Welcome everyone. Thank you very much for coming. If any of you have been to all three this week, well, congratulations, I will be awarding prizes for stamina at the end of the webinar if you've made it through the 3 over the 3 nights.
Just to let you know, we've got a couple of interesting things coming up in the new year. I'm already getting some webinars together. We've got David Argyle, we'll be speaking about mast cell tumours in January.
We're also having an equine webinar week from 10 January, so if any of you either deal with horses through the practise or have colleagues and friends who are equine vets, then you might want to just let them know about this week that we're doing for. For horses, we've got equine dentistry on the Monday, we've got equine analgesia on the Tuesday, we've got infectious diseases on the Wednesday, and then my high point of the week, pruriasis in the horse on the Thursday, and that's with a guy called Stephen White, who's a an equine dermatology specialist from UC Davis. So that's something that we're looking forward to, but .
Back to the present, we're very fortunate tonight to have Clive Elwood from the Davis referrals down in Hartford Bedford border. Clive is a 1989 vintage Cambridge graduate, even, even older and longer in the tooth than I am. I first met Clive when I was a final year student at Liverpool University and he was our house officer, and he went on to do internships and residencies at Liverpool and London University.
And by 1995 was already a diplomat in the European and the American College of Internal Medicine. He then went on to do a PhD on gluten sensitive enteropathy in 2000 and in 19998 it started to work for Davis referrals. He is the winner of the 2009 BSAVA Melton Prize for meritorious contributions to veterinary medicine, which I think he is well deserving of, and since this year has been doing a bit more desk work as the managing director of Davis Referrals, so really looking forward to your presentation, Clive, today, who is going to do a talk on.
IBD and triaditis in Katherine, looking forward to it. I'm going to mute myself. Unless there are any problems, I will stay muted, and then hopefully at the end we can have some questions.
Thanks very much, Clive. Thanks, Antony. Good evening, everyone.
I hope you can all hear me OK. This is slightly surreal because I'm actually sat in my 14 year old daughter's bedroom because that's the one place in the house that's actually got a wired internet connection and I'm looking around at the sorts of things that 14 year old girls have, and I'm about to talk to you about something for . Far away from that, which is inflammatory bowel disease and triaditis in cats.
So this is my first attempt at a webinar. It's a bit interesting not having an audience in front of you, so you may find them not quite as fluent as I normally am, and if that's the case, so I apologise. So, you can see the first slide and that picture of a cat on the bottom is a Picasso cat, and the reason that's there is because I first presented this lecture in the autumn in Barcelona and I had a day on my own the day before the lecture where I wandered around Barcelona and went to the Picasso Museum, so I thought it was very apt to have a little bit of Picasso and I thought I'd keep that in just to entertain you.
So, inflammatory bowel disease and triaditis in cats. We're going to just go through briefly what we're going to cover. We're going to define triaditis, look at the pathologies behind triaditis and see whether we can link them together.
Review some of the presentations that we see in cats with IBD and complications associated with triaditis, the diagnosis of those, and a little bit at the end on discussing some of the management strategies that we need to employ in these cases. So what do we mean by trioitis? Well, it's a word that really is just a flag of convenience that links a spectrum of clinical syndromes that can happen together, and it's diseases of the triad of the intestine, the pancreas and the hepatobiliary system.
And it seems that with underlying IBD or underlying bowel disease, it's not uncommon to have other things happening in those other areas. So we're going to talk a little bit about inflammatory bowel disease first of all, or strictly speaking, idiopathic inflammatory bowel disease, and what do we understand by that and what's underlying it. Inflammatory bowel disease we understand as an inappropriate response of the intestine.
To inflammatory inflammatory response to antigens such as bacteria and food, what we have to remember is that the intestine and the intestinal immune system and coal immune system is firstly an extremely important organ of the body, but I would say that because that's what I did my PhD on, but also very, very clever and adept at ignoring. The massive antigenic challenge from food and from bowel flora in normal circumstances, and in abnormal circumstances, it seems that we can get these inflammatory responses triggered by things that would not normally do so. Now there are lots of poorly understood.
Reasons behind this. Certainly in clinical cases, we often may not know why the mucosal immune system has been reprogrammed, but certainly from both clinical evidence and experimental evidence, then we can think that there may be genetic factors to do with defects or variations in the mucosa and the mucosal immune system. That may be altered cytokine responses, abnormal permeability of the mucosa, which allows access and a number of other potentially genetic predispositions.
And then prior exposure, so you have to prime the immune system to Produce an inflammatory response that requires prior exposure, and it may be that exposure in certain circumstances, so exposure of a benign antigen in the face of a reaction, say, to a, an example might be a parasitic antigen, could induce a allergic type reaction to that benign antigen. And then Subsequently, changes in the local environment, the mucosal bacteria, etc. Etc.
May also predispose to production of these inappropriate immune responses. So this diagram, or these these pictures are really just to illustrate a little bit about what happens in the mucosa when we have certain types of immune responses. And the picture here just shows the normal villas or two normal villa with a relatively normal villa architecture.
And in inflammatory bowel diseases, we tend to see infiltration of the mucosa with inflammatory cells and collapse of those vill villi, and there are consequent effects on digestion and absorption. And this diagram here just illustrates that a little bit more if we think of our antigens here. Being presented to the immune system, that then triggering an inflammatory response, releasing pro-inflammatory cytokines, causing influx of inflammatory cells and breakdown of the collaginous structure, and that's it's those responses that seem to be behind this architectural change and Clearly with inflammation comes loss of function, and that's why we can see diarrhoea or malabsorption of sort of classic signs of inflammatory bowel disease or just intestinal disease in general.
In feline inflammatory bowel disease, there have been some interesting developments relatively recently. This 2009 paper from Kenny Simpson's lab at Cornell used very, very powerful techniques of fluorescent in situ hybridization to identify. Abnormal populations of bacteria in the mucosa of cats with with inflammatory bowel disease.
And this is this picture here is fish, so these fluorescent in situ hybridization, this shows the bacteria within the mucosa and then these tables show that in cats with Gastrointestinal disease, there seems to be a marked increase in the coliforms within the bowel. Now what we don't know is whether that's a cause or a consequence of inflammatory bowel disease, although it's an attractive speculation that maybe IBD is triggered by mucosal bacteria. And one of the reasons this came about this work came about was because in parallel with looking at cats, Kenny and his team have also looked at.
And with others looked at boxer dogs with histocytic ulcerative colitis, and it's been shown, firstly, that they respond to antibiotics, and secondly, that there is an abnormal E. Coli population in those dogs, and that maybe the boxes have some genetic predisposition to particular forms of of infection. With, with E.
Coli. So it's interesting that we, we keep, we keep going full circle with these things when you say. It's not infectious, it's infectious, it's not infectious, it is infectious.
Well, the, the relationship between the gut mucosa and the gut bacteria is, is fascinating and complex, and I guess this paper just illustrates that more. It doesn't mean that we're going to cure every cat with IBD with antibiotics, but it does raise interesting potential for, for different management approaches. And then from that we say, well, OK, what we've got infla inflammation of the bowel, we can understand maybe how inflammatory bowel disease may come about.
The next question is, well, how does that work itself into triaditis? And The sort of simplistic, probably simplistic, belief is that the anatomy of the feline pancreas and bile duct may predispose to that, and it's different from cats to dogs in that the pancreatic duct and the bile duct in the cats fuse and open together predominantly. In some cats there is an accessory pancreatic duct that opens on its own.
And the, the, the belief therefore, is that because those two things open together, if you get problems in the pancreas, you may get problems in the hepatobiliary tree too. That is a legitimate assumption, I believe, although there's nothing that that gives us concrete proof for that. But I also think we need to look way beyond the anatomy.
And consider things like the local function of the intestine, sphincteric function, I guess, changes in the bowel flora, which we just talked about. All of those things may also directly influence. And predisposed to things like ascending infections up into the to the bile duct and into the pancreatic duct and certainly infections in the pancreatic duct could well be predispositions to pancreatitis in cats, although we, you know, stressed that that's that's speculative, not, not proven.
This picture just illustrates that an anatomy showing the bile ducts here and the pancreatic ducts here and here, just to reiterate what I've just said. So we see in triadits we see manifestations from the intestinal. Disease from hepatobiliary disease and from pancreatic disease.
And in cats with intestinal inflammatory bowel disease, the probably the most common presentation is vomiting. Now, what we have to remember is that many of the cats that we're dealing with may well be going outside, they don't necessarily use a litter tray. So it's certainly possible that diarrhoea is less obvious to an owner in a cat than it would be in a dog, for example.
But nevertheless, if you have a vomiting, vomiting cat, we should certainly be thinking of inflammatory bowel disease as a major, differential diagnosis. We can see diarrhoea and we can see signs of maldigestion and malabsorption, so, weight loss, in the face of a normal or even an increased appetite. As a consequence of both inflammatory bowel disease and potentially pancreatic insufficiency, then vitamin deficiencies, particularly carbalamine deficiency, is a significant risk, and the main things we can see with carbalamine deficiency are anemias and leukopeniaas, although they're not the only things, there can be other effects, as we'll talk about a little bit later on.
And then anaemia as a result of chronic blood clot loss, iron deficiency anaemia is another potential consequence of long standing inflammatory bowel disease, and occasionally the anaemia can be the only clinical presentation. Pancreatic disease ranges from pancreatitis through to insufficiency, both exocrine and endocrine. So pancreatitis can be acute and chronic and on the acute end of the spectrum will be associated with pain and shock and potentially syndromes of systemic inflammatory response and multiorgan failure, and Pancreatitis in cats is often not associated with vomiting, interestingly enough, and can be a relatively occult or difficult to identify abnormality and Certainly when I first started doing referral medicine, you know, I think we missed a load of these with the advent of things like ultrasound and some of the newer serological tests.
We we're obviously much more aware of this whole thing and as Anthony said earlier on that you know, even triaditis wasn't invented when Anthony and I were were. Starting out our careers. Exocrine pancreatic insufficiency is also a potential, particularly of chronic low grade pancreatitis, and in these cats we need to be aware that sometimes the the clinical symptoms of maldigestion, for example, may be due to EPI and classically, again, weight loss, despite a good appetite, and potentially steatorrhea could be noted.
And then diabetes melisis again as a result of chronic inflammation in the pancreas, so classic PUPD, weight loss, and potentially diabetic ketoacidosis, and it's not an uncommon combination both in dogs and cats to have a flare up of a pancreatitis that causes both a degree of insulin resistance pushing a cat from coping with diminished insulin production, to no longer coping with diminished insulin production, and also then developing ketoacidosis as a consequence of both that insulin resistant diabetes melethus and the inflammatory and hormonal effects associated with pancreatitis. The combination of pancreatitis and ketoacidosis is certainly a well recognised one and also potentially very challenging combination to manage. They, they require a great deal of intensive evaluation and, and, careful management of the blood glucose and all the other associated problems.
Then, thirdly, as part of our triad hepatobiliary disease, the most striking abnormality in hepatobiliary disease would be our extra hepatic bile duct obstruction, which is typically from pancreatic swelling, may well be associated with very marked icterus and potentially in those cases where we've got complete obstruction to bile flow. Then we can get vitamin K dependent coagulopathies as a result of inadequate absorption of vitamin K, which is a fat soluble vitamin and therefore requires bile to Act as a detergent on fat cells and aid in fat absorption. So that's relevant clinically because those are cats that we may be thinking about doing procedures on, and they may need some clotting tests and vitamin K treatment to allow us to do that.
Chiangia hepatitis, so, infection in the gallbladder and bile ducts, can be associated with fever and pain, potentially with icterus and other signs of general sepsis, such as hypothermia, which in cats can also be a sign of sepsis. And then we have secondary effects in the liver through such as anorexia, sorry, hepatic lipiddosis as a consequence of anorexia from other diseases, and that can in itself lead to liver failure. And then very rarely then we can see cholelithiasis, again, associated with infection and potentially causing extra hepatic bile duct obstruction in its own right.
. Caliotiasis is uncommon, but quite fun. So Just to add a little bit of narrative structure, if you like, and a little bit of clinical interest to the evening, I'm going to introduce Sophie. So Sophie is a 2 year old female British shorthaired cat who had a long history of intermittent vomiting and diarrhoea, and certainly a number of months, and The owners described her as not gaining weight, despite having an exceptional appetite, and then within the previous few days, she had become quite ill indeed, and despite appropriate treatment with fluids and antibiotics, had continued to deteriorate and was really quite unwell when she presented to us.
She was very depressed, she was significantly dehydrated. She was unable to stand and lift her head. Which suggested the possibility of some muscle weakness, and she had palpably thickened bowel loops, when, when we felt her very easily felt, abdomen.
She had no muscle tone, so you could feel those bowel loops very clearly. And I always, you know, when you feel these loops in cats, I always think of a, something like a piece of rope or roo that they have that sort of lost their flexibility and it feels like a coiled up piece of rope sitting in the, in the, in the abdominal cavity. So what other diseases and clinical entities do we need to consider in our triaditis cases?
Well, obviously it partly depends on the nature of the initial presentation, but we need to be ruling out associated metabolic diseases, so that may be renal failure, it may be. Abnormalities, hormonal abnormalities which could form in hyperthyroidism, etc. Etc.
Infectious diseases. So again, if we have a, a cat presenting with diarrhoea and, and fever, then we need to be thinking of, abnormalities such as intestinal infections, maybe, maybe something like salmonella. Neoplasia, for all sorts of reasons, is going to be on our list of differential diagnoses, potentially toxins.
Again, we may be looking at reasons for hemolytic disease through toxins or vomiting as a result of toxin ingestion, trauma. Certainly, if we have a very ecteric cat like this one here, then, bile duct rupture would be a potential traumatic cause of a postipathic jaundice. And then we also have immune mediated diseases in various forms.
As a broad list and within these different categories, we can obviously fill in the gaps as all the other types of disease or definitive diagnosis that we may be looking at that mean that the animal doesn't have triitis, it has some other abnormality. So things that we're going to be looking at and looking for in in cats with triaditis, we're going to start off with just standard haematology, biochemistry panels and talk a little about the sorts of things that we're gonna be looking for and trying to analyse in those and obviously in any inflammatory situation, so if we have a pancreatitis or a cholangio hepatitis. Then, neutrophilas, not unexpected, and if there's a significant bacterial or septic component to that, then we may well see a left shift.
Anemias, we may see anaemia associated with chronic disease, but if we have some iron deficiency, then we need to be looking at the red cell picture and the red cell parameters, as well as the smear comments for a microcytic hypochromic. And as we mentioned previously, leukopeniaas can be associated with curbalamine deficiency as a result of carbalamine malabsorption. On a biochemistry panel, it depends on the clinical status of the animal, but if we have a vomiting, dehydrated cat like Sophie, who I showed just now, for example, then yeah, we're going to be most worried immediately about the sort of emergency end of the spectrum, so electrolytes, maybe blood protein to tell us a bit about hydration status, and that may influence how we have to manage the cat.
And then liver enzymes may well be elevated if there's hepatobiliary involvement. And sometimes the pattern of those elevations can be useful. For example, in lipidosis, which can be a Complication of some of the other conditions.
ALP and ALT tend to be elevated, whereas gamma GT tends to be normal. So that's can be a little clue sometimes that that there's lipidosis going on as opposed to some other cholangio hepatitis or similar. And then of course in our biochemistry we're also going to be looking at our bilirubin to some extent to get a a degree of elevation there although it may be clinically obvious that the animal is ecteric, the tissue bilirubin can take longer to fall than the serum bilirubin.
So having a baseline bilirubin can be quite useful when it comes to actually monitoring our, our treatment. And looking for, for example, resolution of biliary obstruction. Urinalysis should be a component of our our standard minimum database type panel and again bilirubin, which in the cat, remember, is completely abnormal as opposed to dogs where a small amount of bilirubin can be normal.
And we're going to be particularly interested in glucose. Again, stressed cats may well become glucouric, but once they reach the point of ketosis, then you know we, and there are ketones in the urine, then we know we're dealing with diabetic ketoacidosis, and that's going to change our approach to the management. Other tests that start, blood tests that start coming into the picture are the feline pancreatic lipase immunoreactivity FPLI which I'm sure everyone's aware is, is, you know.
Become very much at the forefront in the last few years. Now it is clear from the evidence we have that this test does have very good sensitivity for pancreatic inflammation. Excuse me, one of the potential problems, however, is that its specificity may not be very good.
Well, no, that's unfair. We need to just be aware that pancreatic inflammation can occur when. Actually, the pancreatic inflammation is much less significant than some other disease process.
So a positive PLI test must be interpreted in light of other findings, so. You know, we could have a positive PLI in a cat that has IBD, for example, where the IBD was far more important than the pancreatitis, and there may be no other clinical evidence of, of, of pancreatitis. It may be microscopic pancreatic damage or reaction that's elevating that PLI.
TLI in the cat is. Much less commonly used because EPI is much less common, but it is a good test for diagnosis of EPI. It's not really terribly useful for pancreatitis because it's only elevated for a relatively short period of time and certainly PLI has superseded it.
It's a diagnostic test for pancreatitis. We also need to be aware that potentially if we've got effective pancreatic insufficiency because the blockage of the pancreatic ducts and of the pancreas, then the TLI may not necessarily be low. So sometimes you could have an EPI that's going to respond to enzyme supplementation, where you're not going to diagnose it on a TLI.
Carbalamine and folate, then, where are we with those? So just remind ourselves a little bit that these vitamins are useful, potentially as diagnostic markers. Folate is absorbed in the upper intestine, predominantly in the duodenum and and and chainum, and Low folate, assuming dietary levels are adequate, is usually a reasonably good indicator of proximal small bowel disease.
Carbalamine is absorbed in the distal small intestine, in a carrier mediated absorption, and intrinsic factor is important, which is released from the stomach and from the pancreas, and if we have loss of intrinsic factor or we have distal small bowel disease, then our carbalamine can go down and sometimes it can go down profoundly. It has a number of effects on immune function, on neuromuscular function, because it's such an important cofactor in energy pathways within the cell that curbelamine deficiency, when it's clinically significant, can have broad, broad ranging effects. Vitamin K, we tend not to measure vitamin K, but as we've already said, this fat soluble vitamin can be diminished, particularly when there is significant loss of bile flow, and we will get a vitamin K dependent coagulopathy.
And one of the classic features of that is because it predominantly is involved in cofactors of the intrinsic pathway. That are a measurement of intrinsic pathway function, which is the prothrombin time or one stage prothrombin time, that tends to be prolonged over and above the . Changes in the extrinsic pathway.
So we'll see a pattern of change with vitamin K deficiency where the one stage prothrombin time is prolonged and the activated partial thromboplasting time may be normal. And again, that's important firstly because we may be biopsying these animals, secondly, because there is a big difference between a coagulopathy as a result of vitamin K malabsorption on the one hand. Compared with a coagulopathy as a result of liver failure, on the other hand, in liver failure, we might find both pathways are abnormal and clearly when liver failure reaches the point of there being significant coagulopathy prognostically, that's not very good, whereas potentially vitamin K dependent coagulopathy are, are .
Awkward or a . Frustrating little thing to manage, but we can supplement the vitamin K, get them through that and carry on with our our diagnostic tests as necessary. Moving on from blood tests then, again, partly depending on the presentation, but faecal analysis is going to be really important, particularly in those cats with evidence of intestinal disease.
We need to be ruling out our infectious diseases through culture, microscopy, and here we got a little happy little giardia. Swimming around, and through PCR, for some of the protozoan parasites, tritrichomonas is, is, in vogue these days, although in our practise, it's a very rare diagnosis, but there are various, culture-based and PCR-based tests to identify tritrichomonas infections and . You know, they can be clinically of great significance.
So we use our faeces to rule out infectious disease and also potentially as part of our work up for exocrine pancreatic insufficiency, so large, bulky, very mallodorous steatic stools would be the classic. And the other classic finding in EPI in cats is they'll often have a very, very fatty stained perineum, so greasy perineum, obviously not very pleasant, but that can be a sign that there may be fat malabsorption. So back to Sophie then.
So Sophie remembers a really quite a poorly pussycat and we've got some initial blood test results from her and the significant haematology is here, and I'll just give you a minute while I have a drink of water just to, to look at those and have a little think about those and, maybe mull over what you think might be going on. So when we see a profound neutropenia like this, then we think of increased consumption, so we may be dealing with marked generalised sepsis, just causing a massive neutrophil sink, or it's possible we could we could have an immune mediated destruction of neutrophils, or it's possible we could have some defects in neutrophil production. And as we'll see, we'll, we'll find out from some of our other test results, where we're going with that.
And then on our biochemistry with Sophie, again, have a look at those numbers for, for a few seconds and I'll talk through those and we can see what we think. This is the bit in doing a webinar when having no audience in front of you leaves you completely deaf and blind to whether anyone's still there or whether they've all gone off to get a glass of wine. So yeah, this is a pretty ugly set of blood results and just starting from the top here.
Sophie's pretty profoundly hypokalemic, and we know she's been inappetent, we know she's been diarrhoea, we know she's been vomiting, so it's no massive surprise that her potassium is low, but it really is very low. And similarly, a low chloride is most likely the result of loss of gastrointestinal fluid through vomiting. As we then work down, she's got a really massive CK so her creatinine kinase is, is very, very big.
She's got a very significant myopathy. And that immediately fits in with the clinical suspicion that she's got muscle weakness, and we know that. Potassium can cause a significant loss of potassium can cause a hypokalemic myopathy.
And my initial thoughts with Sophie was that these two things were directly linked and that she had a myopathy because of hypokalemia. If we look at her liver enzymes, her AST and her ALT are both high, whereas her alkaline phosphatase and gamma GT are are in the normal range. Now That can initially be confusing until we realise that.
We have significant amounts of release of AST and ALT if there is this degree of muscle damage, so these enzymes are in muscle cells as well as in liver cells, so at least a proportion of this change could be due to a myopathy rather than a hepatopathy. Having said that, our bilirubin is high and that may indicate some degree of hepatic disease. It may be that she's septic, bilirubin can go up in sepsis in cats.
And her blood glucose is low, which could be because she's so profoundly weak and debilitated again, that could be consistent with the degree of sepsis. And if we link back to our neutropenia, you do wonder whether she's suffering from septic disease. This low blood sugar is probably con contributing to her significant obtunded weak, debilitated state.
But she's not been eating for a for a longish while. She may well have just exhausted many of her capacities for gluconeogenesis. And then fortunately, Sophie passed some faeces.
I didn't get a picture of it, but it was very pale and very steat, really quite an unpleasant smell. So from that I was actually quite suspicious that there might be some pancreatic insufficiency, although, as you can see here, her TLI was normal. And then we got in time, not straight away, but within the next couple of days, we got B12 and folate back and as you can see here, her B12 was unmeasurable, so her carbalamine was completely down in her boots, and I guessed that she'd been malabsorbing carbalamine possibly all her life, and she was profoundly lacking in that.
And if we go back to what we know about carbalamine, one of the classic features of curbalamine deficiency is leukopedias, and that then suddenly becomes much more significant potential reason for her marked neutropenia that we've noted. She's also got a slightly low folate, suggesting she may well have some degree of intestinal malabsorption of folate. The low B12 and lack of secretion or lack of release of pancreatic intrinsic factor might well fit together, so we'll see combinations of intestinal disease and pancreatic insufficiency together going to greatly increase the potential for lobelamine deficiency.
So from these tests, I'm thinking in her that she has clinical evidence of bowel disease just based on on the palpation of her intestines. She has some profound metabolic derangements leading certainly to a myopathy. She may well have some hepatopathy.
She's got marked hypocabauminemia and consequences. That she may well have a significant neutropenia, and I'm also thinking that she may well have some pancreatic insufficiency also based largely on the, on the appearance of the faeces. So how are we going to use other tests in cases like Sophie to see whether we can get a little bit more information and try and define our, our pattern of disease?
Because really, you know, that's the question in these cases is trying to work out just what is involved. Is it one system, is it more than one system, if it's more than one system, how are those various things fitting together? So radiography, plain radiography is of relatively limited benefit, but you are looking for obstructions and mass lesions, ruling out other diseases, we can potentially look for evidence of whether the small intestinal movement is full of fluid or gas.
We may be looking for for distended loops. Contrast studies, we no longer do. Barium studies for intestinal disease in cats and dogs, other than as a marker of motility abnormalities.
Theoretically mucosal irregularities and thickening, can be seen, but frankly ultrasound is so much better and and easier that, you know, I would. I guess I'd probably throw my hands up in horror at the thought of doing a barium series these days, and I, I guess, also, you know, most practises have ultrasound machines, and although you, you may not be the greatest ultrasonographer in the world, . It's still potentially very useful for looking for for big abnormalities like mass lesions or obvious dilated loops of bowel that might be associated with other diseases such as such as obstructions.
So I'm much more a fan of ultrasound than I am of X-rays for intestinal disease. This picture, however, shows us why a radiograph may be useful in that we can see this beautiful collection of choleliths in this cat's gallbladder, which Yeah, we don't see very often, but it's a, it's a nice finding and you can imagine quite. Significant potential for these to migrate south and cause obstructions.
This is a big problem in people, you know, virus, gallbladder and gallstone disease. It's much less common in cats and dogs, but we occasionally see see them and occasionally they become surgical cases. So moving on to, to ultrasound then.
I think ultrasounds has probably been the one modality that has revolutionised our understanding of this whole area because it's moved from the, the sick cat being something of a black box to having capacity to do some really useful and clinically helpful studies and and identify. Entities like pancreatitis, which certainly 20 years ago were were really not thought of. So ultrasound can be useful for assessing the intestinal wall, first of all, and these are the features of listed features of inflammatory bowel disease, loss of the distinct wall layering, focal thickening, and potentially the mucosa looking hypoechoic or diffusely hyperechoic.
Sometimes, particularly if you've got components of lymphaectasia as a consequence of IBD, then it seems that those essentially dilated lactals potentially with fatty fluid in them are quite choic, and the first layer of the wall can become quite quite bright. The mucosa can be thickened and enfolded. We'll sometimes see the muscularis layer is thickened and then we'll also see abnormal mesenteric lymph nodes, all the sort of ultrasonographic components of inflammatory bowel disease.
This slide just illustrates that muscularis hypertrophy. So here we've got a bowel loop from inside, sorry, from serosal to luminal, and this is the outer layer, and although the ultrasonographic layers probably don't directly correlate with the anatomic or histopathological layers, nevertheless, it's convenient to say look, this, this is probably close to the muscularis layer and that looks. Relatively high atrophy and and that could be enough for an experienced doctors in order to suggest that there may be some inflammatory bowel disease.
And here we've got some mesenteric lymph nodes, sorry, I just. Clicked on a video loop, which I didn't intend to, so I'll go back to that slide and hope it ignores it. Mesenteric lymph nodes here just showing.
A mesenteric node, which in most normal healthy cats, you won't notice, but, in, when the nodes are reactive because of IBD, then we can begin to detect them. We do need to use a little bit of judgement on those because . We can find that, in younger animals, particularly where there's quite a lot of activity going on as part of normal immune development in the bowel, then the mesenteric nose can be relatively more obvious than in, in older animals.
So there's not an absolute, cut off to say what is normal and what is abnormal. We need to lose a little bit of, judgement and just add it to our overall picture. And again here we have a a mesenteric node that we can see on a.
Normal ultrasound picture. The pancreas then in ultrasound and pancreatitis, like the combination of findings that we're looking for are enlargement of the pancreas. And irregular pancreatic margins.
The pancreas can be hypoechoic, which may reflect acute inflammation and necrosis or hyperechoic, and sometimes if there's been chronic pancreatitis, then you'll get fibrosis and that potentially will increase the ecogenicity of the pancreatic tissue. If there's a lot of inflammation around the pancreas, it's not unusual to see the peripancreatic mesenteric fat as hyperechoic, and we may see local or more generalised accumulations of peritoneal fluid. Masses, cavitating lesions or cystic lesions or abscesses can be complications of pancreatitis.
We can sometimes see dilatation of the pancreatic duct and accompanying pancreatitis, we can see bile duct dilatation through extra hepatic bile duct obstruction. And we may also see changes of of liver enlargement or increased ecogenicity accompanying pancreatitis. So this image then just shows the right limb of the pancreas here, which is swollen, has some indistinct, irregular margins and is relatively hypoechoic to this area of relatively hypoechoic peripancreatic fat.
So that would be interpreted as likely representing some acute pancreatitis. Now, probably the single biggest key in this from a technique point of view is actually being able to get the probe in the right place and be confident that what you're looking at is actually where the pancreas should be, and that's skill and time, but nevertheless, very useful tool. This image also shows an image of pancreatitis with the duodenum here, and this is probably a more chronic pancreatitis lesion where we can see the pancreas here.
This will be the portal vein, I think, and you can see the pancreatic tissue is pattily hyperrechoic. And then this shows the left limb of the pancreas with the spleen here, which we use the spleen and the splenic vein as the landmark to identify where the pancreas is. This area here would be the pancreas again with the portal vein here, and that left limb to me looks a little bit bright relative to the splenic tissue.
And if we're lucky, we'll see biliary obstruction. And this is a very clear enlargement of the bile duct. This can be a very, very tricky area to image.
The area where the pancreas and the bile ducts and the upper duodenum can be really difficult to get lovely clear images and. Nevertheless, if you get the images you need, they can tell you such a lot of useful information that it's well worth, the time spent sometimes and, I potentially. You know, if I'm suspicious that there's an abnormality in that area, then, you know, I'll spend a long time trying to acquire images because I do think they're gonna help us substantially in in making decisions about treatment.
So, ultrasonographic changes associated with hepatic diseases, then we can see some biliary tract dilatation, and I'll show you some pictures of those, potentially gallbladder edoema with thickening of the gallbladder wall, colonothiasis, obviously shadowing echo abnormalities, and then potentially bright eitecture to the liver associated with lidosis. So this picture then just shows the the changes we see associated with bile duct obstruction and dilatation, which we, we can see biliary dilatation in things like cholangia hepatitis as well as with obstructive disease. So this is the liver here.
These structures are properly dilated bile ducts, but this structure is the normal hepatic vein, but there's an extra. Visible Structure here which is the dilated bile duct. So when you see this double pattern here of a vein and normally the hepatic veins have just got one bright border here.
When that bright border looks as though there's actually a duct there, that's because the bile ducts are dilated and you actually see the fluid within the bile ducts giving you this classic picture. This is a very exaggerated extra hepatic bile duct obstruction. I put it in really just for illustrations of very severe changes.
So all of these structures here are dilated bile ducts, but this was associated with a near plastic obstruction to bile flow rather than our IBD triaditis. But just to show you that it can get frighteningly enlarged. And then not the greatest ultrasound image in the world for which I apologise, but we can see this is the gallbladder here and we saw those radiographic images of the coliliths, but this is what they look like on ultrasound, and ultrasound's very sensitive to, to picking these things up.
And then Here we've got spleen, and when we're looking at the eco texture and the ecogenicity of the liver, the liver should normally be less ecogenic than the spleen, and as we see here, it's actually much more ecogenic, and that would be very suspicious for fatty infiltration from lippidosis. You're going back to Sophie then, remember we're, we're halfway through trying to manage and decide what we're gonna do with Sophie. Well, here we can see that she's got some dilated bowel loops and.
Possibly some mucosal hypertrophy, but there wasn't clear evidence of hepatic or pancreatic disease on those scans, remembering that if she has EPI, there's every possibility that she's actually got significant reduction in pancreatic mass, and we're not going to find a pancreas on an ultrasound. And then we've got a little bit of evidence of some biliary tract dilatation here. This is the gallbladder.
So there was some evidence that she may have some bile duct disease, possibly through obstructive disease, remembering that our bilirubin was up, but also possibly we'd say some cholangio hepatitis. So we've identified through our blood tests and clinical pathology and maybe through our imaging, particularly through our ultrasound, our areas of abnormality, we then have a variety of options to try and sample and define our disease processes further. Needle aspiration of bile can be very useful for culture and for cytology, potentially any masses or lymph nodes and potentially the liver.
Remembering that even when we're sticking needles in these things, we might be worried about clotting and . I'm not the most aggressive er tester in the world, but I would probably make sure I've done some platelet counts and clotting tests and potentially buckle mucosal bleeding times if I was worried. Endoscopy.
Very useful obviously for examining and biopsying the mucosa of the stomach and small intestine. When we move up to masses or perhaps diffused liver disease, then we may be talking about percutaneous true cut type biopsies, endoscopy again, put that in twice. Laparoscopy, can be a very useful technique for obtaining, .
Pancreatic biopsies, hepatic biopsies, and as a facilitator from what the surgeons call a mini laparotomy, so they pull a loop of bowel through a very small, laparoscopy wound, so they can do, bowel biopsies as well that way, on a relatively mini, minimally invasive fashion. And then finally we have the option of of full exploratory laparotomy surgery. So we have a range of sampling techniques and we'll obviously need to decide in an individual case for clinical and economic reasons where we might wish to go with those things.
So, if we've got an animal with cholangio hepatitis, we may be suspicious that there's some intestinal disease, although there may be less overt evidence of that on the clinical presentation. So should we be considering IBD in these cases, so whether we think there may be a triaditis, and should we therefore be thinking about endoscopy, for example, and biopsy? There isn't an absolute hard and fast answer I can give you on this one, but the things that I would be considering would be the previous history.
So is there evidence that this animal may have had intestinal disease, so it may be a chronic vomiter, it may be that there's been some some poor poor weight gain or other signs of low grade GI disease preceding the primary presentation. There may be physical examination findings, for example, we are in Sophie's case when we have those thickened bowel loops, there may be changes in our blood tests, for example, our folate and carbalamine levels, and there may be imaging changes that would suggest that yes, there is indeed some intestinal disease and that the diagnosis of IBD may modify our management strategies. So that's where recognising the potential for triaditis.
Actually becomes quite important because it may be that these other diseases as primary presentations have a background where there's intestinal disease and managing that intestinal disease may ultimately be the way to go with managing the case overall. So endoscopy in cats, it's very important to take our endoscope in vomiting cats all the way through to the small intestine. Now technically, that may be quite difficult and it is one of the more difficult skills in small, small bowel endoscopy is to get through that pyloris into the upper small intestine, but it's really quite important.
However, it has some limitations in that although we can get biopsies in the stomach and duodenum, there may well be more significant disease more distally in the bowel, and we're not going to be able to biopsy those with our endoscope. We are only taking mucosal biopsies, so we're only looking at the the superficial surface of the bowel, although the diagnosis of IBD is based on that, that area predominantly. Endoscopically, the bowel may look normal, and we know there's quite a poor correlation between the histology of the bowel and the endoscopic appearance.
So, it's always wise to take biopsies when you endoscope, even if you put them in a pot and put them on the shelf. Much better to do that so you can submit them later than to have to repeat an endoscopy because you haven't biopsied and you wished you had. So what the changes we see in endoscopy in in IBD in CAT, well, we will see changes in the stomach, we will see visible changes in the duodenum.
But of course, yeah, we have. Only 5 of 18 cats that had that had IBD and were vomiting that had visible changes in the stomach. So again, we must try and get through to that duodenum and biopsy the duodenum, if we suspect there may be vomiting as a result of the gastric or intestinal disease, we've got to make sure we rule out IBD or at least look for IBD with our duodenal biopsies.
Bio aspiration, I think it's funny, it's one of those things that cystocentesis fills, well, certainly new nurses who join us with horror, the thought of putting a needle into the bladder, and the same sort of degree of horror is often aimed at putting a needle into the gallbladder. Personally, I'm reasonably relaxed about bile aspiration. You know, we use a thin blue needle, obviously the animal has to be appropriately, analgesed and restrained, but, the risks are, are, are no different, I think, from cystocentesis, and sometimes it can make a profound difference.
So this cat took here, this is what I drew out of his gallbladder, and this was, it was pus effectively. And this is what it looked like under the microscope. So, you know, no question that bile aspirate in him was absolutely the way to go to make a diagnosis of a of an acute cholecystitis.
And then we've got our pathology as a as a sort of final diagnostic test if you like. So yeah, we may be looking for changes in our, in our . In testing, so villas.
Height loss, crypt hypertrophy, infiltrative change, etc. Or in here, for example, we've got a liver section where we've got some infiltration around the bile ducts and we've got some lymphoplasmacytic cholangitis. I should have a picture of a pancreas in here, but I don't, sorry about that.
You can imagine that we may have pancreatic biopsies as, as the pretty much the gold standard for diagnosing pancreatitis. Treatment then. Well, the treatment is going to vary substantially depending on the range of the particular pattern of presentation, but in the acute stage.
Supportive care through fluid and electrolyte therapy, antibiotics are potential requirements intravenous antibiotics because of the potential for bacterial infection and complication. Nutritional support can also be a significant requirement, remembering the risks of lipiddosis in particular. You know, if the, and the fact that these animals may well present having not had a good appetite for, for a period of time.
And nutrition support through placement of feeding tubes, esophagostomy tubes, potentially, peg tubes, even ginostomy tubes in some cases, can all be important supportive management, and also, particularly with pancreatitis and some of the inflammatory liver diseases, then they're gonna be, really quite uncomfortable and, and we need to be considering their, their needs for analgesia. In the longer term, then hopefully if we've got an animal that's not too sick or has got through an acute crisis and we need to be thinking about diet, if we go back to our original presumptions about the potential role of antigenic triggers in IBD. And the other pathologies going on, then, then I'm going to be thinking, well, maybe I want something that's lowish in fat because I don't want to, over challenge the digestive absorptive capacities of the pancreas and of the bowel, something that's highly digestible.
But I also potentially maybe be thinking about exclusion diets and using novel proteins, either a proprietary diets and the various. Propriety exclusion diets available for cats, or even using home cooked foods. And also on the diet front, we may also need to consider if there's significant liver failure or that we may be wanting to give something that's appropriate protein and biological value and caloric value for some sort of hepatic support diet.
And I freely acknowledge that we may not be able to achieve all of those things. We may not be able to get one diet that ticks all those boxes, so we're gonna have to make some judgments in the individual case as to to what's more important. Antibiotics we choose to use, well, certainly, referring back to IBD and the potential role of bacteria there, then you combinations of metronidazole and tetracycline, I would consider, you know, trialling those in, in clinical cases as well as potentially using diet.
The types of bugs that are involved in ascending infections of the bile ducts and possibly triggering pancreatitis are largely going to be coliforms and anaerobes, so we may be selecting bean type drugs, moxicillin, clabaleic acid and cephalosporins. Then potentially some of our nutraceuticals, which I think are are very attractive deoxycholic acid is really in the drug capacity because there's pretty good evidence that it has a pharmacologic effect on the liver. Some of these other drugs, Sammi and melt thistle, there is less evidence.
There is human evidence, there is less evidence, but there's also little likelihood that they do any harm. According to steroids, I suppose again the $64 million question, should we be using steroids? Well, certainly they are appropriate for management of IBD and some of the inflammatory liver diseases.
I would like to be reasonably confident that we're going. Be on top of any bacterial infections. But once I start using them, and I'm gonna be using them at initially, immunosuppressive dosages.
So 2 mix fork would be my standard starting dose of prednisolone. And then potentially other immunosuppressive drugs may come into the picture for management of IVD, cyclosporin. Chlorambuil, which we'll also use in some of the low grade homas, and methotrexate are on the list, although I rarely end up using those, maybe because I, I give all my lymphoma cases to the oncologists at work.
So let's look at Sophie then, we're coming to the end and I'm conscious of the time for everybody here. So Sophie, we think has presumed hypokalemic myopathy. She's hypocabalainemic, she's suspected to have EPI and we think she may well have an IBD, and there's also some evidence of a of a hepatopathy of some form.
And so we've got some, you know, pretty, big nuts to crack, when we're treating Sophie. So we started off with intravenous fluids, we supplemented her potassium, we gave her carbalamine parenterally, we gave her intravenous antibiotics, and despite that, despite improvements, measured improvements in her potassium, etc. She continued to vomit and was profoundly debilitated.
Now she was a very high risk, I felt for general anaesthesia. And whilst I would ordinarily wish to to get biopsy confirmation, I felt it was all or nothing with Sophie that we really couldn't justify the risk of anaesthesia to get endoscopic biopsies. So I opted to start her on corticosteroids anyway.
On the assumption she probably had an IBD. She could have had lymphoma, but that if she did so it was likely as a consequence of longer standing bowel disease, given that her history was, you know, a number of months. So within about 48 hours of starting corticosteroids, there was a profound overall improvement in her condition.
She started eating a commercial hydrolysed diet, as an exclusion diet, and over the next few days there was a progressive improvement and progressively normalising laboratory changes. And this is actually a picture of her that her owner sent me about 6 months down the line where she was. Behaving much more like a normal playful cat, and they were slightly embarrassed, I think, to realise that what they thought was normal for her, prior to her, her more obvious illness was actually a cat who was still feeling pretty crummy because it had gut disease and, you know, they were very happy with the, with the outcome and Sophie, who was, you know, pretty sick and, had some pretty significant.
Consequences, . So summary then, we use the term trioitis to remind ourselves that there is a complex combination of interlinked pathology. There are quite wide ranges of presentations and combinations possible, so we need to try and define the extent of the pathology, identify and manage all our problems.
In initial management, we need to prioritise our treatment. But we need to recognise that there may well be long term disease, particularly long term intestinal disease, and managing that may be the, the best way to manage the, the overall case. Thank you very much, and a bit more Picasso to finish.
Oh, thanks, Clive. That was great, really interesting and fascinating move through the intestine, pancreas and liver of the cat. So that's taught me a loss anyway, so I really appreciate that.
Do we have any questions at all? Anybody want to ask Clive anything while he's got he's on? See if .
If anything comes up there, the . The ultrasonography, my, my difficulty, it really is just practise, isn't it, getting to see those quite . Discreet lesions.
Do you have an ultra sonographer at Davis, or do you do a lot of your own stuff? I I used to do all of my own stuff and I still fill in for the ultrasonographers on occasion. I get called in to fill in gaps, but we have, well we have 4 images, so they tend to share the ultrasound out.
So we had a couple of people off here today and I got dragged in. So I do less than I used to, but I used to do all my. And are they human ultra sonographers who overall?
No, they're they're they're diagnostics. OK, question here, . Recommended analgesia for treating these cases, I would tend to go with opiates rather than any nonsteroidals.
I think there's lots talked against opiates in. Historically with pancreatitis, particularly the concerns mooted about opiates affecting pancreatic duct tone and the like, I'd rather do that than give a nonsteroidal and have potential risks of loss of mucosal integrity and ulceration. And part of the shock in these cats, particularly the cats with pancreatitis, I'm sure the pain is a significant contributor to.
To shock and and all the sort of hormonal consequences of that. So I mean pancreatitis is extremely uncomfortable in people. And I'd want the best analgesia possible if it was me, so that would be where I would be going with it.
I don't really see enough clinical evidence that using opiates is detrimental. I suppose also these days our anaesthetists would be potentially thinking about things like lgnocaine infusions and ketamine infusions. That's all a bit new hat to me.
I need to go and see one of our anaesthetists to get involved with that sort of thing. Again, as you say, quite controversial, the use of steroids, but nothing should die without the benefit of steroids, as we say, so I suppose that was the. The case in this case, what was the rationale in the end?
Well, the rationale in Sophie's case was initial management without steroids hadn't got us where I wanted to be. I, I didn't have any wriggle room really. Yes, she was very sick.
She was very sick and I needed to do something. I did have, I felt strong clinical evidence that she was a cat with IBD, certainly just palpating her intestines. It was enough for me to be very suspicious.
So I wasn't that, you know, you like to get the best evidence and do do what you can, but clinical realities intervened and it was a question of well she's going to need that and if she if she doesn't respond to that, she hasn't responded to anything else. But if I don't give her that and she needs it, well, yeah, of course. Dogs with pancreatitis, you, you often, you know, again, there's that controversy, do you give steroids or, or don't you?
Is that very similar or are they different? I, I suppose I should say I'm giving I'm giving steroids for the IBD, not for pancreatitis. And that's sort of where the question comes, should you be how hard should you be trying to identify for the presence of IBD?
Very rarely use steroids. In fact, I don't really see any place for steroids in most cases of pancreatitis in dogs. There is some, .
Potential is this condition in humans called autoimmune pancreatitis, which is very steroid responsive, and there's a suggestion that some cases of canine pancreatitis may be similar, but no one's really been brave enough yet to give them steroids. They're pretty much off the menu for pancreatitis. Yeah, yeah, that's great.
Clive, I think we've exhausted all the questions there, but I think, you know, I've certainly enjoyed the talk. I really do appreciate you taking time. Out of your busy schedule to come and chat to us and hopefully we can we can drag you along another time to give us another webinar on a topic of your choice.
I'd be delighted and I hope everyone enjoyed it. It's been a pleasure. Thank you very much, Clive, take care and I'll speak to you soon and thanks very much, everyone.
Next week, Thursday, we've got. We've got Martha Cannon talking about difficult hyperthyroid cases, so we've had a very much a feline focus lately, so please do come along to that. I hope you'll enjoy it.
And if not, I think I'm allowed to say happy Christmas now and happy Christmas to you as well, Clive. All right, take care. Speak to you soon, bye bye.