amazing things with their lives. It’s been so much fun getting back in touch with them, hearing what’s happened to them, where they’ve been, where they’re going. It’s just been, like I said, just an absolute blast. Today is Tuesday, March 18th. So if you are interested in joining us for the April cohort, there’s still a few slots left, but registration does close out tomorrow. And that will, because we’re going to go ahead and get started getting everybody into it this weekend, we’ll have our first meeting the week before April 1st to make sure everyone’s set up and ready to go.

And then April 1st, we will be off and running. If this is not a good time for you, if you think you want to do it in the future, I usually run these or I do run these every other month. It gets a little weird towards the end of the year because December is not a good time for anybody to do it. Plus they don’t offer the exam in December. But if you’re looking at doing it in the future and making plans, I do offer them every other month. So I think it’s April, it’s June, then August. And then you’d have to go and look at the website because it gets a little funky there to try to make it work out at the end of the year so that we fit everything in the way that we want to.

But that is that. And so if you’re interested in more than content, if you’re interested in becoming the best student, you can possibly be, if you’re interested in learning to retain more faster with less studying. If you’re interested in getting higher scores just by showing up because you’ve got better skills. If you’re interested in getting rid of imposter syndrome and you’re interested in feeling like you belong, feeling like you people decided and chose you to be in your cohort for a reason. If you’re at risk or you know someone who’s been labeled at risk, please, please, please get them some information on this program. We’ve just been able to do some amazing things and I want to be able to do that for more people moving forward. Anyway, today we are going to be covering encephalopathic disorders.

This is going to be a good one. Encephalopathic disorders. So this should be a lot of fun, at least better than cranial nerves. Real quick, these are brain dysfunctions, commonly caused by things like metabolic issue, toxins, infectious problems, inflammation problems, those kind of things. The key to these is going to be differentiating them from each other. Right, and from other cognitive issues. That’s where your questions are going to come from.

That’s how things are going to work here.

Let’s jump into some priming questions. What is the hallmark distinguishing feature of Wernicke’s encephalopathy? What’s the hallmark distinguishing feature of Wernicke’s encephalopathy? How can hepatic encephalopathy be differentiated from other causes of altered mental status? How can hepatic encephalopathy be differentiated from other causes of altered mental status? So that’s the key, right? We need to separate out these from other types of altered mental status and from each other.

What is the classic EEG finding in metabolic encephalopathy? What’s the classic EEG finding in metabolic encephalopathy? Which toxins are most commonly implicated in toxic encephalopathy? Those are fantastic questions. Really, really should lock in for you what we have to do moving forward. And at the end, hopefully you’ll be able to get those if you can already. First one we’re going to do is Wernicke’s encephalopathy.

This is acutely reversible neurologic syndrome due to vitamin B1 deficiency, also known as thiamine. So this is commonly seen, and this is really key in alcoholics, people who are malnourished. And then the other big one is in post bariatric surgery. Those are the big ones. So there’s a B1 deficiency, usually due to malnutrition, alcoholics. And if I remember correctly, it always confused me that alcoholics had this. And it wasn’t that the alcohol was the problem.

It was that they don’t eat. It’s that they become malnourished if you’re a severe alcoholic. I think that was the connection. And that took me a while to understand because I was kind of like, I don’t get why this would be an issue for alcoholics in particular. And the answer was it’s not really. It’s just that it’s more people who don’t pay attention to food. So they become malnourished, which might be my children.

Some days I just can’t get them to eat anything, which is so weird to me. Anyway, clinical presentation, the classic triad for Wernicke’s encephalopathy. This is something you should absolutely know. If anything is called a classic triad, I would hold on to that. That would be a flashcard for me. It’s ataxia. Here’s a good word for you.

Ophthalmoplegia. I think I got it. And confusion. So ataxia is impaired coordination and gait stability. Ophthalmoplegia is weakness or paralysis of the eye muscles. We just finished the cranial nerves, so you’d have to be able to differentiate there. Hopefully they won’t put these up against each other on a test question.

That would be mean. Confusion, obviously you know what that means. This may also progress to Korsakoff syndrome, which is, if this is ongoing, you get an irreversible amnesia with confabulation, meaning that they start to create these fake memories that they don’t know that they’re having. Also kind of sounds like my children. Lab studies. I told you to clean this up. No, you didn’t.

I did clean it up. Never mind. Lab studies and imaging. The mammillary body atrophy is a late finding. Don’t know if you’ll need that. This is a clinical diagnosis. Thiamine levels may be low, but are not required for the diagnosis.

It’s going to be really through that classic triad of presentation. Treatment and management. As you can imagine, the key here is to replace thiamine, to replace vitamin B1. So we’re going to do IV thiamine. But here’s the important part of this that you absolutely have to hold on to. And I can totally see this being a test question. If I were writing questions, this would be a great question.

You have to give it before glucose. And the reason is that metabolizing glucose requires thiamine. So you get lactose and then lactic acid buildup. So you get lactic acidosis if you give glucose without thiamine, and that can cause more severe issues and can lead to screwing up your diagnosis and more severe issues for the patient, right? Because you still get confusion. You get mental status changes, all those things, because of the lactic acidosis that you have now created. So it’s important to remember that for this part.

All right, let’s keep moving. Hepatic encephalopathy. This is an issue due to accumulated ammonia and neurotoxin in liver failure. This can happen secondary to a GI bleed, an infection, dehydration, or to sedatives. Clinical presentation, altered mental status, asterixis, which is the flapping tremor of the hands. This is really important for hepatic encephalopathy. You’ll see it in other places.

In fact, you’ll see it in other places today. But it really is the hallmark for hepatic encephalopathy that it should send off alarm bells for you. And if you see asterixis, that flapping tremor of the hands, you should be thinking hepatic encephalopathy until proven otherwise. They can have hyperreflexia, exaggerated deep tendon reflexes, lab studies and imaging. So serum ammonia, often elevated, but does not correlate with severity. Liver function tests, they’ll show an elevated AST, ALT, bilirubin, and INR. For your electrolytes, you get hypokalemia, metabolic alkalosis, can worsen the symptoms.

You’re going to get a CT or an MRI to rule out other issues because you’re looking at this altered mental status, but it’s not obviously going to show you hepatic encephalopathy. Treatment and management, first line is going to be lactulose, which reduces ammonia absorption. Second line is going to be rifaximin, which also reduces ammonia-producing gut bacteria. The biggest issue is we’re going to correct the underlying issue. So if they have an infection, if they’re on sedatives, if they’re on something that’s causing this, we’re going to stop that. Again, that asterixis really strongly suggests hepatic encephalopathy, so pay attention to that. Moving right along, toxic and metabolic encephalopathy.

This is encephalopathy secondary to systemic illness, metabolic issues, or toxins, right? So what are our common causes here? This was one of our priming questions. Think for a second. What are our common causes of metabolic or toxic encephalopathy? Well, we just said before, to be sure to give thiamine before glucose, right? Because a common cause of encephalopathy is hypoglycemia.

So glucose is a mainstay of treatment. You can also be caused by hyperglycemia, by hypoxia, by uremia, by drug overdose, by opioids, benzodiazepines, sepsis, all these things, right? Clinical presentation is going to be changes in mental status. Hyperreflexia, like we just said before. Myoclonus would be sudden brief involuntary muscle jerks. Lab studies and imaging. EEG shows generalized background slowing.

This is a classic finding for metabolic encephalopathy. So write that down. Underline it. Generalized slowing. Triphasic waves may be seen in a hepatic or uremic encephalopathy, so they help show us that there’s an encephalopathy, but they don’t that doesn’t the triphasic waves don’t really differentiate it for us, so that’s not going to help us in a test question. You’re going to want to check, obviously, glucose levels, a complete metabolic panel, so glucose, sodium, potassium, calcium, and renal renal and liver function abnormalities. You’re going to be looking for all of that to try to figure this out, right?

So, when you think about this, I’m listing all of these, for each individual diagnosis, but you’re going to see a patient walk through the door with altered mental status. So then you’re going to have to do these things in order to differentiate what’s going on, what’s causing this altered mental status. So the fact that you’re going to do an EEG, the fact that you’re going to do a complete metabolic panel, that all might be just part of what you do when you have someone walk in in this state, depending on what kind of state they’re in. You might get an ABG, which may show acidosis, hypoxia, hypercapnia. All of those things could be causing this, right? So you’re sort of just looking for your cause. If you think it may be sepsis, you’re going to get a blood culture, right?

And again, that CT or MRI of the brain not really going to help us for toxic or metabolic encephalopathy, but is going to help us to rule structural issues out, to rule tumors out, to rule masses out, to rule out all of these other issues, all of these other things. So there’s a good chance you order one. Treatment and management. So obviously, what’s going to be our main thing for treatment here? What am I obviously going to say for our first line of treatments? It’s addressed the underlying cause. If you have hypoglycemia, give glucose.

They need oxygen, give oxygen. If the electrolytes are not balanced, we’re going to balance electrolytes, right? So all of these things are based off of what we find the issues to be. Then we’re going to tune them up and then supportive care in the meantime. So we’re going to be looking for those reversible causes so we can fix them because they are, I don’t want to say easy, but we have labs. We have ways of showing. We have ways of demonstrating.

So if you find things that are off, let’s tune those up and assume that that’s the problem until we find something more tangible. What was the EEG finding? Do you remember for metabolic encephalopathy? Background slowing.

Let’s talk about uremic encephalopathy. This occurs in advanced renal failure due to accumulation of uremic toxins, common in patients with end-stage renal disease who are either missing dialysis or having some kind of problem with dialysis. So for clinical presentation, again, altered mental status, myoclonus. They can get to seizures. Asterixis is also possible here, but really I want you to think about hepatic encephalopathy, not uremic encephalopathy. Could they put it on there for uremic? Yes, they could.

But I would think, I don’t know, 75% to 80% of the time on an exam, it’s going to indicate hepatic. Lab studies and imaging, you can get an elevated BUN and creatinine. This is the hallmark of renal failure, right? So typically a BUN over 100 and creatinine greater than 10. That’s bad, right? That’s pretty severe, but that’s end-stage renal disease. You can get electrolyte abnormalities.

And again, you may show that generalized slowing or triphasic. So this is going to fall really, I pulled this one out. I pulled uremic encephalopathy out. I could have just said that it’s encompassed within toxic and metabolic encephalopathy, but I just, I don’t know. I felt like it should get its own discussion. So that’s why you see that slowing, generalized slowing here as well and some of those same symptoms. And labs.

Treatment and management. So what’s the treatment and management going to be for uremic encephalopathy? Pretty simple. It’s going to be urgent dialysis. Like do it right now. That’s the definitive treatment. We’re going to correct any electrolyte imbalances and we’re going to watch for seizures and treat with antiepileptics if necessary.

They will get better with dialysis. That’s the nice thing here. And just like that, we’re to hypertensive encephalopathy. You wouldn’t imagine how long this takes me to put together for how quickly we go through it. I’m not even going to give you the time involved because you would be hysterical. Hypertensive encephalopathy. This is a severe hypertension leading to cerebral edema and dysfunction.

Severe hypertension leading to cerebral edema and dysfunction. This is part of your hypertensive emergency situation. When I talk about this, the blood pressure’s got to be like over 180, over 120 at least to cause these symptoms. So what do you think they come in with with a hypertensive encephalopathy? Take a guess. I’ll give you two guesses. And please start with altered mental status.

Excellent. They have altered mental status. They have severe headaches, vomiting, seizures, and papilledema, which is that optic disc swelling due to increased intracranial pressure is also possible.

Now, if you have someone come in with severe headaches, altered mental status, there’s a good chance you’re going to get a head CT, right? Because you’re going to want to rule out a stroke. We’ve been talking about strokes. So, you have to think about this in context. These are easy questions when all we’re talking about are encephalopathies. But when you’re talking about the whole world of problems, you have to separate everything out. So, that’s whether you’re in the office or on your exam.

What do you think the treatment is for a hypertensive encephalopathy? Hopefully you don’t need me to tell you this. What’s the treatment for hypertensive encephalopathy? Lower the blood pressure.

All right, so we’re going to lower the blood pressure. We’re going to do it gradually, usually with IV medications, nicardipine, labetalol, clevidipine, that sort of thing. So we want to lower the blood pressure gradually. We want to avoid rapid blood pressure drops to prevent ischemia because you can cause other issues there. So it’s going to be a slow reduction in blood pressure.

Fantastic. All right, so just real quick at the end of this, I just want to run, do a quick summary of everything that we talked about. Actually, let me do that. Let me move this down. We’ll do that after. We’ll talk about the summary and then we’ll talk about the priming questions. But first I want to talk about the study tip, our study tip for today.

I’m a big fan of Jim Rohn. If you haven’t discovered him yet, he was, unfortunately he passed away, a fantastic human being, gave unbelievable discussions on things. One of the things I recently saw him talking about was the idea. I think I might’ve shared it here. I can’t remember. Of how you get paid, what you get paid for. And the idea was that you do not get paid for a time.

You get paid for value, right? Because if you got paid for time, then you just wouldn’t have to do anything when you got there. You get paid for value. You get a return on value. So you get more valuable as time goes on. You’re in school to become more valuable per hour of unit time worked, right? But it’s really about that.

So anyway, that’s the kind of thing he talks about. It’s just a little bit different ways of thinking about things. The specific thing I wanted to cover today that he makes me think about was what he called majoring in minors. And I’ve been noticing a problem in myself that I only recently, after years and years of majoring in minors on it, I think I just solved it over the last, I don’t know, 30 days or so. And when Jim Rohn talks about majoring in minors, what he’s talking about is we spend so much time mired in the details and the little things that we don’t actually act, that we don’t do anything because we’re so concerned about all the little pieces. And it’s kind of the idea that we don’t have to have all the lights green before we get started on the entire trip, right? So, if you’re going to plan a trip from here to the grocery store, you don’t wait till every single light is green to get started.

You just start moving, right? All the pieces don’t have to be perfect. Everything doesn’t have to be in line for things to work. And I apply that to a lot of times when I’m working with students. They’ll come to me very concerned about some minor, minor detail. And they will go around in circles for weeks, stuck on this thing. And again, I do it to other areas of my life.

I’m not trying to berate anyone. I’m just trying to point it out to you and to me, as I constantly do, that they will be looking for something. And one example of this, it’s not a fantastic example. But one example is I’ll have students I’m working with for the PANRE, right, and they’re trying to get ready for the PANRE. And they’re very concerned. They spend a lot of time on the differences in the blueprint and when they go through their review books and the thing, the review books are geared for the PANCE, not necessarily the PANRE. So how is that different for them?

And although it matters, it matters, let’s say like 1%. So if you spend an hour on a topic like that, it’s probably worth it out of 200 hours, you’re going to spend studying or 300 hours, you’re going to spend studying. But if you spend 10 hours on it, you’ve wasted so much time. It just isn’t worth it. You’re majoring in minors. You’re using major time on minor things and you’re slowing down your progress. Like I said, I see that in students who come to me, not because they’re anything particular, but just because I get the same questions over and over.

So look around and think about, is there a spot where I’m doing this? And can I solve the big problems rather than solving the little problems that aren’t actually going to move the needle, but are taking up so much time. So for me, one of my things is has, for the last few years, has been diet, I’ve been, you know, I’ve been struggling with my weight, not ridiculously, but just slowly creeping up over the years, and I’m doing less exercise than I should have for a period. And I’m like, holy crap, I got to solve this, right? So then you go down the rabbit hole of nutrition, you know, intermittent fasting, high protein, this or that, all these different things. And the end result is, I just started tracking my calories with this very, very simple calorie tracker, working towards hitting 150 grams of protein per day, not necessarily mandatory, but that’s kind of the goal. And then staying under a certain number of calories per day and making sure that I exercise a minimum of 45 minutes per day, just that I’m moving at all.

And it’s amazing what happens. You don’t have to have it dialed in.

Now, will I get better at it? Yeah. Over time, maybe I’ll dial in the macros more. Maybe I’ll dial in the exercise more. But you know, it’s better than reading about all these things and trying to find the perfect thing, getting started and doing it. So that’s the difference. Just pay attention.

Don’t major in minors. Major in majors. Use major time for major things.

All right, let’s talk about our priming questions. What is the hallmark distinguishing feature of Wernicke’s encephalopathy? What’s the hallmark distinguishing feature of Wernicke’s encephalopathy? It was the first one we did today. It’s the classic triad, right? Well, it wasn’t. Do you remember?

Ataxia, ophthalmoplegia, and confusion. How can you differentiate hepatic encephalopathy from other causes of altered mental status? This is a big one. Asterixis. What’s the classic EEG finding in metabolic encephalopathy? Generalized background slowing. Which toxins are most commonly implicated in toxic encephalopathy?

Opioids, benzodiazepines, sedatives, carbon monoxide, heavy metals, and uremic toxins, which we talked about separately, like in kidney failure. Those are kind of our top ones. Fantastic, excellent work. So glad to have you with me today. So excited to start with the April cohort. You know, maybe it’s just that we kicked in daylight savings time. That may be what has me perked up.

The days are getting longer. Things are getting better. I’m always excited this time of year to see the daffodils start to poke through. I just bought a little garden box I’m excited to plant. There’s so many fun things happening. My son has his first varsity baseball game today of his entire life. Really excited to see that.

My other son is in middle school playoff basketball starting today. Excited to go watch that. So there’s so many fun and exciting things. I hope you’re taking some time to enjoy them. Although I know you’re busy, you can find some space to enjoy at least some little things as the sun’s coming out. Go for a walk, get outside, give yourself a little bit of a break and a reprieve. I guarantee your books will be there when you get back.

All right. Well, once again, thank you so much for being here. Thank you so much for participating in this community. It’s an absolute pleasure for me. I couldn’t enjoy it anymore. And if you’re interested in getting better in all aspects of being a student, test taking, please join us for the 33 Days to Pass the PANCE program. You can get more information at physicianassistantexamreview.com/33