Diarrhea | Clinical Medicine

What's up Ninja nerds? In this video today, we're going to be talking about diarrhea. This is a part of our clinical medicine section. If you guys like this video, it helps you, it makes sense, please support us. And some of the ways that you guys can do that is by hitting that like button, commenting down in the comment section, and please subscribe. Also, really urge you guys, if you have the opportunity, please do so, which is going to be go down in the description box below, click on the link that'll take you to our website. When you go to our website, there's a lot of cool stuff that we offer here that I think will really augment and help in aiding in your learning process. So we offer things like notes, illustrations, quizzes, or even developing exam prep courses, and so much more. So go check it out if you have the time.

All right, without further ado, though, let's talk a little bit about diarrhea. So we're going to do this in kind of a couple parts. First thing is, I want to talk about diarrhea within the acute setting. So a patient comes in with acute diarrhea, we'll talk about, well, we'll define it now. It's pretty straightforward in the sense that you have to have at least three or more loose stools, right, per day for at least two weeks in duration. All right, we say at least less than two weeks in that particular scenario because if you cross over that two-week barrier, then you're into the chronic diarrhea. So again, we say greater than three or more loose stools per day for less than a two-week duration, that's acute diarrhea.

But then when we take a patient who comes in, they're saying, "Hey Doc, I've been having diarrhea for a couple days now, and it's been pretty intense." You have to then kind of create a framework in your head. And I think the frameworks that you should start thinking about is, is this an acute non-inflammatory or secretory diarrhea, or is it an acute inflammatory diarrhea? This is really important. All right, the reason why is in a patient who has an acute non-inflammatory diarrhea, often times these would just kind of get better on their own. You just kind of give them supportive care with fluids, etc., and just hopefully they'll get better, and they usually won't require any treatment.

The concept, the pathophysiology, though, behind a patient developing acute non-inflammatory diarrhea is interesting. The location of the actual GI tract that's most commonly affected is going to be the small bowel. So this is the area here, I'm just representing a piece of it, but that's the ileum. But it could be the ileum, the jejunum, or the duodenum. So I think the big thing to remember for acute non-inflammatory diarrhea is you're going to have what's called small bowel involvement. And I think right away, this should hint to the way that these will present. Now, the small bowel is primarily responsible for absorbing most of your nutrients. It absorbs a decent amount of volume of things as well. So if you damage the small bowel, right, you injure it for whatever particular reason, you're going to affect absorption pretty significantly. And whenever you have a massive decrease in absorption, and plus a lot of that is actually getting pulled into the bowel, but I really want you to think about decreased absorption to make it easier for yourself. Massively decreased absorption. One of the problems is that you have intensely voluminous stool, right? So whenever there is decreased absorption, it's not going to be moving from the small bowel to the bloodstream. It'll continue to transit through the small bowel, eventually into the large bowel. The large bowel will try its best to absorb some of those things like water and liquids, but it won't be able to do as good of a job. And so one of the things about this stool is that this stool is going to be super voluminous and extremely watery. All right, so that's one of the big things I think that's really helpful here is that this is going to be more of a, let's term this a watery, but let's kind of use this term high-volume stool. So you're going to be like peeing out your butt, right? And I think that's really one of the best things to remember here with these patients, that they're going to have very heavy, voluminous, watery appearing stools that usually indicates small bowel involvement.

Now, if we take this at the macroscopic view and say, "Okay, there's injury here, we're not absorbing things." I get that, that's basic physiology. But if I take and say, "How exactly is this happening a little bit at the microscopic level?" I can go into that. So one of the big things about acute non-inflammatory diarrhea is that the actual pathogens that are causing this, they don't directly damage the mucosa. So that's really important to remember, is that there's no direct mucosal damage, right? That's really important. So let's actually write down, there's no direct mucosal damage. All right, what happens, which is super kind of like cool in the sense, is that these pathogens over here that we'll talk about, what they do is, let's actually just represent one here, we'll do it in this kind of color here. Let's say here is a pathogen, and we're just going to use the bacteria as an example here. What it does is it releases something called an exotoxin. And there's so many, we're not going to focus on every type of exotoxin here, but they can release these things called exotoxins. And exotoxins, what they'll actually do is they'll act on these mucosal cells. And when they act on these mucosal cells, what's really kind of cool about this is they activate specific channels that are present on these cells. So imagine here, I just kind of highlight a couple channels here on these. These channels are super sensitive to these enterotoxins, and it'll activate like these different second messenger systems, which is kind of cool but a little bit too deep beyond this kind of concept, so I won't go into it. But the whole point is that you'll stimulate these things, and what will happen is they'll drag things out into this particular area. So these cells would begin to secrete things into the lumen. And that's what's really interesting. You're not damaging them per se, you're causing them to become kind of utilized by these enterotoxins and say, "Hey, secrete things." And what it does, it secretes things like sodium, and potassium, and chloride, and lots and lots of water. And so if I'm secreting a ton of these particular things, what do you think is going to happen to the actual volume of my stool? If I'm containing lots of water and electrolytes, it's going to be pretty intense, right? Because first off, these are going to be hindered in a way that you can't absorb. But on top of that, you're going to have a significant degree of secretory activity. So that's why often times we call this type of diarrhea an increased secretory type of function or an increased secretory type of activity. That's why it's sometimes also referred to as a secretory diarrhea. All right, but there's no direct mucosal damage in that sense. It's just this is really kind of impairing absorption by kind of shutting these mucosal cells down and telling them, "Hey, secrete a bunch of different things." So that's kind of interesting.

Now, the question then comes, "Okay, if there's not direct mucosal damage, exotoxin-mediated, lots of these, where are these exotoxins coming from?" Well, it's coming from the pathogen, right? And that's something that we have to be able to talk a little bit about. So there's a couple of these different types, and I think some of the big ones that we're going to hit here, um, I think you should definitely take some time to try to memorize. So I think one of them should be Staphylococcus aureus. And I think one of the particular things that may kind of cue you off, uh, to think about this one, to think about picnics. And I'll explain what I mean by that in just a second. So in picnics, you're having a lot of family members who bring over potato salad and things that are rich in mayonnaise, and it sits out in the baking sun a lot of the time. That's a potential nidus for lots of Staphylococcus aureus. They release these pre-formed toxins, and you can get pretty bad vomiting and diarrhea pretty quickly. Another one is called Bacillus cereus. And I want you to think about rice. So usually in people who eat a lot of rice, and then they go and they preheat the rice, sometimes this is just one of those bacteria that can sit in that rice a lot and can cause again, this acute diarrhea along with vomiting associated within the couple hours after eating it. Another one, really high-yield one, is called enterotoxigenic E. coli. This is a really big one that people often hear. This is like traveler's diarrhea, in the sense of Montezuma's Revenge. So this is a really big one when those people who go and they go and travel, they go to Mexico, they drink some of the water, they eat some of the food, and they end up with this terrible, terrible diarrhea. That's a really, really common one. Another one would be, uh, Vibrio. So Vibrio cholera is another one that I don't want you guys to forget as well. This one's definitely associated with travel as well, um, and usually one of the key terms or buzzwords that you'll kind of think about with this one is you hear that word, "rice water" kind of stools, heavy, voluminous stools. Usually, this is more of kind of an endemic. So you'll definitely see this in kind of more of those third-world country areas where it's less fortunate. But I'd say that these are some of the big ones to potentially think about as enterotoxin types of causes.

Now, with that being the bacteria, the other ones are viruses. And these are often times pretty much the most common, 'cause they, they're pretty self-limiting. And I think they're going to be ones that you'll definitely see on the exam in some way, shape, or form. One is called the norovirus. And I want you to think, when you hear norovirus, think about cruise ships. This is usually one of those where people are on these cruise ships, they're either kind of coming in contact with another person who has that, or there's it's in the water. It's just one of those common areas where this can get passed pretty quickly. Another one is called the rotavirus. And this one is a virus that I think is best to remember in daycares. So it's usually in kids who kind of pass this along. They touch particular things after they've touched their, you know, their boo-boo, boo-boo, and then they go and they kind of pass that along via the fomite. That's a big one to also remember, daycares.

The next one is parasites. And I think there's two that I really would want you guys to try to consider. One is called Giardia. And Giardia is one of those I want you to remember, river water. This is like also sometimes they call it Beaver Fever. So this is one of those where Giardia is a very nasty protozoa that sits within river water, and if people kind of ingest that, they can definitely get this and get some really nasty diarrhea. The other one that I would also want you guys to consider here would be, uh, Cryptosporidium. So this would be the other one I want you guys to remember is called Cryptosporidium. Now, Cryptosporidium is interesting in the sense that you have to be immunocompromised to really get this one. And I really want you guys to just associate this with AIDS patients with a CD4 count that's usually less than 100. That usually can tip you off in some way that this patient's immunocompromised in some way, shape, or form, and they've encountered this. Usually, um, this can be potentially travel, foodborne, contact, a lot, but you need to be immunocompromised because it's an opportunistic infection. But with that being said, we kind of have an idea here about this particular process.

One thing I want you to understand, though, is that do you see any white blood cells here? No. There's no break in the mucosa that's causing these cells to be directly damaged. So because of that, one thing I really want you to understand here is that we kind of use this as a diagnostic test. There are no fecal white blood cells, and there's no chemical that these fecal white blood cells release. So there are no fecal white blood cells and no molecule they release. So I'll write this down: no fecal white blood cells and no chemical that they release called fecal calprotectin. All right, and this is a chemical that's usually released by these particular types of fecal white blood cells. And then lastly, do you see any blood that's present in the stool? Did we break the mucosal barrier and cause this blood to leak in? No. So there should be no blood within the stool as well. Now, take that with a grain of salt, um, and the reason why is sometimes when people have diarrhea, they wipe and they wipe and they wipe, and then they kind of create like these little areas of hemorrhoids or irritated tissue that they can have blood. That doesn't mean that there's actually blood coming from their stool, though. It's just from them wiping aggressively. All right, that covers the first part here of the diarrhea.

The second part here is again, same patient, they come in, they're saying, "Hey Doc, I've had three or more loose stools within a day for a couple days, as long as it's less than two weeks." And then you say, "Okay, could it be acute non-inflammatory or could it be acute inflammatory?" And I think one of the questions is, "Does your stool look bloody? Does it look mucousy?" Right? "Have you had high voluminous types of watery stools, or have you had the next one?" And so in this one, small bowel is preserved. That's not the issue. It's usually the colon, and it's usually more the descending colon, um, more than anything that gets hit. You might get a little bit of the, the last part of the transverse colon, but you're going to get really large colon involvement or large intestine involvement. So with this being said, what you're going to see here is you're going to see colon involvement. Now, with that being said, because there's involvement, it's not going to be, this helps to reabsorb just a little bit of or absorb a little bit of water from the stool, not a ton. The interesting thing with this one, that the stool, and we'll explain why in a second, is going to be bloody, right? And it's going to be mucoid, which means it's going to have like some mucus kind of look to it. So it's going to look kind of stringy, if you will, and have some bloody tinge to it, but it won't be like high volume, right? And I think that's the important thing to remember because you preserve the small intestine in this one. So when you hear this term, "bloody mucoid diarrhea or stools," you think of a very special term that we often utilize here, and it's called dysentery. And so whenever you hear the term dysentery, thinking about bloody mucoid containing stools because of colon involvement, but preserved small intestine involvement.

Now, we talked about how this was related to absorption. This isn't really related to absorption. Why am I having bloody mucoid stools here? I'll explain. In this scenario, you're actually having pathogens. I'll just represent it here in this again, same kind of concept. They may, they very well may be releasing enterotoxins. That's definitely possible with a lot of these. They do that, but they're often causing direct mucosal injury and damage. So do you see how this guy is all jacked up? This one's all jacked up, right? So you're definitely getting heavy, heavy mucosa damage. Now, when you damage the mucosa, you alter the barrier here, right? First off, you're going to cause damage, it's going to trigger an inflammatory reaction. So when you trigger an inflammatory reaction, what kind of cells are going to come to the area? White blood cells. And they're going to try to come into the lumen to fight off whatever is causing this. And so what often ends up happening here is that you're going to get a ton of these fecal white blood cells, and these are essentially kind of like your neutrophils, if you will, and they're going to be like, "Okay, I got to come into this area and I got to try to help out." And so what they'll do is they'll often move through the bloodstream and they'll kind of come out here into the lumen a little bit. And so that's one thing. And all right, they'll try to fight off some of this. But what's going to end up happening is they're going to propagate more inflammation. When you propagate more inflammation, you know there's these special cells here, I'll kind of squeeze one in here, let's do it right here. Here you have a cell, it's called a goblet cell. They're kind of naturally there, and whenever there's lots of inflammation, they hate inflammation. And what they'll do is they'll start secreting a lot of mucus. So here, this goblet cell is spitting out a bunch of mucus in response to a lot of this inflammation into this area. So you're going to get a lot of mucus because of the inflammation. You're going to get a lot of white blood cells. But also, have you damaged the barrier here? Yeah. So what else can start kind of leaking out here if you continue to cause more damage? You can start having blood leak out here. So now I'm going to have mucus, I'm going to have blood, and I'm going to have a lot of fecal white blood cells out here. So I'll notice that there's going to be lots of mucus because of, like, inflammation, direct inflammation, lots of blood because of, again, mucosal damage. And then on top of that, I'm going to have lots of fecal white blood cells. And then with lots of fecal white blood cells, what do those bad boys release? They release a lot of what's called fecal calprotectin. And so what should happen to the fecal calprotectin levels? They should go up as well. And so you're kind of noticing here that in this one, no blood, no fecal calprotectin, no fecal white blood cells. Here, fecal white blood cells, fecal calprotectin, blood, and again, that mucous appearance. And again, this is what's giving, lending to this bloody mucoid appearance of the diarrhea. All right, and again, it's not usually a high volume. And I think that's one of the other big things to be able to remember.

So the question then arises, "Okay, if these are causing direct mucosal damage, which is leading to all this kind of downstream cascade, causing particularly colon involvement, not small intestine involvement, dysentery-like appearance of my stools, what are the potential pathogens that would directly cause this damage?" And there's a lot of them. So I think some of the ones that I want you guys to remember here is going to be Salmonella. And I think a lot of you guys know this just in general, it's going to be undercooked, like poultry or eggs and things like that. So I just want you to remember that it's going to be more foodborne. All right, but I think the, the key thing is here, I'll just put down some type of poultry or again, could be undercooked, like eggs as well. Another one would be Shigella. All right, Shigella is a really scary one, um, and the reason why Shigella, again, it can be related to travel, and it can be related to foodborne, and usually poultry as well. But this one, man, it can release toxins and it can cause direct damage. All right. Another one is going to be, um, you have another one called Campylobacter. And Campylobacter is another nasty one as well. And again, I would go with the, the fact that this is again, more of a foodborne one. Often times the test question that comes up with this one is Campylobacter is linked to that Guillain-Barré syndrome. But again, we're not going to go too crazy down that rabbit hole. The next one that I want you guys to remember is going to be, I think probably one of the big ones, this is called EHEC, so Enterohemorrhagic E. coli O157:H7. Right? Uh, this one is really nasty, and this is usually again, this is foodborne, and this is one of those that can really wreak a lot of havoc on the body. This can cause what's called hemolytic uremic syndrome. And so can this one as well, but definitely scary one to remember here. Um, another one that I would actually definitely want you guys to not forget here, um, I think it's probably one of the likely ones that you'll get tested on in some way, shape, or form. We're going to have a special lecture on this by itself, but it's going to be Clostridium difficile, often kind of termed C. diff. And the big thing to remember about this one is think about antibiotics. Has the patient been on any recent antibiotics? This is usually a cause and it kind of triggers this kind of like process to occur. All right.

The last thing is going to be parasites. And parasites, usually for these, the ones that I would want you to remember here, there's really only one specific one. Um, it's a really nasty one, it's super scary if you ever get it, it's called Entamoeba histolytica. And this one again, is more travel, it's more of that like river water type of a kind of things that you can to become exposed to. It's a nasty, nasty amoeba that can cause a lot of problems. But I definitely don't want you guys to forget this one. So if a patient comes in and they have this mucoid bloody diarrhea, I want you to think, "Okay, how would I tell? Is there blood? Fecal white blood cells? And a mucus appearance of their stool?" Think about these particular pathogens and think about the organ that's most commonly affected within the GI tract. If I think about acute non-inflammatory type, but they're coming with a volume that's really, really high, it's watery appearance, it's likely affecting the small bowel region. And think about these particular pathogens in this scenario. And again, think that this is not going to have inflammatory markers that I'd see here. All right.

With that being said, that covers the acute diarrhea. What about the patient who has more than three loose stools per day for greater than two weeks? Now we're in the chronic diarrhea camp. Let's talk about that.

All right, my friends. So now, if a patient comes in and they have the chronic diarrhea picture, right? So they've been having at least greater than three or more loose stools per day for more than two weeks, more than 14 days, we're in that chronic diarrhea camp. And I think the best thing to do is to start asking yourself the question, "Okay, if it's not acute diarrhea, so it's not the non-inflammatory or inflammatory, then we're in the kind of areas of where we may repeat some of these that we talked about in acute." And so it's helpful, but we're in three camps here if it's chronic. One is, we're in the secretory camp, the osmotic camp, or the inflammatory camp. And so let's talk about these in comparison to what we talked about with acute diarrhea, which was the small bowel, large bowel involvement. Believe it or not, in all of these, whether it's secretory, osmotic, or inflammatory, it can hit any part of the bowel. So it could be in any of these, it could be small bowel or large bowel. So that's not going to be super helpful in that sense, right? And then even when you look at the diarrhea itself, if you ask the patient like, "What's their diarrhea look like?" Which I know sounds terrible, um, but it's can be helpful. Sometimes for secretory diarrhea, it'll appear watery. So it won't be like bloody or mucoid or anything like that. It'll definitely be more of like a watery type of diarrhea. And then you would be like, "Oh, well, Zach, that's off of what we talked about before, wouldn't that be more small bowel involvement?" It definitely could be, but it also could be large bowel involvement. So it's not necessarily like specific for one or the other in that particular sense. You could definitely be hitting multiple parts of the GI system. So, okay, if that's not super helpful, then how can I really visualize this? Well, it's the same concept. Is that there is something in, you know, the acute, uh, non-inflammatory diarrhea that were due to pathogens, they enterotoxins that were stimulating these GI cells to secrete things. In this situation, it's the same thing, except this something that's actually binding onto these, uh, enterocytes and causing them to secrete things is usually something like a hormone or a stimulant of some sort. And so let's just use this as an example. Let's say that this is the hormone or this is the stimulant laxative. What does it do? It's the same concept we talked about, guys. So you're going to stimulate these enterocytes, and there are specific channels on them, and what they'll do is they'll secrete, that's the name, things like sodium, potassium, chloride, and water. And then with this, guess what you'll get? You'll get a diarrhea that's relatively watery, right? But it doesn't point to where in the actual bowel you've actually affected. It just may say it could be hitting the small bowel, could be hitting the large bowel as well. But then the question comes, "Okay, I know that I'm going to have lots of like things like sodium and potassium and water in my actual stool. Okay, that's helpful. I'll use that later when I talk about the stool osmolar gap. We'll get into that. But I got to ask myself the question, "Okay, what are these hormones?" Because this could be diagnostically useful, right? If I know that this is rich in electrolytes, and I know, "Okay, that's a secretory diarrhea," then I have to tie this to hormones. What are some hormones that can definitely stimulate this process? Well, I think a couple of them that would actually want you guys to remember is if you have elevated levels of VIP, vasoactive intestinal peptide. And this is actually sometimes seen in a disease which we call a VIPoma. And that's important to be able to remember. So elevated levels of vasoactive intestinal peptide is helpful. Another one is if you have elevated levels of gastrin. So there's a tumor, and I think a lot of these are going to actually be pretty straightforward. Uh, gastrin is another one that can cause secretion. And guess what it's released by? Oh, you'll never guess it. It's a gastrinoma. So these can be seen in that disease called Zollinger-Ellison syndrome, where you have like a pancreatic tumor or a tumor of the small bowel that's pumping out lots of gastrin. The other one is usually going to be something like increasing levels of a molecule that eventually is related to serotonin. And I'm just going to put down here, it's called, um, you have a molecule called 5-hydroxy tryptamine, but it's related to this one. And we call this one carcinoid syndrome. So it's related to serotonin and carcinoid syndrome. So this is a tumor that'll pump out these kinds of molecules that can cause diarrhea and wheezing and things of that effect. Okay. So if it's hormone-related, I can then say, "All right, I know that this secretory diarrhea, which is rich in electrolytes, could be due to a hormone or could be due to a recent laxative that they've been taking." And these stimulants are exhibiting the same type of effect. And often times, there's just two types of laxatives that you want to be able to look for: one is called Senna, and the other one is called docusate. And often times they can be given together. But in these scenarios, if a patient is taking stimulant laxatives, this could give them that secretory diarrhea rich in electrolytes, or if they're making too many of these hormones, it could give them the secretory diarrhea. All right, so we now know that this could be more of a chronic secretory diarrhea from these mechanisms.

What about the osmotic type? Well, the osmotic type, it's the same exact process. I'm not going to write them down, I'm just going to highlight that often times you definitely hit the small bowel, but you may also hit the large bowel as well. So there definitely can be a mixture of small and large bowel involvement. When you look at the stool, though, this is what's interesting and it could be clinically helpful. The stool sometimes could have, let's say we represent half here is watery, and the other half, it could be fatty. So sometimes you can have a watery diarrhea in this osmotic state, or you can have a fatty diarrhea. This fatty diarrhea, we actually use the term steatorrhea, which is a fatty, like kind of stool, fatty, greasy stools, or it could be watery. And I think the reason why this is kind of helpful to know is that in certain types of diseases, such as Celiac disease, or pancreatic insufficiency, um, or Whipple's, or tropical sprue, things to that effect, they lose a lot of fat that can actually occur. And anything that's a global malabsorption syndrome, they lose lots of fats in their stool, and that can usually make you think about a malabsorption, a maldigestive type of syndrome. If it's a watery stool, though, it's likely not malabsorption or maldigestion, it's probably some type of laxative. All right, so that can be somewhat helpful. But with that being said, a patient comes in, they have stools that are maybe watery or fatty. The thing to think about here for this type of osmotic diarrhea, it's actually pretty straightforward, is you have some type of osmotic substrate. It's the, we're just going to represent that in blue here. This is a substrate that can actually pull water into the bowel. So here's your substrate, and it's literally yanking water from the vascular system around these cells into the actual stool. And whatever this osmotic substrate is, the concept is that it's really yanking and pulling in water and other types of molecules into the stool. So this will be a very watery type of stool. It'll have lots and lots of water and osmotic substrate. And I think that's the big thing to remember is you're going to have lots of, we're going to call this guy here your substrate, and we'll talk about what these substrates are, but you have lots of them, and they yank out a lot of water into this stool. That's what causes this diarrhea. Question is, is what are these osmotic substrates? Well, these could be variable, man. So I think it goes back, ask yourself the question, in this particular scenario, is it any kind of malabsorbed, um, or is it a maldigested substrate? If it is, the things I would like you to think about would it be something like Celiac? Right, Celiac disease. I would want you to think about, um, what we call EPI, which is exocrine pancreatic insufficiency. I would want you to think about another disease, uh, called tropical sprue or Whipple's. So think about tropical sprue or Whipple's. And I think the other one to not forget as well, besides these, is could it be lactose intolerance? So let's actually make room for that. It's either malabsorbed or maldigested material that are acting as these osmotic substrates. And if they're acting as osmotic substrates, they'll yank water into the actual bowels. And so this would be the diseases that would cause this. All right, and again, I think the important thing to remember, MERS, we will cover all of these in a separate lecture on malabsorption, okay? But these are going to cause lots of malabsorbed and maldigested osmotic substrate, pull water into the bowel. All right. The other one is, it actually could be due to laxatives, but we call these osmotic laxatives. And we give this to people who are having constipation, um, or other diseases, and it's unfortunately leading to diarrhea. The ones I think that are important to remember are three. One is called lactulose, which is commonly given in patients who have some type of underlying liver disease with hepatic encephalopathy. Another one is called polyethylene glycol. All right, this is often times, um, given to patients again, who have issues with constipation. The last one I think that's also helpful to remember that can act as a laxative as well is magnesium citrate. So these are something I think that's important to remember when you have a patient who comes in with chronic diarrhea, ask the question, if it is osmotic, is there any chance that it's kind of a maldigested or malabsorbed kind of like substrate that's causing this yank of water, or is it a drug that we gave them that's causing this yank of water into the bowels?

The last one is going to be a chronic inflammatory diarrhea. And again, I think it's important to remember that again, this could affect the small bowels, or it could affect the large bowels, right? The big thing to remember for this one, though, is that this type of diarrhea is bloody and mucoid. So you're going to have that bloody type of appearance of the stool, and you're going to have that mucoid appearance of the stool as well. And I think that's really, really important to remember. And it may say, "Oh, it's dysentery." No, they're not really going to be in that dysentery type, but this will be kind of like bloody and a mucoid appearing stool. Okay. Now, with that being said, if you have a mucoid bloody containing stool, and it's again, greater than at least three or more of these a day for greater than two weeks, we're not thinking about dysentery anymore, we're thinking about a chronic type of diarrhea, but we are knowing that this is going to be inflammatory. So what we know is there is mucosal damage. And from that mucosal damage, we already talked about this a little bit, you're going to cause activation of immune system cells. So you cause damage here to these mucosal cells, it'll alert your immune system. Your immune system, particularly your white blood cells, will try to come to the area and fight off all of this particular problem that's causing this. In this particular scenario, it's usually an inflammatory reaction in like IBD or a chronic infection. But these immune system cells will try to leak into the bowels to fight off whatever is causing this. Usually, it's unfortunately kind of like an autoimmune condition. But there is damage, there are white blood cells, there is going to be damage to the actual mucosa, which leads to blood that appears within the stool. And there's going to be so much inflammation that it actually causes goblet cells to produce lots of mucus. And so you get the point of why we get this bloody mucoid stool. But the other important thing to remember is is that yes, you'll have blood, you'll have mucus, but you'll also have lots of fecal white blood cells and the calprotectin molecule that they release. And all of these things usually kind of lead you to think that this is some type of inflammatory diarrhea. All right, you don't see this in osmotic, which is rich in water and and a substrate. You don't see this in secretory diarrhea, which is rich in electrolytes. You're seeing this in an inflammatory type, and it's usually disease that's been associated with chronic inflammation of the bowel. And the two types that I think are important to remember are going to be really inflammatory bowel disease, so Crohn's and ulcerative colitis. And the last one is sometimes patients can have chronic infections like CMV, um, especially in immunocompromised states. But chronic infections would be another one that you could definitely consider. But I think by far the most common one to remember is going to be inflammatory bowel disease. So with that being said, we have a patient who comes in with chronic diarrhea, think, is it secretory? Lots of electrolyte-rich stool, hormones, stimulant laxatives? Is it osmotic? Substrates, lots of water-rich stool, think about again, if it's steatorrhea, malabsorption, global malabsorption, or maldigestive materials. If it's not, it's more watery, think about the osmotic laxatives. And then lastly, is it inflammatory? Think about the inflammatory mediators and things like that that would be present within the stool, and think about IBD.

All right, now let's talk primarily about the complications only of acute diarrhea, because for chronic diarrhea, we're going to talk about malabsorption more specifically on its own in a separate video. So we're going to focus only on the complications of acute diarrhea.

All right, my friends. So now we're going to move on to the complications of diarrhea, right? So when a patient has acute diarrhea, I think the biggest things to remember is when they come in with this intense either watery diarrhea or the bloody mucoid diarrhea, it's important to be able to look out for these following complications. I think one of the first ones is hypovolemia, right? If, especially if a patient has more of that like non-inflammatory type of diarrhea, they're having tons of high-volume, very voluminous watery stools, they're going to lose a lot of like fluids within their GI tract, right? So if you're not absorbing things, and on top of that, you're secreting heavy amounts of fluid, this is definitely a problematic issue. And so what happens is, is you're not getting a proper absorption of straightforward water, right? And even to some degree, electrolytes like sodium and water. I would also include something like that as well. So sodium and water. With that being said, if you don't absorb these, what happens to your blood volume? It drops. And if your blood volume drops, what happens? Well, now we consider this patient to have hypovolemia. How does hypovolemia present? Well, it really depends upon the severity of hypovolemia, right? This patient can present a variable amount of ways. So they could present with tachycardia, maybe they have a high heart rate. This is usually one of the signs of like a really bad hypovolemia. Um, they could have low blood pressure, so they could be hypotensive. I'd say that this is usually when it's pretty bad. I would also say that you're starting to maybe see signs of like, you know, physical exam findings, so dry mucous membranes, right? So we'll say that they appear dry. So we'll say dry mucous membranes, dry membranes. We also use that term, skin turgor, that their skin turgor is definitely affected as well. And I think these are some of the definite findings here that would be suggested that the patient is hypo. Maybe the urine output's a little bit low as well, and they have an acute kidney injury as well. But these are some of the findings I would watch out for.

The other thing is that you also have a lot of problems, particularly with electrolytes, right? So you, you know, you're you're constantly not allowing for proper absorption, especially of potassium. And that could definitely lead to patients developing low potassium, which we call hypokalemia. So watch out for hypokalemia. But I think one of the other ones that's really helpful, 'cause it's like, it's one of those that you constantly are being tested on between vomiting and diarrhea. And vomiting, you're losing lots of protons. In diarrhea, you're losing a lot of your basic bicarbonate. And so because of that, you're not giving an adequate amount of contact time for the absorption of bicarbonate. And so bicarbonate is not going to be absorbed. And if bicarbonate isn't absorbed, what does that call whenever your your bicarb is really low within the bloodstream? That's called a metabolic acidosis. So if you have low bicarb, we can see this patients developing what's called a metabolic acidosis. And usually this is of the non-anion gap phenomenon type, right? So I think this is important to remember that in patients who have diarrhea, this is small bowel, large bowel, but you're impairing all of these processes. And that's one of the big things. So really, really watch out for checking their chemistries to look out for any features of electrolyte disarray, looking for features of a patient having hypovolemia, and watch out for that metabolic acidosis.

The other thing I would really watch out for in these patients more particularly is the patients who have that mucoid or bloody diarrhea. So in those patients, you're definitely concerned that they have that dysentery type of appearance, right? And with that being said, that definitely suggests more colon involvement, right? And so these patients will often times, we'll kind of highlight this in red here, have intense kind of like colitis, inflammation of their large intestine. I'd say we see this a lot with your EHEC, your Shigella, your Salmonella. So these are really, really scary ones. So one of the things that you'll have is if patients develop colitis, is they'll definitely have abdominal pain. The other thing is that this is definitely inflammation, it's going to really crank up your white blood cells. You're going to develop a cytokine storm. So you're going to see these patients developing high white blood cell counts and fevers. And so I would really, really be cautious in these patients if you have a patient with really terrible abdominal pain, they have an increased white blood cell count, and they have fevers in the setting of really bloody mucoid diarrhea. And so in the scenario of dysentery, I would definitely be concerned that these patients have a really bad colitis, and they can get a lot worse. So sometimes if this back, you know, these bacteria have the opportunity to, these can really continue to cause a lot of damage, and sometimes they can even translocate across the gut into the bloodstream and cause sepsis. So really, really careful to watch out for that one.

I say the worst-case scenario, though, is if this continues. So if a patient continues to have colitis, as we talked about here, what happens is this chronic inflammation, it just shuts down the contractile activity. And so what happens is these kind of these colon, like the muscles and the myenteric plexus here, you just shut down a lot of the motor activity. And so these muscles and nerves in that inflamed area of the colon stop working. And so because of this massive inflammation here, we'll kind of continue to represent this, this massive inflammation here of the colon, you start to shut down the motor activity. And as that happens, the colon begins to dilate. It's kind of like if you think about it like localized ileus, if you will, right? You're just kind of shutting and paralyzing this portion here. And so this causes massive dilation of the colon. The problem is, is if this dilation gets to greater than 6 cm, we just don't call this dilation, we give this a very specific name, we call it megacolon. So it's a toxic megacolon. So whenever this point has gotten to greater than 6 cm, we now have a patient who has toxic megacolon. What's the fear of a toxic megacolon? The fear is if this is really, really big, you can start to increase the risk of that intraluminal pressure being high enough that it can lead to perforation. And if these patients perforate, if they develop a perforation, then this can cause them to go downhill extremely quickly, right? Because perforation can then lead to sepsis, it could lead to peritonitis, right? So sometimes these patients can then quickly kind of deteriorate via the peritonitis, or they can deteriorate via sepsis. And so I think that's important to be able to remember in these patient populations. So again, patient comes in, they have fevers, abdominal pain, elevated white counts with this mucoid and a bloody diarrhea, think about colitis. You'll be able to pick this up off of imaging. If that kind of gets to the point where their abdominal pain gets much, much worse, and then radiographic films show that there's massive dilation to the point where it's greater than 6 centimeters, they have toxic megacolon due to that infection. The scary thing about that is there are a high risk for perforation. They can develop peritonitis, pneumoperitoneum, and sepsis.

Finally, the last complication, I don't want to add it in here, but I think it kind of comes up a couple times, and it's called hemolytic uremic syndrome. So in patients who have hemolytic uremic syndrome, I think the big things to watch out for here are two particular types of bugs, all right? Two particular types. And this is going to be your Enterohemorrhagic E. coli and your Shigella. These are the ones that I really, really want you guys to be very cautious of. If you see these somewhere within the question stem, these are two of the bacteria that are scary in the sense that they can undergo, especially if they have massive inflammation. So if they cause that, sorry, that colitis factor that we talked about, remember how it causes massive inflammation here? I told you that these bacteria can translocate. And so if they do translocate, so here we're going to say that there's a little bit of bacterial translocation here, so there's some bacterial translocation. What's the potential problem with this? The potential problem here is that these bacteria, once in the bloodstream, can definitely kind of throw off your clotting process. And what they'll do is they'll unfortunately lead to lots of clots. The mechanism of this isn't completely understood as to why, but it may increase some of the inflammatory cytokines, which activates your procoagulant cascade. And so what ends up happening is these patients start to experience some type of like coagulopathy.

Where they start kind of clotting now. The crazy thing is, is that as red blood cells start moving across this of clots, they start shearing some of the red blood cells up and consuming more of the platelets. And so what ends up happening out of this is two things.

One is you actually consume platelets. And what is that called whenever you consume the platelets and they drop? It's called thrombocytopenia. And so they'll develop something called thrombocytopenia where those platelet levels will will start to drop.

The other concept is that you will chew up the red blood cells. What's that called when you chew them up and you drop the red blood cell levels? Anemia. But we call this hemolytic anemia. So now a patient has hemolytic anemia, which is going to be busting open or ripping up one of those red blood cells. Consumption of the platelets and that's now called thrombocytopenia.

The other problem is is that these kind of clots, they start to occur in some smaller vessels in the body. And one of the most, like, unfortunate areas is the kidneys, in these actual glomeruli. So another thing that actually happens here is that these glomeruli get plagued. And now you're altering the renal perfusion and the filtration process. And so what ends up happening here is these patients, because of these altering the renal perfusion and the filtration process, you drop off their GFR. And if you drop off their GFR, you can potentially lead to two things.

One is you could drop their urine output. And the other one is you could potentially increase their creatinine, which is kind of an example of a kidney injury. And this would be an acute kidney injury. So if these patients have, well, we've kind of like in this particular sense, say an acute kidney injury, which is kind of based on a rise in the creatinine, a decrease in the urine output, I apologize, decrease in the urine output. And on top of that, an increase in another molecule that's also helpful here, which is BUN (blood urea nitrogen). Increasing the BUN, increasing the creatinine, and a drop in the urine output suggests an acute kidney injury.

If on top of that, you have thrombocytopenia and hemolytic anemia, you have the triad, if you will, of hemolytic uremic syndrome. So again, acute kidney injury, thrombocytopenia, and hemolytic anemia suggest hemolytic uremic syndrome in the setting of EHEC and shigella.

Okay, now we've covered the complications of acute diarrhea. Now let's move into the diagnostics. We talked about acute diarrhea, which can cause a lot of complications, right? It's really important to be able to identify that. So let's actually go through this patient. First thing that we have to do is rule out any kind of complications that they may have from their diarrhea, which was hypovolemia, hypokalemia, metabolic acidosis, hemolytic uremic syndrome, toxic megacolon, or perforation.

So if I get a CBC and BMP, this will help me to identify the HUS and it'll help me to identify any acute kidney injury, hypokalemia, hypovolemia types of complications. If I see that their hemoglobin, hematocrit's low, their platelets low, and they have an increase in their creatinine, oh, this is HUS. That's a complication. I'm scared that they have some type of EHEC or shigella infection.

If I see that BUN, creatinine's high, and I see that their potassium's low, that definitely tells me that they have hypokalemia due to the poor perfusion of the kidneys. And low potassium is because they're they're actually kind of not allowing for the absorption of that potassium.

The next thing is I have to remember that if a patient has hypovolemia because of their diarrhea, they have colitis. Which is maybe they have an increased white blood cell count, maybe they have a fever, they have, you know, some definite large amounts of diarrhea. Or they have an immunosuppressed state. Maybe they have HIV, maybe they have some type of medication that they're taking like an immunosuppressant medication, or they're just post-transplant, they're on immunosuppressants to prevent them from having a rejection of their transplant. These patients are super high risk and can get really, really sick.

So hypovolemia, they can go into shock. Colitis, they could develop toxic megacolon and perforation. Immunosuppression, they could develop severe sepsis. And if they're having diarrhea for three plus days and they're not getting any better, they could start to develop severe hypovolemia. This is a patient that's very high risk and they deserve a further workup of the type of pathogen that they have. In that scenario, and only in that scenario, would we obtain a stool analysis.

If they're hypovolemic and requiring lots of fluids, if they have a very high fever, leukocytosis, and I apologize, and I've had persistent diarrhea for more than three days, you need to get a stool analysis.

What does this consist of? The first thing that you want to look at is the fecal white blood cells and the fecal calprotectin. If it's elevated, that tells me right away, oh, this is an inflammatory type of diarrhea. That's not good. All right. I just don't know which type yet. I get the stool culture. And the benefit to that is it tells me what type of bacteria it is. And believe it or not, that's very, very important because we don't prescribe antibiotics, preferably, to patients who have enterohemorrhagic E. coli because they're at high risk for HUS. So stool culture will help me to guide which type of antibiotic I'm going to prescribe.

Ova and parasites will tell me if I have any type of parasites. Do I have Entamoeba histolytica, Cryptosporidium, Giardia? And then norovirus and rotavirus testing will help a little bit to at least more particularly guide maybe, um, separating people from one another. In other words, if I have the norovirus, I should probably have this patient avoid human contact. I should isolate them away from other people so they don't spread that infection. If they have the rotavirus, I should maybe have my child stay home so that they don't go to the daycare and pass that on to another individual. So that may be the benefit of that. Either way, it'll help me to identify the type of infectious diarrhea that they have and guide my management.

All right guys, let's move into the next part here, which is the diagnostic approach of chronic diarrhea. So we have a patient who comes in, they've had greater than three loose stools per day for greater than four weeks. Pretty terrible. We should definitely be able to figure this out. I think the first thing that's really helpful to determine is if it's inflammatory or not. That really kind of gives you the first start here. So obtain right away the fecal white blood cells, the fecal calprotectin. I didn't even get a fecal occult blood test. The reason why is if these are elevated, automatically tells me that there's inflammation. In the fecal occult blood test, there's usually going to be some degree of blood in the stool. That's going to help me right away to determine if this is inflammatory or not.

If it comes back elevated or positive fecal occult, then it's inflammatory. I just have to figure out if it's chronic infection or if it's an autoimmune disease or autoimmune attack in the form of IBD. So what do I do? Get a stool analysis. If I get a stool analysis and it shows me that the stool culture, the ova and parasites are negative, it's unlikely a chronic infection that they've been kind of colonized with. It's likely going to be IBD. Get a colonoscopy. This will tell you if it's ulcerative colitis or Crohn's disease based upon the appearance of the colonoscopy, the biopsy findings. And then from there, you've diagnosed it as IBD. Treat that accordingly.

If you do the inflammatory testing, again, shows you that the fecal white cells are up, shows you the fecal calprotectin up, shows you if fecal occult blood test is positive, it doesn't tell you if it's a chronic infection or if it's IBD. You just know that it's inflammatory. Get the stool analysis. If the stool analysis at this point shows you that it's positive stool culture, maybe it contains a particular type of bacteria like C. diff, or their ova and parasites come back positive and it shows you that they have a chronic infection with Entamoeba histolytica or Cryptosporidium. Cool. You know that it's a chronic infection and you'll treat that accordingly.

Once you've ruled these out, so in other words, you say, okay, I have no fecal white blood cells, no fecal calprotectin, my fecal occult blood test is negative. Then I just need to say it's either osmotic or it's secretory. So then what I'll do is I'll get a stool osmotic gap. The purpose of this is you're just taking 290, subtracting it from a multiplication factor of two from their stool sodium and their stool potassium. That right away should make me think, okay, if my stool sodium and my stool potassium are high, which is in secretory, I'm taking 290 and subtracting from a big number, that means that they'll have like a smaller osmolar gap. And if I take a patient who has osmotic diarrhea, they'll have a normal sodium, normal potassium. So their osmotic gap should be like a little bit on the, let's say, higher side, because I'm taking a big number and subtracting it from like a normal number.

So if my osmotic gap is less than 100, what that's telling me is is I'm taking 290 and subtracting it from a big number. That means that there's a lot of sodium and potassium in their their stool. This has to be secretory diarrhea. From there, I'll say, okay, it's either hormones or it's laxatives. Remember I told you that check their VIP levels, their serotonin metabolite levels, and gastrin levels. If VIP is elevated, it's probably VIPoma. If their 5-HIAA levels are elevated, it's probably carcinoid syndrome. And the gastrin levels are elevated, it's probably gastrinoma. Right away, that's pretty easy, right?

If these come back negative, then it's probably some type of laxative abuse or a stimulant laxative. And again, we took the example of senna and docusate sodium being the example. Think about this in a patient has chronic constipation, they're taking these regularly. The other one is osmotic gap greater than 100. That tells me that the stool sodium and the stool potassium is normal. They're not very high. All right. So in that scenario, if the osmotic gap is greater than 100, it's osmotic diarrhea.

In this scenario, I told you it's either maldigested or malabsorbed nutrients, or it's potentially some type of osmotic laxative. So how do I determine this? First thing I need to think about is in malabsorption and maldigestion, one of the biggest things is is I can tell if they have lots of fat in their stool or not. So what I want to do is I want to get a fecal fat test and a hydrogen breath test. And this will make a lot more sense when we go through the malabsorption lecture. The reason why is if the fecal fat test is positive, that tells me it's a global malabsorption. Something like celiac disease, tropical sprue, um, maybe Whipple's, or even exocrine pancreatic insufficiency.

If my fecal fat is negative and my hydrogen breath test is positive, it tells me that there's probably some type of large amounts of undigested carbohydrates in my GI tract, such as lactose intolerance. And that's an example of a partial malabsorption. And if in this scenario, the fecal fat is negative and the hydrogen breath test is negative, it's no malabsorption or maldigestive syndrome. It's likely the laxatives. And then look for a history of lactulose use, magnesium citrate, or polyethylene glycol.

All right, we've gone through it, my friends. Now we've got to talk about the treatment of diarrhea. And these patients who have diarrhea, acute, greater than three loose stools per day for more than, at least in this case, less than two weeks, is what we would define it as. For these patients, it's all about treating the complications first. Do they have features of hypovolemia? Do they have low blood pressure? Do they have compensatory tachycardia? Do they have dry mucous membranes? Do they have decreased skin turgor? Are they not making a lot of urine? And maybe they have an acute kidney injury because of this. Give them fluids. If they can ingest fluids, great. If they cannot ingest fluids, you want to give them IV fluids. Often times it's a combination of both. Just make sure that you, as you're giving them fluids, you're monitoring for improvement in their blood pressure, their heart rate, their urine output, or their appearance of their dehydration.

Severe colitis. So if this patient has a high fever, they have a white blood cell count, they have evidence of a very inflamed colon on their imaging, that's a very sick patient. And I really should consider if this patient has these to really start antibiotics on them. Another indication for antibiotics is if they're immunocompromised. The reason why is if they have an infection like an infectious diarrhea, yes, it could be cleared, but if they're immunocompromised, they may not have the immune response that they can mount that's good enough to clear that infection. And these patients are candidates for antibiotics.

Question comes up, okay, which type of antibiotic do I put them on? It really depends upon the type of pathogen. That's why you would do a stool culture or stool analysis. For example, if it's really something, for example, like C. diff, that's usually vancomycin or metronidazole. If it's Giardia, that's usually metronidazole. Um, and generally, if it's something like Campylobacter, that would be more like azithromycin. Really any other invasive pathogen, you could treat with, you know, ciprofloxacin. So that's the big thing to remember is often times a fluoroquinolone is going to be sufficient. Azithromycin may be better for Campylobacter. Um, metronidazole is going to be more preferred for Giardia. And then vancomycin or metronidazole is preferred for C. diff.

Now, with that being said, I think it's important to remember that hemolytic uremic syndrome is a definite complication of EHEC or shigella infections. If it's combined with an acute infectious diarrhea, and again, in these particular patients, it is of utmost importance to avoid antibiotics. The reason why is there's been a lot of studies that have showed that the utilization of antibiotics like for example, fluoroquinolones in a patient with EHEC or shigella, it can actually cause a worsening destruction of those bacteria. They pop open, they worsen the coagulopathy, they worsen the hemolytic uremic syndrome.

Same thing if you give them loperamide. Loperamide basically prevents them from having diarrhea. So it decreases the contraction of the the actual bowels. Problem is is that you don't clear the effect, the elimination, or you don't clear the infection. So I'm not eliminating the infection out of my stool. Therefore, it stays in larger amounts in my colon and then worsens the the infection of the colon, worsens the release of these bacteria and seeding of them into the bloodstream, which would can worsen their HUS. So it's often times really important just to provide supportive care. Don't give them platelets because it actually could worsen the thrombocytopenia. Try to, you know, give them hemoglobin or give them, um, red blood cells only if their hemoglobin is less than seven. And just monitor them for any severe acute kidney injury. Do they need dialysis? In other words, do they have refractory hyperkalemia? Do they have a metabolic acidosis? Do they have, um, severe hypovolemia? In those particular scenarios, they may need dialysis.

The last thing I think that's important to remember is if you're going to treat acute diarrhea with an anti-diarrheal agent, it is of utmost importance to avoid loperamide so that they can clear the infection. One that can be potentially beneficial and doesn't increase the risk of hemolytic uremic syndrome or worsening of their colitis is bismuth subsalicylate. So that's something to potentially consider.

Chronic diarrhea patients. This is a little bit different. You really have to be able to identify their underlying cause. So you have to say, are they on some type of like laxative? Discontinue that. Osmotic or, um, stimulant laxative? Is this some type of like hormone-related problem? You have to treat that underlying hormone-related problem. Is this some type of malabsorption or maldigestive disorder? You have to treat that problem. And again, is it some type of inflammatory bowel disease? You have to treat that problem. So that is of utmost importance for the other component here, which is these patients, they're not really, as long as it's not some type of infection that if it is blocked off, it won't cause a worsening colitis, you can give these patients anti-diarrheal agents like loperamide. That is safe. It's just best to avoid this in acute infectious diarrhea.

All right, my friends, that was a lot. And I really hope that this made sense. Thank you guys for watching this video. I hope it helped. I hope that you learned a lot. As always, love you. Thank you. And until next time.

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