Hi everybody, and welcome to this session on chronic diarrhoea. So the idea is that we're going to talk through how I approach these cases in order to achieve, a diagnosis. And as we go through it, a lot of what I will say will be based on anecdotally, what I find works, but a lot of it as well will be based on information that's out there in the literature as well.
So try and highlight those points, as we go through the talk. So first off, let's define diarrhoea, and talk about why it's so important, in small animal internal medicine. So diarrhoea is one of the most common reasons for presentation to veterinarians, as you'll all know.
And whilst acute diarrhoea is often self-limiting and requires minimal investigations and often minimal to no treatment, chronic diarrhoea is very different in that it often requires, multiple tests and or trial treatments, often over a period of several weeks, with quite a variable expense incurred by the clients as well. So, What I often do from the get-go with these patients is really start the ball rolling on managing client expectations. You know, these are not the kind of patients that we can just wave a magic wand and get a diagnosis and solve that problem.
It can take a long period of time to get an answer in these patients. So, most cases of chronic diarrhoea, can certainly be successfully diagnosed and managed in first opinion practise. However, there are some cases, that might benefit from referral, and those are often, the ones that fail to respond to routine management or therapy.
Those with severe signs of disease, for instance, patients with really quite, bad protein losing. Enteropathy, or those in which a diagnosis has not yet been made. So that's, that's where, referral clinicians like myself come in.
But pretty much all of this will be talking about how we approach these guys in first opinion practise, OK? Having been in first opinion practise for many, many years, myself as well. So a little bit on the pathophysiology, literally just one slide, so don't worry too much.
Diarrhoea is defined by the passage of faeces with excess water and or nutrient content, which changes the character of the faeces. And it's often due to one or more of the following processes. So the first one is osmotic diarrhoea, and that is a process whereby you have increased levels of unabsorbed or undigested nutrients within the gut lumen.
And that causes an increased oncotic pressure, osmotic pressure, sorry, within the, gut lumen that draws fluid into it. So a really good example, of a disease that causes this would be, exocrine pancreatic insufficiency, where we have maldigestion of our food and therefore lots and lots of nutrient, passing through the bowel. That's undigested.
We then have secretory diarrhoea, and that is a path physiological process whereby often infectious organisms, cause inflammation of the crypts that line the intestines, and when they become inflamed, they often hypersecree fluid into the bowel lumen, and the bowel lumen is not able to keep up with that and absorb enough water to compensate. We then have motility disorders, and there are two forms, hypomotility, which is by far the most common, and we see that with lots of different inflammatory diseases of the bowel, and it basically causes areas of reduced segmental contractions, which reduces the efficiency of nutrient digestion, absorption. And fluid absorption as well.
So you see this in lots of different, disorders. We may see hyper motility as a cause of diarrhoea in some patients, because of, very much increased motility. And a good example of that would be a cat with, hyperthyroidism.
We've then got the group of disorders that come under abnormal permeability, and these are diseases that cause damage to the paracellular, tight junctions between cells. And that can be secondary to inflammation, erosion or ulceration, and that causes excessive loss of fluid, but also, in more advanced cases, protein as well into the gut lumen. So this is one of the, main, pathophysiological processes that occurs in patients with protein losing and turopathy that we're gonna touch on again later on.
So let's talk a bit more about defining the problem. Well, the actual definition for chronic diarrhoea is, a patient who's had diarrhoea for more than 3 weeks that has failed to respond to symptomatic therapy. OK, that's easy enough to remember.
We then can start to think about how we, determine the nature of the problem. And this is something I'll touch on. Quite a few times throughout this talk, and we're basically talking about this patient's diarrhoea and saying, does this appear to be primary small bowel diarrhoea, primarily large bowel diarrhoea, or a clear, mix of both types of diarrhoea?
Because that can help us guide our treatment plan, but also how we investigate these patients as well. It's also very important to divine, the severity of the problem from the outset as well, so that again, we can manage client expectations, but also we can decide how aggressively we need to investigate and then treat these patients. And finally, don't forget as well that some small intestinal diseases do not cause diarrhoea at all, OK?
So, there being no diarrhoea does not exclude a small intestinal disease altogether, and that's because the colon has a large absorptive capacity for excess, . Faecal fluid. So if you've got a normal function colon, you might not have any diarrhoea whatsoever with with quite moderate small intestinal disease.
So a little bit on to how we can look at disease severity and score these patients, and there's a couple of scoring systems that I want to briefly mention. They're things that I use quite regularly in my patients to help me, assess their severity, and the first one is the SIBDI score from 2003, . And it was published in the Journal of Veterinary Internal Medicine.
Basically, it's a scoring system that we use an initial presentation, and we re-score them using the system after treatment to help us, decide how well our patients are doing. And we tend to refer to complete remission of signs as an over 75% reduction in the CIDA score, whereas partial remission is 25 to 75% reduction in SIDA score. So this is the SII score itself.
It's something that's really, really easy to institute in practise. There's 6 parameters for attitude, appetite, vomiting, stool consistency, still frequency, and weight loss. We score them from 0 to 3 for each of those, sum 8, the values, and then we can use this nice table at the bottom.
To, stick our patient into one of 3 or even 4 disease categories. I tend to find it really useful when I've got a client who's quite resistant to investigation, and I say, look, if your dog is in this severe category, you know, there is certainly some strong but there are some strong reasons why we should. Investigate this as much as possible, and vice versa, when you've got, a client who's really panicking about their patients' GI signs, if they have a very low, SIDI score, you can sort of reassure them that, you know, the lengths to which we need to investigate and treat perhaps aren't quite as extensive.
The CSI score, came out 4 years later in 2007, and this also included scoring for albumin concentration. The presence of ascites or peripheral edoema, obviously linked with concentration, and the evidence of any pruritus. So it was the CIA score plus these three parameters and lo and behold, it was even more powerful to accurately predict outcome than the CIA score, as you can imagine, because as we'll talk a bit later on in this talk, the presence of hypoalbinemia in particular is certainly a negative.
So we're gonna talk about the causes of diarrhoea now, and this is something that I always have in the back of my head before any patient walks through the door. A long list. James, I'm sorry to interrupt you.
I think your microphone has moved. You've gone very dull. Can you hear me?
Yeah, perfect. Thank you. I'm sorry to do that to you.
No, that's OK. So when I'm thinking about my differentials, I group patients often into two types of categories, patients with primary gastrointestinal diseases within the small or large intestinal or both, and patients with extra gastrointestinal diseases. So disorders outside of the GI tract.
And often these patients, have other clinical signs, as well that can help us differentiate them from patients with primary GI disease. So this is a table, that I've put together of what I believe to be the most common causes of chronic diarrhoea. And I'll just touch on a few of them, now, we'll we'll cover parasites in, in, in faecal analysis.
But small intestinal dysbiosis, otherwise known as antibiotic responsive enteropathy or antibiotic responsive diarrhoea, is a very, very important one, that we'll talk about. And, and certainly this is something that's becoming more and more important, . In human medicine, and perhaps you'll know of this under another guise, and we used to refer to this as, small intestinal bacterial overgrowth.
It's now been renamed, but it's the same thing basically. We've then got inflammatory bowel disease, which is a very large group of patients. And this is an idiopathic disorder, so it's essentially a diagnosis of exclusion, and we have to bear that in mind as we're investigating.
In these patients. And this, disorder may also be referred to as simply chronic enteropathy or even steroid responsive enteropathy as as we'll get onto it later on. We've then got the patients who respond to diet, and there are a huge numbers, certainly, around the 50% mark, of cats and, and even dogs with chronic diarrhoea will respond to dietary manipulation alone.
And within dietary responsive enteropathy, we've got two different, types of, of, of dietary responsive disease. Either a dietary allergy, which is based on an immune response or dietary intolerance, which is, not an immune response. OK?
We've then obviously got neoplastic causes, intestinal lymphoma being a particularly, nasty one in dogs. And certainly the large cell variant of this in cats can be very nasty, but do be aware of, feline small cell lymphoma of the intestines, which is actually a relatively, treatable disease that carries a pretty good prognosis, and it is even, you know, converable to, to the prognosis that's associated with IBD in a lot of cats. We've then got some of the other sort of more, you know, less common ones.
And then within the secondary causes of diarrhoea, EPI Xocrine pancreatic insufficiency, it's a very important rule out that we're gonna, talk about a bit later on. Chronic pancreatitis, certainly it could cause diarrhoea and abdominal pain and hypoorexia, but it also will cause diarrhoea. Lots of different hepatic diseases, renal diseases, and then other endocrine diseases.
So hypoadrenal corticism in dogs, hyperthyroidism in cats, and then don't forget cardiovascular disease. They can be quite sneaky ones. Patients in particular who have right-sided heart failure and don't have left sided can certainly present with vomiting and diarrhoea because of GI, wall edoema.
So we'll just talk about those a little bit later on as well. A paper that was published in 2017, took a retrospective look at, the causes of diarrhoea and the cases that they diagnosed. And lo and behold, 90% of, of those patients who presented with chronic diarrhoea had a primary enteropathy, only 10% had a secondary.
And within those primary patients, the vast majority were dietary responsive. And then there was a lot of diagnosis of, of idiopathic or inflammatory bowel disease. 11% were antibiotic responsive, then infectious in neoplasia.
And within the secondary causes, EPI was the most common diagnosis. In total as well, 87% of dogs had clinical remission, in this study, which is quite reassuring, whereas only 13% died or failed to respond to treatment altogether. And those that didn't do very well, generally had diagnoses of severe inflammatory bowel disease or neoplastic disease, which kind of makes sense, .
And, the presence of an increased disease severity score, the presence of anaemia, severe hypoalbuminemia, and or severe hypocabauminemia were all associated with the poorer prognosis. So again, useful little things to keep an eye out for when investigating these patients to help us prognosticate. So this is my really simple 6 step approach to investigating and diagnosing these patients with chronic diarrhoea.
So history and thorough physical examination, rule out and treat endoparasites. Then we're going to try and differentiate primary from secondary causes of diarrhoea and characterise the disease process, and that's gonna be done with blood work and imaging. We'll then move on to therapeutic trials as long as they're not contraindicated, for instance, the patient with PLE has too severe disease, and then patients who fail therapeutic trials will move on to histopathology on GI biopsies for a definitive diagnosis.
So let's go through signalment. It's a pretty important thing to have running through your head before that patient's even walked in the door. What disorders is this patient most likely to have?
You can be refining your list of differentials before they've come into the consulting room. So older animals are more likely to have neoplasia or extra gastrointestinal diseases such as chronic kidney disease. Younger animals, are unlikely to have those, but are, you know, more likely to have infectious or dietary diseases, and may also, be at risk of developing, into susception.
When we're thinking about breeds, there are some really strong, breed predispositions. So some breeds even have their own enteropathies, such as Sharpei enteropathy, which is a form of a protein losing enteropathy, which is not very nice to treat. And there are also some breeds that unfortunately are predisposed to multiple enteropathies, so EPI, IBD, and antibiotic responsive diarrhoea in German shepherds, for instance.
Sex and neuter status generally is not so useful. So we're then gonna move on to the history taking. And, and this is definitely a very, very important part, of the workup as well, but some things are more important than others, and I'll highlight those as I go through it.
We're going to want to ask the clients how long has the patient, been ill. Are there any other animals in the household, and if so, are they ill, because that would increase the index of suspicion that this is something, infectious or potentially dietary. They all be the same thing.
Has there been any previous response to trial treatments, and if so, which medications and, and what dosages, as we'll touch on a bit later on. Do the owners have diarrhoea? Certainly zoonotic diseases such as jardiasis, could cause the owners to have diarrhoea as well.
And then a really, really important one for me to ask, has this patient maintained normal weight or lost weight and what's the patient's appetite like? And this is really important because it can really help us refine differentials. So patients who are, You know, normal appetite, normal weight, you know, generally don't have too severe disease, OK?
Patients who have reduced appetite and losing weight, often have quite severe disease, and often diseases that are quite inflammatory such as advanced inflammatory bowel diseases or neoplastic diseases. They feel sick and don't want to eat and are losing weight. Whereas patients who have weight loss despite an increased appetite, they're a really important group of patients because, These are patients who are polyphagic but losing weight, often because they have one of the following three things maldigestion, so they're unable to digest their food to absorb the nutrient, malabsorption, they're unable to absorb the nutrients, or malassimilation.
They're able to absorb their food, but not able to utilise the calories appropriately. So a good example of maldigestion again would be EPI, malabsorption, you can see with almost any small intestinal enteropathy. And malasimilation is something you can see perhaps in a diabetic patient who's losing lots and lots of calories in their urine through glucose.
We're going to ask the clients, are there any clinical signs of extra gastrointestinal diseases such as PUPD things like that, and we're gonna ask the clients if that pet is vomiting. And I do that because vomiting is often associated with small intestinal disease. However, cats can vomit with disease of the colon, so they are a bit tricky and don't follow the textbooks, so just be aware of that.
But it is a question that I do like to ask because it it helps me, decide if there is also, you know, small intestinal and or gastric involvement in whatever disease is going on. When we're asking about the regurgitation, vomiting, sorry, we also have to be very cautious, that that patient isn't actually regurgitating, and we all know how to do that by asking the right question. An important thing to rule out at this stage.
We're then gonna start talking about diet. So we're going to ask them, are they on a dry diet? Are they on a wet diet?
Is it a commercially available one? Is it prescription? Is it raw, lo and behold, how do they feed their pet?
Is it ad lib or restricted? When was the diet last changed? What effect did that have on the diarrhoea?
Do the clients tidbit, which is an important question to know now when we're thinking about, elimination diets a little bit later on down the line. Has the patient been lethargic or weak, and then the usual questions of vaccination, roaming status, long term meds illnesses, and or travel history. And then we're gonna get to the part where we ask the clients lots and lots of, very unusual questions about their pet's diarrhoea, such as how watery is it, what's the volume, how frequent, what's the colour like?
Is there any tensmus or straining associated with it, mucus, hematochezia. Melina. And also, does the diarrhoea, occur at times of stress or dietary indiscretion, you know, because patients who have, colitis type diarrhoea during periods of stress often have a diagnosis of irritable bowel syndrome, which is something that's, you know, diagnosed and treated in a very different ways to, enteropathies.
So this is a little table. Of the questions and the tick list that I go through in my head to help characterise that patient's diarrhoea. So small intestinal diarrhoea is generally large, watery, and explosive in nature, very rarely with mucus or fresh blood, but you may see digestive blood melena .
If there is ulceration or erosion, you'll sometimes see fat within it. The colour is often very variable, yellowy brown, and it may occasionally have, undigested food in it. There is very little, straining associated with small intestal diarrhoea, and it is frequent but not that frequent.
We're expecting patients to have 2 to 4 episodes of diarrhoea per day, perhaps. And they're not that urgent with it. They can hold on to it until the back door's been opened and get out.
And as I say, patients, will quite often vomit with small test of disease, sometimes have flatulence, and sometimes have weight loss, and sometimes have, hypoorexia or reduced appetite. Large bowel diarrhoea, however, is often small and semi-solid, in its nature. It's very common for it to be mucus in there and fresh blood, .
The colour is often quite bright and vibrant, as I'll show in the next slide. We don't tend to see undigested food in there, and it's really common for these patients to have tinesmus and straining. A lot of clients I find mistake colitis or constipation, as they see their pet straining unsuccessfully and then passing small amounts of faeces and presuming they're constipated, when they're not, .
Often with very increased frequency, defecating multiple times per day and multiple times per walk, often with quite a degree of urgency, and it's very uncommon, as I say, for vomiting to occur in large intestinal disease. We also very uncommonly have weight loss or hypoorexia in these patients as well. On the left is a good example of some small intestinal diarrhoea, .
It's from one of the pets that's owned by one of our receptionists at work. Thank you very much. And on the right, was one of my patients who had really classic colitis type diarrhoea, lots of fresh mucus, blood, fresh blood, sorry, mucus, and very vibrant colour to the stool, that's sort of semi-formed and not not as watery as the one on the left.
OK, so we're gonna move on to the physical examination now. And unfortunately, there's not a lot that we can tell about these patients from their physicals. They're often very, very unrewarding, as you know yourselves.
One thing that we definitely want to do is bodily conditions score these patients, because again, that'll tell us a bit more about perhaps the severity of the patient's disease. It'll also help us to monitor, their treatment response nicely as well. We're gonna check hydration status, and of course, we're going to do a deep abdominal palpation.
We're primarily looking for evidence of masses, You know, of any of the abdominal organs, any evidence of pain that might be referable to pancreatitis, any abnormalities of the small intestine, and often they're really, really very boring to palpate. I think the exception to that is the, those cats with small cell lymphoma of the intestines and you feel those guys and they've got really, really rubbery tubular intestines that are really quite characteristic. And sometimes as well.
Patients I've found with EPI, cats, that is with EPI, their small intestines can feel really distended and full of all this undigested food that's passing through. They can be quite spectacular to palpate as well. And we might in cats be able to palpate in large lymph nodes, but not in dogs, and of course we're going to check the kidneys as well in cats.
We'll always perform a rectal exam, although it's something, that I think can be overlooked, in, in that sort of 7.5 to 10 minute consultation, but we really do need to do that. Firstly, to check the stool again, the owners may not have reported Molina, but you can, do a digital and just check the colour of the.
Faeces, if there is any evidence, have a good feel around, and check for any evidence of hematochezia, any changes in the mucosa, or any masses such as rectal polyps, which quite easily, you know, be diagnosed. And then we're gonna obviously screen for patients with cardiovascular disorders, as well. So on to testing, we've done a physical exam and history and we're already refining differentials, but all of our diarrhoea patients need a bit of faecal work.
So what do we need to bear in mind about faecal testing? Well, generally, it has a high specificity, but a low sensitivity. So, if you find an organism in that dog's faeces, that organism, you know, is there.
But if you don't find an organism, it does not mean it is not there. OK, so we do need to bear that in mind. And also, as we'll talk about in a few of these other specific, infectious diseases, identifying, an organism within the faeces does not prove causality that that organism is, is causing the diarrhoea.
There are a lot of, bugs that can be innocent bystanders that we need to be on the lookout for. So what would be, My general approach, well, I perform, a faecal smear in-house, a sedimentation and a flotation externally to for over larvae and oocysts. I'll perform ardia antigen testing, potentially a ZN stain for crypto young animals, salmonella and Caylobacterculture.
In cats that I think are at high risk of tritrichomonas, I'll perform a PCR, so tritrichomonas is, . A protozoal cause of large bowel diarrhoea in young pedigree cats. And it can be really, really, quite uncontrollable, large bowel diarrhoea, and in some individuals often lead to a degree of faecal incontinence where they just continuously dribble, diarrhoea, from, from the rectum.
So that's one that we need to have on our radar. So I'll do all of these tests, and even if they are all negative, I will send all of my patients home on a 5-day course of fenbendazole at 150migs per kg once daily, just to be 100% sure that we've covered, for any, worms, but also for Giardia as well, because, as I've said, not all of our tests are, that sensitive, for these, infectious diseases. OK?
So just a bit about each of these individual bugs. So Giardia, can be tested for most accurately on an elizer. It's much more sensitive than just doing a microscopy, alone.
So, that's, that's something I would recommend in all patients. We can do it the external lab or we can do that, in-house on an IDEX, snap test, which is now quite readily available. And that's reported to have really pretty decent sensitivity at about 90%, and 100%, specificity as well.
Do bear in mind when we are testing for Jardia, that jaardia and tritrichomonas as well can be found in the faeces, of normal animals as well. OK, so potentially, you know, we will identify that organism, but it's not the cause of the diarrhoea. I'm sure we're going to treat that individual, but if they don't respond to that treatment alone, we do need to start thinking about, other causes that patient's diarrhoea as well.
It's a nice and easy one to treat, as we all know, with a short course of fenbendazole, or metronidazole. But infection is not always eliminated in every case. So sometimes, these patients will still remain positive on their snap tests even after treatment.
And some patients as well are at risk of, reinfection. So we need to make sure that clients, are disinfecting their households really nicely, so that patient doesn't reinfect itself from, for instance, a dirty litter tray. Tri Trichomonas, as I said, something we're looking for in cats, and we do a PCR to test for this, because it has a much higher sensitivity than other methods of testing.
Couple of take home messages about that though, the faeces really does need to be as fresh as possible. So what I tend to do is contact the lab that I'm sending it to, ask what days they run the test, and then, figure out, what day is best to collect that faeces from the clients so that. It arrives to the lab as fresh as possible because the older that sample is, the lower the sensitivity, and often once it's more than sort of 4 or 5 days old, even the sensitivity really, really, really does drop.
And we would recommend the owners again pull multiple faecal samples, to send away for analysis of this. And we might even perform a faecal wash, where we instil 20 mLs of warm saline into the colon and aspirate that to send for analysis. If we do an in-house, Smear or a wet mount, as it's otherwise called, these organisms will be seen swimming around, hopefully, if they're there, and they often have this jerky, forward motion which can help differentiate them, from Giardia.
The treatment of these is, is very specific, and that's why we do need to always screen for this if there's any, suspicion of this disorder, and that's with Renidazole at 30 metres per k once daily for 2 or 3 weeks. A little bit on salmonella and Campylobacter. So there's lots and lots of species of Campylobacter out there that cause, you know, enteric disease in in dogs and cats, but they're most significant in young animals, because they have a naive immune system.
So certainly Campylobacter, juni is, is sort of something that we should be looking for in young individuals with diarrhoea, as it could be causing their signs, but also because it has a synergistic role with other enteric pathogens such as parvovirus, jardia, and salmonella as well. As I've mentioned already, there are innocent bystanders, and Campylobacter is a common one. OK, so Campylobacter, can often be found in the faeces of diarrheic animals, but it's actually not commonly the cause of their diarrhoea unless they're quite young, for instance.
And, and in one study in cats, Campylobacter, interestingly, was isolated more frequently in, in cats without diarrhoea than those with diarrhoea, so. Things to bear in mind that even if this is the cause of the diarrhoea, normally, you know, these clinical cases are quite uncomplicated, uncomplicated, pardon me, and self-limiting, and resolved with supportive therapy alone. So isolation of compyloact does not confirm causation and treatment is often not warranted in a lot of cases with this.
The sort of exception, to that would be patients that are very immunocompromised, febrile. Or with evidence of severe hemorrhagic diarrhoea, or that are owned by immunocompromised humans, and we're worried about, the risk of zoonosis. And in those patients, we would recommend treatment with erythromycin, these sort of standard dosages.
Onto salmonella, salmonella, very uncommonly causes, diarrhoea in cats and dogs, although it, it can be seen causing clinical diarrhoea, in puppies or in, in kenneled populations or raw fed dogs. Antibiotics are generally not indicated in patients of salmonella because it's normally self-limiting, and actually, putting these patients on antibiotics can, can select for a very antibiotic resistant strain of salmonella and more severe infection, plus antibiotics potentially can alter your gut flora, and your gut flora naturally is there to help fight off, these more pathogenic organisms. And so only supportive therapy is required in in some generally.
So we've done our physical and history and our faecal analysis and we've ruled out, parasitism. We're now going to move on to looking at excluding gastrointestinal diseases and learning a bit more about the the primary GI diseases. So at this point, my standard approach would be a full biochem with urinalysis and haematology, PLI, TLI, folate and carbalamine.
In all patients, I would do a basal cortisol in dogs at this point, and I'll talk about that in a few more slides, and also a total T4 in the older cats to screen for hyperthyroidism and a fib and valve as well in cats. Bile acid stem as well would be appropriate if we are suspicious of hepatic dysfunction or shunting diseases. So the BUN and creatinine.
On our biochemistry may be elevated if our patient has a pre-renal lasotemia because they are dehydrated because of the diarrhoea, or because they simply have, renal aotemia and, and the cause of their diarrhoea is chronic kidney disease. So this is where we need our urinalysis to help differentiate those two because with pre-renal lasotemia, we would expect appropriately concentrated urine in a highSG, whereas we wouldn't see that, with, chronic kidney disease or renal failure. Total proteins are a very important one to look at on the biochem, and we're really looking to see if there's any evidence of PLE.
So patients with PLEs often have reductions in both the albumin and the globulins, because of loss through the GI tract, which differentiates them from patients with PLNs, protein nephropathy, who generally just lose albumin through their kidneys. The total calcium in a patient with low protein levels will also be low as a large percentage of calcium is protein bound, so we don't get too excited, about that. ALT and ALP elevations, so they will obviously be seen in patients with primary hepatic disease and that could be causing the diarrhoea, but they will also be seen, secondary to many other gastrointestinal tract diseases, mild elevations in these liver enzymes.
As a reactive hepatopathy to to what else is going on in the abdomen. Just bear in mind that this is certainly the case in dogs, but less so in cats. Even mild liver enzyme elevations in cats can be significant because they have much shorter half lives, OK.
We're going to have a look at the cholesterol level as cholesterol is often low in patients with small intestinal malabsorption. And we're going to check the electrolytes, primarily because they could be low in patients with chronic diarrhoea and need some form of supplementation, but also to have a look at their sodium potassium ratio. And we're doing this to screen for any evidence of Addison's disease.
So an abnormal ratio is considered below 27, certainly below 24, you'd be getting a bit suspicious about Addison's and below 20 to 21, I'd be very suspicious about Addison's disease. Do bear in mind though that our sodium potassium ratio will only become low. In Addisonian patients, who, are unable to produce mineralla corticoids, so that would be your straight up regular Addisonian patients.
Do be aware that atypical Addison's disease, is the disorder in which these patients don't have glucocorticoid. Production but maintain normal mineral or corticoid production and therefore an atypical Addisonian will have a normal sodium potassium ratio. So that normal sodium potassium ratio does not rule out all forms of Aans, OK?
Hyperbilirubinemia may be seen in patients with extrahepatic biliary duct obstructions such as pancreatitis. But we should also consider other differentials like, feline infectious peritonitis and even hyperthyroidism in cats with elevated bilirubin. The haematology is often quite non-specific, but we may see a non-regenerative anaemia in patients with chronic diarrhoea, because of anaemia or chronic disease.
We may have a regenerative anaemia if there is concurrent gastrointestinal tract ulceration or erosion, and we may even have an iron deficiency anaemia. So, a hypochromic and microcytic anaemia, if patients have chronic gastrointestinal blood loss. And a good example of that would be a patient with an ulcerated small intestinal mass, often referred to as silent tumours, as often they're very hard to diagnose, on imaging, and, and sometimes patients don't even have diarrhoea at all, but just present with, an iron deficiency anaemia.
I enophilia, may be indicative of parasitic, parasitic or hypersensitivity disease. And neutrophilia and stress loop grammes are common in our poor patients with diarrhoea. So what about the more specific tests that we can use for the GI tract?
Well, the PLE PLI sorry. Is used to screen for pancreatitis as a cause of the diarrhoea, but also as a possible comorbidity. And what I mean by that is that it's not uncommon for patients with IBD to have mild elevations in their PLI, and those that do carry a slightly poorer prognosis than those that have a normal PLI concentration.
PLI is really important to screen for exocrine pancreatic insufficiency. It's a great test because it's very, very sensitive and specific. So we should be doing this in all of our diarrheic patients, in my opinion.
But we do have to remember that it needs to be a starved sample because if they've been fed, prior to the test, it will increase their TLI level and could push it into the normal range. Folate and carbalamine. So we run these, to look for a few things.
One of them is evidence of, small intestinal malasorption and to see where the small intestinal malabsorption is localised. So folate is absorbed in the ginum and a low folate level tells us that there's a disease in that region and carbalamine, is absorbed in the ilium. And the same goes for that region.
So with carbalamine, this is slightly different to folate, having a low level of carbalamine on a blood sample does worsen your prognosis, OK? And it does mean that you need to supplement that patient with carbalamine because patients who have hypocabauminemia and aren't supplemented with carbalamine do poorer than those that are supplemented, OK? So that's not quite the case with folate, you know, I don't, I don't believe low folate level confers a poor prognosis, and I don't tend to supplement folate generally.
But do bear in mind both of these tests folate and cabalamine, they're not 100% sensitive, so you certainly can have diffuse small intestinal disease and a normal folate and cabalamine. And then briefly mention, folate to carbalamine ratios because I was certainly told at university that high folate and low curbalamine, is indicative of small intestinal bacterial overgrowth, but I think we're really, stepping away from that now and, and we're diagnosing, you know, bacterial overgrowth or, dysbiosis based on, response to appropriate antibiotic therapy now. CRP is something that's readily available in the UK.
It's an acute phase protein and a non-specific marker of inflammation, and it is often elevated in cases of IBD. And it's nice to use this to monitor treatment response and to make sure that what we're doing is reducing that CRP level in combination, with our scoring systems we talked about earlier. It also might help us, decide on, on what we reach for, from the medication drawer as well, because in one study, a CRP of over 9.1 indicated the need for glucocorticoid therapy in patients with IBD with a reasonably high sensitivity and high specificity.
Basal cortisol, . Will be performed as well in dogs, as I said, to screen for Addison's disease. And if the basal cortisol is normal, we forget about it, that's fine.
But if the basal cortisol is low, we then have to stim our patients, OK? Because you can have low basal cortisols for a variety of reasons, and, and a lot of those, you know, are not because of primary Addison's disease. So any low cortisol level needs stimming, and if it remains low, then we have a diagnosis of indeed.
And we talked about bioasss briefly, and we're now just gonna go over imaging. So, imaging, is something that I perform in pretty much all of these patients. I'll tell you why in the next couple of slides.
But I think it's important to remember that radiography is of little to no benefit when we're imaging patients with chronic diarrhoea. Ultrasonography is much, much more, sensitive. And specific, OK?
But obviously ultrasonography is very operator and equipment dependent. The main things you're going to look at are the stomach, small intestines, colon, pancreas and lymph nodes, but also assess the other abdominal organs as well for evidence of disease in there. But the main, utility that ultrasound has in these patients is to diagnose, sorry, to exclude diagnoses, sorry, of neoplasia.
Chronic foreign bodies and interception in these patients, OK? And we have to bear in mind that ultrasound is unfortunately very rarely definitively diagnostic. And this was nicely highlighted in this retrospective paper from the RVC where they looked at ultrasonography in patients with diarrhoea, and they found that it had a moderate utility in the investigation of these patients in only 38% of dogs and no utility in 53% of dogs with chronic diarrhoea.
OK? And interestingly enough, it was definitively diag definitively diagnostic in only 3% of cases reported of systemic shunts and foreign bodies and things, whereas actually it misdiagnosed 7% of patients, OK. So it really helps you, understand the limitations of abdominal ultrasonography in the investigation of these patients.
But the things we might look for are gut wall thickness, which in some patients can correlate, with presence of disease and disease severity, but not all. We may look for hyperchoic, linear mucosal striations, as you can see on this image here, which is indicative of lacteal dilation. Within the mucosa, which certainly could be because of .
The disorder lymphaectasia, or it may simply be secondary to one of many chronic inflammatory diseases in the small intestine. We may see mucosal speckling, which, we used to say is indicative of, of infiltration within the mucosa, but it's more recently been shown to be more associated with just the time that patient was last fed. We may see hyper ecogenicity, so an increased brightness of the mucosa, and that certainly in cats has been shown to be consistent with disease in that layer of the intestines.
We may see thickening of the muscularis layer, which is this skinny little black layer here. I'll show you an image of of that just shortly. And that can be seen in cats with small cell lymphoma.
We may see enlarged lymph nodes. It's quite common to see mild to moderately enlarged lymph nodes in any patient with chronic diarrhoea, but if we're seeing really big lymph nodes, we might start thinking about, neoplasia and actually aspirating those lymph nodes for cytology. We're gonna look for pancreatic changes as well and obviously free abdominal effusion, .
So this is a nice image of a cat that I diagnosed with small cell lymphoma. So compared to this nice thin muscularis layer here, OK, on a dog, but, it should look similar in a cat. You've got this really thickened, black muscularis layer here.
And when you see changes like this, changes involving the deeper layers of the small intestine, this might be one thing that points us, towards full thickness biopsy. In preference to endoscopic biopsy, you know, is the muscularis layer is not something that we can readily sample endoscopically. This is an image of a patient's enlarged, mesenteric lymph node.
A patient who's got loss of layering within this, severely inflamed region of small intestine. This is an image of a, an enlarged pancreas on a cat just adjacent to the stomach here. And then, neoplasia, OK, if you pick up something like this on the abdominal ultrasound scan, we can then things start changing our diagnostic pathway about how we're going to sample this and not worry too much more about biopsies and trial treatments.
Fab. So we've done all of our imaging, our blood work, and at this point, We've er essentially excluded neoplasia as best that we possibly can do, foreign bodies in interception, and we're left with quite a shortish list of differentials. So our patient could still have dietary responsive enteropathy, antibiotic responsive enteropathy, fibre responsive enteropathy or steroid responsive enteropathy.
So I put the, the aliases of all of these next to them, but I quite like to think of them, by, the treatment that they respond to, just an easy way to, to sort of remember them. We also haven't fully excluded things like lymphaectasia and lymphoma, you know, as they can have very variable ultrasonographic appearance. So at this point, we have a discussion with the clients, about the options of either progressing to the final step in workup of, GI biopsy for histopath or to just put the brakes on and do some trial treatments.
Now, I would generally recommend trial treatments at this point, as long as the patient isn't too severely ill. That patient has a PLE. And I'm worried they're gonna succumb to their disease in the next 2 weeks.
I'm gonna push them to go straight for, for biopsy, OK. But generally, trial treatment is, is warranted prior to biopsy. And the most, common way that this is done is to start either a dietary trial, first, and then if patients fail to respond to that, you can then move them onto an antibiotic trial.
And then if patients respond to that, potentially move on to, to biopsies. So whilst that's probably the most common approach, I do it slightly different, and I combine the two at the same time. And the reason for that is that I find clients have, You know, only so much sort of patience, and they will only go through so many weeks of failing trial treatments before they lose faith in you.
So what I tend to do is start them on both an antibiotic and a dietary trial at the same time, and after week 3, I discontinue the antibiotic trial. As long as I've got a clinical response. And if that patient stays well, I keep them on the diet for another 5 weeks.
If that patient relapses at that point, I pop them back on the antibiotic and discontinue the diet instead, OK? And that can help tell me which of the two, you know, the antibiotic or the diet that they're responding to, and it just saves a few weeks for the clients. So a little bit about elimination diets.
As I say, I would start them on the diet and reassess their response. And if there is no improvement by week 3, there is no point continuing it any further. If they do show improvement by week 3, though, continue it to at least week 8 to be 100% sure that they remain in clinical remission.
So I tend to reach for a commercially a prescription hydrolyzed, protein diet. As I just find they're just so user friendly, really. The other options would be to look at a novel protein prescription diet or a home prepared, novel protein diet as well.
Do bear in mind that we're using this trial treatment as a, as a, you know, a diagnostic test. And, you know, there are other diagnostic tests that we can consider, for dietary allergies and intolerance, but they're really, really not very good. So intradermal skin testing, skin patch testing, and blood work for, for food-based allergies that are causing chronic diarrhoea are really of no, diagnostic value, much better doing a dietary trial instead.
Do bear in mind that some patients require several dietary trials, however, so I've had a couple of patients who will respond to hypoallergenic, who have failed, you know, ZD. So there's nothing wrong with doing two dietary trials, just to be sure. I very rarely if ever rechallenge these patients.
And, we just need to be careful as well that we don't supplement them, with anything that contains, a source of protein whilst they're on, an elimination diet. So 100%, just that hydrolyzed prescription diet and nothing else. You've got to make that very, very clear, with the clients.
So onto the antibiotic dietary trial, sorry, on the antibiotic trial. This is, as I say, used to treat small intestinal dysbiosis, but also in combination with the diet, we'll treat mild cases of IBD as well. And we basically use this to eliminate any undiagnosed enteropathogens, to modulate the intestinal flora, and also because these drugs have some, we think mild immunomodulatory or anti-inflammatory effects on the bowel.
So I tend to use these for 3 weeks, OK? And if I'm using this alone as an antibiotic trial and they're responding during those 3 weeks, I then continue it but taper the dose over the next few weeks going forward until hopefully they come off of it, or until they're at least on the lowest effective dose, long term. And the 3 drugs that I think are the most appropriate ones, are metronidazole.
Oxitet, and Tylasin at the doses are listed here. But do obviously just be aware of the potential side effects of these drugs. Fibre, just gonna touch on it very briefly to say that it's really important that we do supplement fibre, in patients with large bowel diarrhoea, OK?
As it is definitely, been shown to improve outcome in these patients, and basically a lot of that is due to the soluble fibercium, that's found within, you know, these supplements, that significantly, improves colonic health. Improves faecal consistency, in these guys. So, protein do profiber, which contains psyllium as well as, probiotics and things, but you can also get canned pumpkin as well, from the shop, which contains decent amounts of psyllium.
So just gonna very quickly go through GI biopsy before wrapping up on steroids. I think GI biopsies are essential prior to the use of any immunosuppressive therapy. And really endoscopic biopsy is the technique of choice unless you think there's transneural disease.
And the reason for that is that, there is decreased morbidity compared with Xlap and full thickness biopsies. There is no risk of dehissance. We can start immunosuppressive therapy, almost as well, as soon as we've got those biopsies back rather than having to wait for wounds to heal.
You can biopsy the colon as well in these patients. You can visualise the mucosa, and it is often cheaper than ex lap in some places. The disadvantages obviously are that we can only get to the stomach, duodenum, colon, and ilium, so we'll miss most of the jujunum, and we know that disease can be very segmental in in some individuals.
And we're only able to, sample the mucosa as well. Plus the fact it's quite technically challenging, and expensive equipment that's not readily, available. The biopsies are then sent to an appropriate lab, whether they're endoscopic or full thickness, and they're assessed based on some WSABA guidelines that were reported in 2008, where they look at these morphological criteria.
And screen for these inflammatory cells. And essentially at this point, what we're doing is we're excluding things like lymphoma and lymphangectasia, and we're left with often a diagnosis of exclusion of inflammatory bowel disease, and we can decide which type of inflammatory bowel disease it is based on which. These satellites is most prevalent.
Do bear in mind as well though, that, the severity of changes when you're looking at things like, how much, fibrosis there is an atrophy, the severity of changes don't always correlate particularly well with, clinical disease severity, so we do have to bear that in mind. So we've worked our patient up and achieved a diagnosis of steroid responsive enteropathy or inflammatory bowel disease as they've failed their other trial treatments and . You know, the, the, the diagnosis has been, has been found on the biopsies.
And we're going to start prednisolone at this point, and we tend to start prednisolone at 1 to 2 migs per gig, twice a day. We do that for about 2 weeks, at which point we're often starting to achieve clinical response. And then it's at this point, we start to lower the dose by 25% every 2 to 4 weeks, to achieve the lowest effective dose.
So do be aware that dose and duration must be appropriate. So these are pretty hefty doses, used for pretty long periods of time, OK? So this is really why we need that biopsy to be able to justify doing this causes the side effects, as we know, of prednisolone can be really quite profound, particularly in large breed dogs.
Patients who are refractory to steroid therapy, often benefit from a second immunosuppressive agent. And we most commonly use, chlorambil in cats, and azathioprine, cyclosporin, or chlorambuil in dogs. I'm not going to talk about those in any more detail.
It's beyond the scope of this. Sulfasalazine may be added in as well for patients who've got large bowel diarrhoea. Just bear in mind, that it does have quite a side effect profile of caratic conjunctivitis, Zika, vomiting, allergic dermatitis, and it can induce jaundice, and that when we do use it, we really use it for as shorter periods of time as possible, OK?
And when patients do need to be on this regularly, we try and use the lowest effective dose, OK? Finally, probiotics are something that we can consider whilst the evidence isn't particularly, robust, about how important they are in patients with chronic diarrhoea, there are actually lots of different reports in the literature of improvement, of inflammatory bowel, disease activity scores and improvements of faecal scores in patients with diarrhoea, and reduction in the duration of diarrhoea as well in individuals. Prebiotics also very similarly, there's some, Evidence out there that they can improve diarrhoea in dogs, but it's not particularly strong or robust evidence.
And then absolutely finally, just to finish on, cyano carbalamine is something that, as we said earlier, is something that we have to supplement in patients with low serum carbalamine levels as they will then do much better on treatment. And we can use that drug. So via injections weekly and then monthly or orally in the form of Kabalaplex from Protective.
So at this point I think we open up for questions and I'll just leave this slide on which is just a final summary of the diagnostic pathway, that I use in my patients. James, that was absolutely fascinating and, and so logical. Sometimes one can kick yourself when you think of a case and you think, oh, I, I missed that or I should have thought about that.
But that was great. Thank you so much. Not a problem.
Not a problem. It was very interesting to hear what you were saying about ultrasounds and that sort of thing because it's it's often a diagnostic tool that we all jump to nowadays. And I was quite surprised to see the Well, relatively poor results that, that the study gave us.
Yeah, absolutely, I mean, you know, clients when they're being asked to pay anything from 100 to 300 pounds for for an ultrasound study think they're gonna get some. You know, some real results from it and potentially a definitive diagnosis, but we have to make them very aware from the outset that's often not the case. What I often find as well is that the size of the patient can play an important role, and there are studies that have looked at, other imaging modalities and often patients who are over 25 kilogrammes are actually better having CT, because you're more likely to spot lesions, within the GI tract, than with ultrasound just because of the size of the patient.
But yeah, it's quite frustrating that you do these imaging studies, you know, and you see all these little changes and you think, ah yes, I'm going to find this here and I'm going to find that there when I scope this patient, and often your biopsy results come back and it's all back to front. The disease was actually more severe in areas that you thought it wasn't going to be and vice versa. Yeah.
Yeah. Couple of comments coming through about pre and probiotics and the controversy and I, I mean I've been around for long enough to have seen these things come and go in fashions and that sort of thing. What is your feeling on, you know, may not do any good but certainly won't do any harm or do you think they can do harm?
Yeah, I mean, I really like the idea of using them, in acute diarrhoea, and there's more evidence very recently about it improving outcomes in acute diarrhoea, because it gives you something to treat those patients with rather than sending the client home with nothing having, you know, paid for, for your time for a consult. But I think in chronic diarrhoea, it's certainly something that if the clients suggest it, I'm, I'm all for it, if I have a patient that's, You know, got relatively mild signs and they're not quite controlled on diet and or antibiotic, and I'm a bit hesitant to look at prednisolone. I might try them.
But I would say the vast majority of my patients, you know, don't go onto a pre or a probiotic, and touch wood, they all seem to do pretty, pretty well other than those of PLEs, of course. And of course not to be doing that during a diet trial. Yeah, that's right, yeah, absolutely, yeah.
OK, excellent. Some, some, comments coming in about supplementing with the B12 and the folate and that sort of thing. I think you commented and said you don't tend to supplement for folate, if I remember correctly.
Yeah, as far as I'm aware, there's no strong evidence to say that the low folate actually confers a poorer prognosis and that supplementation improves outcome, whereas it's the opposite of that with carbalamine, . So whilst we, you know, have Kabbalaplex now, which has both in as far as I can remember, you know, then we can supplement both no problems. But prior to that, you know, we were injecting B12 subcot, and you could get folic acid, you know, from the human pharmacy.
And I know there are some vets who do. Supplement with that. But I think from an evidence-based medicine point of view, I don't think there's, you know, any strong evidence to say that, that we need to.
And certainly, if it's a case of polypharmacy of another tablet or supplement the owner's got to pay for and get into their pet, I think we need a decent level of evidence to say, you know, that we'd recommend it. OK. Ian's written quite a long story and that sort of thing, but the, the gist of it is, you know, do you think things change, patterns to chronic diarrhoea change?
He's talking about, recently having diagnosed a number of cases of lymphangiotasia, not having ever seen it in his career before. OK, yeah, I mean I certainly have fits and spurts of, of that disease, and. You know, I suppose.
Lymphatic taser is a bit of a difficult one because you, I've had patients that I'm I've scanned them ultrasonographically and they have lactal dilation, and then you scope them and you see relatively dilated lactteals as well, and you biopsy them and actually it's just inflammatory bowel disease with lactal dilation. But I certainly have had quite a few, patients who have confirmed lymphaectasia, who generally don't do brilliantly well. I've had quite a lot of them that do quite well upfront for the first few weeks, but then really drop off the edge of a cliff.
But there is a very interesting form of the disease that I have seen once, and when he talks about the disease changing, there is a, a process whereby these lcteals can get bigger and bigger and bigger, and then they can rupture. And what they do is they leak lymph into the intestinal wall, and then that lymph sits there and the intestines react to it in the form of a granulomatous type inflammation around it. And you call this a lipogranuloma, and the intestine at X lap can look neoplastic, really thickened, irregular inflamed, but what you do see are these white blebs on the outside of your Intestine that looked like little mothers of pearl.
And these are these lipogranulomas. So I have seen that once in a patient that was called into theatre. We scanned the patient, it looked near plastic.
We opened it up and they said, what are these white labs, and these were lipogranulomas. So that might be one really unusual form of lymphatasia to look out for, just in case you ever, you know, one of these patients up to biopsy. So yeah, that, that can be a progression of, of lymphaitasia.
OK. David is asking for clarity when you were talking about anti well I'll put my false teeth back in. Antibiotic responsive diarrhoea.
You said you mentioned three drugs. Do you use a cocktail of the three or do you just use one at a time? Yeah, sorry, it's one of the drugs, .
Oxitet, or Tylacine. So the anecdotally, there is some evidence that Tylacine, is the most effective of the three, and certainly it's the one that I use most commonly. It's also got, you know, a bit less of a side effect profile, than the other ones.
So yes, you'd select one of these drugs, . And you'd have that patient on it for 3 weeks. If they are responding to that drug, brilliant, that is consistent with the diagnosis of small intestinal dysbiosis.
We'll then try and taper them off of that drug over the next few weeks, see what happens. And some patients actually never need to go back onto the antibiotic, they don't relapse. Some do and need to go back onto it and perhaps stay on it long term, .
But patients who don't respond to the 3 week antibiotic trial, you can safely say, OK, this doesn't look like it is small intestinal dysbiosis, let's move on. OK. Catherine, that slide hopefully has answered your question as well.
Joe is asking, and this is the last question we've got time for tonight, comments on live yoghurt. Oof Sorry. No comment.
I have absolutely no experience. I know clients often ask me and I probably should do some more research, but I can't see it doing any harm. And and how would you rate it together with pre and probiotics that come in.
You know, one of the commercial forms. I mean, is that another no comment one? Yeah, but there, there is evidence for the pre and probiotics and that it can improve disease state in some patients with chronic diarrhoea in some patients with acute diarrhoea.
But as I'm not, as far as I'm aware, there's not that same evidence for, for live yoghurts. You know, and I think at the end of the day, if they do a little bit of good and are guaranteed to do no harm, why not try them? Yeah, yeah, absolutely.
Excellent. Well done on balancing on the fence on that one. Yeah it could have gone either way.
James, it's been an absolute pleasure to listen to you and I look forward to working with you and listening to you chat in the future again. So thank you for your time. Not a problem, for having me.
Folks, thanks for attending tonight. That's all we have time for to Les, my controller in the background, thanks for all your help and it's good night from me.