129b: Quick Encephalopathy Review for the PANCE

All right. So just as I sat down to record this episode, a whole team of landscapers descended on my neighbor’s yard to mow his lawn for the first time this spring. But we’re going to carry on and hopefully it’s not too obnoxious for you. Today we’re doing one of our companion episodes. So we’re doing 129B on encephalopathic disorders. And the conditions we covered in episode 129 were were Wernicke’s encephalopathy, hepatic encephalopathy, toxic and metabolic encephalopathy, uremic encephalopathy, and hypertensive encephal encephalopathy. I didn’t think I could get through all that without screwing up at least one of them.

So, there you go. One of the things I was thinking about as I was putting this show together was I was trying to understand how these were in like an encephalitis. And I didn’t quite get it because I’m like, I’m thinking that there’s no inflammation in Wernicke’s. There’s no inflammation in hepatic encephalopathy. So what am I missing? And it’s really straightforward, but it’s what I want to, the reason I’m pointing this out is because it’s so many times that the simplest things can have a big impact on your memory because all of a sudden something clicks and then it sticks in your brain. You’ve got it.

And I think that may be how this is for me. And the problem is you can’t tell what will do it for one person or another person. I was thinking about this idea the other day when we talk about high yield information. Probably 60 to 70% of high yield information is the same for everyone, but the other 30 to 40% is different for everyone, depending on what you already know, depending on what you need to learn, and depending on what’s easy for you, what’s hard for you, et cetera. So it’s one of the things I teach in the 33 Days program is how to discern all of that stuff. But anyway, I’m getting way off track here. I want to get back to the idea of encephalitis versus encephalopathy.

And when you pull it up, I mean, the definition’s really straightforward. It’s not hard, but it’s just a piece I was missing, an information gap, a knowledge gap. So encephalopathy is a global brain dysfunction. So your brain’s not working correctly. Encephalitis is brain inflammation, which may lead to an encephalopathy, but they’re not the same, right? They’re similar, but not the same. So something to hold on to, something to think about in how all this comes together.

So let’s run through real quick our different diseases that we covered in the last episode. Then we’re going to go through some questions and see if we can lock some of this together. So what was Wernicke’s encephalopathy? What were the key main points there? Well, it was an acute reversible encephalopathy caused by a B1 deficiency, thiamine deficiency, confusion, ataxia, ophthalmoplegia in a malnourished or alcoholic patient. I feel like these were always alcoholics. It doesn’t have to be, but certainly that was a common presenter.

So it’s a B1 deficiency. You’re going to treat it with IV thiamine before glucose. We went into why in the last episode. I’m not going to do that here. Complications, this can progress to Korsakoff syndrome, which is irreversible.

Next, we have hepatic encephalopathy. This is a neuropsychiatric dysfunction due to ammonia buildup in the liver. You get asterixis with this. Triggers for this might be a GI bleed, an infection, sedatives. Treatment is lactulose is the first line treatment. Labs, you could find ammonia being elevated, but that’s not diagnostic on its own. Toxic and metabolic encephalopathy, this is diffuse cerebral dysfunction caused by systemic illness or metabolic toxic imbalances.

An EEG shows generalized background slowing in altered mental status. That generalized background slowing seems to be one that comes up over and over again here. Common causes are things like hypoglycemia, sepsis, hypoxia, and other toxins. Symptoms, myoclonus, hyperreflexia, fluctuating mental status. You’re going to do an ABG, CMP, EEG, and a toxicology screening if you would think this is possible. Treatment. Fix the underlying issue.

Pretty straightforward stuff. Uremic encephalopathy. This is due to accumulation of toxins and advanced renal failure. BUN would be greater than 100. Plus an altered mental status in patients with end-stage renal disease. Again, here you can have asterixis, myoclonus, and seizures. Treatment.

What’s the treatment here? What’s the treatment for someone who’s in end-stage renal disease with uremic encephalopathy? Well, it’s urgent dialysis. It’s get that done immediately. On EEG, you may see triphasic waves possible, but they’re not super specific. The last one we covered was hypertensive encephalopathy. And this is when it’s easier to wrap your brain around.

This is a dysfunction due to critically elevated blood pressure causing edema, generally talking about greater than 180 over 120. You may see papilledema, headaches, vomiting, seizures. You might get a CT to rule out a stroke. And you’re going to want to bring down blood pressure, but not super rapidly. You want to do it slowly with something like labetalol or nicardipine.

Excellent. So what I want to do first, like we usually do on these episodes, is run through just some short final step type questions. These are building block questions. So this is where you can lock in some key information and the things that I would put on my flashcards if I were building out my own flashcards. I was just talking about last night with the April cohort of the 33 Days to Pass the PANCE program how there’s value in using other people’s flashcards, right? There’s value in using question banks. There’s value in using what other people have already created because it’s faster, right?

So whether that’s The Final Step, whether that’s an Anki deck, whatever you find, right? Because it’s fast. It’s easier than writing it out yourself. But there’s also value in having to choose which things to create, which things to decide to study, which things to decide to make a question about. There’s incredible value in that. It does take longer, and it’s not easy. But if you have the time, there’s a bigger payoff.

But you always have to decide and weigh the value of each piece. Is this worth it? Is this not worth it? If I only have so much time, what do I do? You know, obviously, you don’t have infinite time. So you have to make decisions based around the time that you have and choose. You know, there’s a lot of things you could do to learn things better over longer periods of time, but you just simply don’t have it.

So you have to make some decisions. But I will say creating these on your own better than using someone else’s or having something else create them for you. But I get there’s a time crunch.

All right, so let’s run through a couple of these that I made. What’s the classic triad of Wernicke’s encephalopathy? Classic triad. Ataxia, ophthalmoplegia, and confusion. We just said what’s the first line treatment for hepatic encephalopathy? First line treatment for hepatic encephalopathy? Lactulose.

What about the EEG of metabolic encephalopathy? What do you think you’ll see there? Well, we would hope the question would have generalized background slowing. And these are things that, like I said, you may not see in practice all the time, but I’d like to hope that in your test questions, they’re going to give you these things to make your life reasonable on your exam. What triggers should you always look for in hepatic encephalopathy? What triggers? GI bleed, infection, dehydration, sedatives.

That seems like a good place to start. What’s the definitive treatment for your uremic encephalopathy? This is a simple one, right? Dialysis.

Perfect. Let’s jump into some PANCE style questions. And what I do first is these first couple just take what we did a minute ago and we build a bigger question out of it. So as much as people don’t think this is true or don’t want to admit it, not every question on the PANCE is a long paragraph style question. There are those, but there are also short, straightforward questions. So when you say a minute per question that you have to balance that a little bit. It’s not a minute on a short question and a minute on a long question.

You’re making up time on the short questions. And then you’re using two minutes on the longer questions, or a minute and a half. So for starters, which of the following is a hallmark finding in hepatic encephalopathy? A, papilledema. B, myoclonus. C, asterixis. D, ophthalmoplegia.

Which of the following is a hallmark finding in hepatic encephalopathy? Papilledema, myoclonus, asterixis, ophthalmoplegia. Here it’s asterixis. That’s pretty straightforward. You either know it or you don’t. And if you don’t, it’s just a knowledge gap, right? So you have to go back and fill that in if you don’t know it.

But if you don’t know it, this is not one I spend a lot of time on. Really, I just grabbed this. This is a five, six, maybe ten second question at most on my exam. A 59-year-old with end-stage renal disease presents to the emergency department with progressive confusion and drowsiness over the past two days. According to his family, he has been increasingly forgetful, slow to respond, and intermittently jerking his arms during the rest. On physical exam, he is alert but disoriented to time and place. When asked to extend his arms and dorsiflex his wrists, you observe brief, involuntary flapping movements.

Additionally, he exhibits occasional sudden involuntary twitches of his upper extremities. BUN is 108, creatinine is 11.4, potassium is 6.1, calcium is 7.4, bicarb is 16, and pH is 7.3. So, there’s a ton of key terms and key ideas. Oh, sorry. Which of the following is the most appropriate next step in this patient’s management? A is administer intravenous thiamine. B is initiate treatment with lactulose.

C is begin empiric broad-spectrum antibiotics. And D is initiate emergent hemodialysis. So this should be pretty straightforward also, right? This is just like the question we did before, but I just took it and made it into a longer form PANCE question. But it’s really just a one-step question. You see the patient has end-stage renal disease. You see they have some confusion.

So you should immediately be thinking uremic encephalopathy. That shouldn’t be a jump at all. The BUN of 108 confirms that. Physical exam confirms that. Everything’s pushing you in the same direction. So you wind up with an answer of D, initiate emergent hemodialysis. We’re not going to give them empiric broad spectrum antibiotics because we don’t have any signs of infection.

Lactulose is for what? Well, that was hepatic encephalopathy. And intravenous thiamine was for what? Well, that was for Wernicke’s encephalopathy, right? So none of those are going to fit into our situation. Here’s another one. Try this.

A 62-year-old man with a history of cirrhosis presents, so it’s cirrhosis. There you go.

Now, it’s harder if we’re not in the encephalopathy category, right? If it’s all mixed together, this becomes more difficult. But we are here. We’re just doing this real straightforward stuff. A 62-year-old man with a history of cirrhosis presents with confusion, slurred speech, and altered sleep patterns. His wife reports he recently had a bout of constipation and has taken his usual medications for several days. Has not taken his usual medications for several days.

On exam, he is oriented to person only and demonstrates a flapping movement when asked to hold his arms out and extend his wrists. Vitals are stable. AST is 78. ALT is 62. Bilirubin is 3.1. Ammonia is 86. INR is 1.7.

Which of the following is the most appropriate treatment.

Now, you may not remember what an ammonia level is. I don’t know if this is normal or not. Off the top of my head, I have no idea what the ammonia level is. But I don’t let that worry me. The fact that they’re giving it to me tells me I’m in the right direction. Maybe they’re trying to fool me a little bit, but I’m in the right direction. But the history of cirrhosis and all the other conditions make me think I’m dealing with the hepatic encephalopathy.

Now, what again, would I know that mixed into 60 other random questions? I don’t know. That would be difficult. But I wouldn’t let me not knowing the ammonia levels screw me up. We just pause here for a second and pull that up.

All right. So, as I look at normal ammonia levels, so you’re looking at like 15 to 45, maybe up to 80, depending on the lab. Greater than 100 is what you’d be looking for, hepatic encephalopathy. So in this question, we have an 86, which is a little high, but not crazy high, right? So it’s not enough to confirm. It looks high. So it just pushes me in the right direction.

So in this case, I’m going to be thinking about lactulose. I’m not going to be thinking that I have an end-stage renal disease, right? He’s not getting dialysis. There’s nothing in this question that points me towards renal problems.

Now, you may not remember what rifaximin and what intravenous thiamine are for, so you may struggle there. I think if I remember from what we just did, rifaximin is the secondary treatment, and obviously thiamine is for Wernicke’s. How about this one? Which of the following physical exam findings is most characteristic of hepatic encephalopathy? A, papilledema. B, flapping hand tremor when wrists are extended. C, pinpoint pupils.

D, Babinski sign. Here the answer is B, flapping hand tremor when wrists are extended. Papilledema is for increased intracranial pressure. So that would be more like a hypertensive encephalopathy, something like that. Asterixis is a common finding with hepatic encephalopathy. That should be something that you know. Pinpoint pupils, what does that make you think of?

That should make you think of opioid toxicity, right? And Babinski sign, not really involved for hepatic encephalopathy.

All right, let’s get a little harder here. A 70-year-old woman with a history of cirrhosis presents with progressive confusion and lethargy. She is oriented to person only. Physical exam shows non-rhythmic flapping of the hands when her arms are extended. Labs reveal elevated ammonia and mild hyponatremia. Her BUN and creatinine are within normal limits. Which of the following best supports hepatic encephalopathy over the other causes of altered mental status.

Perfect. So we run through this stem, and do you see how it’s built out? So yes, could you just skip to the question? You could. We’ll not get into that today. But if you look at the stem, they tell you it’s cirrhosis. They tell you about the non-rhythmic flapping of the hands.

They tell you the elevated ammonia. So they give you everything to tell you that this is a hepatic encephalopathy. And then we go so far as to share with you that her kidneys are normal. So you’re feeling really confident this is a hepatic encephalopathy before you hit that question. But now, A, normal renal function with elevated BUN. B, presence of myoclonus and papilledema. C, elevated ammonia and flapping tremor.

D, triphasic waves on EEG. Well, this is kind of straightforward, right? Because these aren’t all in there. But your answer is going to be C, elevated ammonia and flapping tremor. Is A true? Yes, A is true. But it’s not really the best thing that supports it.

It’s the thing that is helpful in supporting it, right? It pushes you in the direction. And again, just be a little careful because that’s a place that I usually screw up. I, generally speaking, have trouble picking the best answer, and I will often pick here. I might have picked normal renal function with elevated BUN because that points me towards hepatic encephalopathy. Well, really what it’s doing is pointing me away from uremic encephalopathy, but by default it’s pushing me towards hepatic encephalopathy. So I want you just to think about that.

So don’t just hit those answers, and some of you are like me, and think, oh, I see one that’s right. That’s got to be the right answer. They’re looking for the best answer. That’s something that was very hard for me in PA school and on my PANCE to do well with. I’m actually only recently improving my ability to see through that problem. I’m very fixated on the first thing I see that’s correct. And I have trouble seeing past it.

So it’s something I want you to just to be aware of in yourself. See if you’re someone who does that. And if there’s a way you can catch yourself a little bit.

All right, that brings us to the end of this particular companion episode. I think this is really helpful. I love going through these and talking about how to think through the questions, talking about the most important pieces that we need to retain of the diagnoses, of the treatments, all these things. I think it’s a lot of fun. I think it’s very valuable to help this stuff sink in and really work for you. So, all right, fantastic. We’re making our way through neuro slowly and steadily.

Can’t wait to talk to you guys again next week. And I really look forward to hearing from you. Let me know how your exams are going. Let me know how your rotations are going. I do absolutely read through every single email and it does keep me going and keep me energized to keep working. So thank you so much. I do appreciate it.

Take care and I’ll see you next week.