Good evening everyone. I see people are joining. Welcome to today's webinar.
We will starting little by little. I want to introduce myself. My name is Victoria Saluk, and I'm a science and nutrition lead in Nestle Purina Pet Care.
First of all, I wanted to say thank you to the webinar web for this collaboration. Thank you all for joining us today, and a special thank you to our speaker for taking the time to share her expertise with us today. Before we begin, just a few quick notes.
If you have any question to our speaker during the session, please type them in the Q&A box. And if you have any other questions or queries or comments, feel free to use the chat box. Also, I wanted to let You know that we have the simultaneous translations today, so you can choose one of the five languages which are Italian, French, German, Spanish, and Portuguese.
You can just click on the globe icon and choose your channel with the language you prefer. So we hope you enjoyed today's session, and within that we can start. First, let me also introduce the brand, the Pro Planned Veterinary Diets.
This is the brand that sponsors today's session and the brand I work for, and I'm pretty sure that most of you are familiar with this, with this brand where our expert nutritionists and veterinarians strive to create the most advanced and effective nutritional solutions for pets in different health conditions. Pro planned Veterinary diets is a part of Purina and Nestle, and Nestle Purina is a global team, includes specialists in nutrition, veterinarians, behaviourists, immunologists, biologists, and so on and so on, spread over 5 continents in North America, South Africa, Europe, Asia, and Oceania. Purina has been a pioneer in the science of pet health, leading breakthroughs that have redefined the industry's understanding of pet nutrition.
Purina has also published more than 500 papers in scientific journals and currently has more than 7000 granted and patented patents worldwide. Our ultimate goal is to understand and improve every aspect of the pet's overall health and well-being. Related to our today's topic, I wanted to introduce you to our new diet that just has been launched last month.
You may already be able to find it on the shelves in your country, and this is the new EN gastrointestinal low fat. So this diet has to reduced fat content. It's highly digestible gastrointestinal diet.
It also contains a special fat source. Containing the medium chain triglycerides, and it has an added ulin as a prebiotic to improve and support the microbiome health in dogs. This diet may be recommended in hyperlipidemia, exocrine, pancreatic insufficiency, pancreatitis, protein losing enteropathies, gastritis, or vomiting.
I also invite you to join our vet centre where you can find all the detailed information about all our products and besides that, a lot of e-learning, scientific publications, webinar recordings, and so on. So please enjoy and join the vet centre. We have it in different languages and in different countries.
And finally, let me introduce our fantastic speaker for today, and this is Dr. Penny Watson. After graduating from Cambridge in 1989, Dr.
Penny Watson spent 4 years in farm, equine, and small animal practise before returning to Cambridge to Cambridge to undertake a small animal medicine residency. She spent 29 years at the Queen's Veterinary School Hospital, becoming the RCVS and a Queen diplomat. And recognised specialist in small animal medicine, she became a fellow of the RCBC in 2016.
She recently retired from clinical practise and moved to France, but continues with research and lecturing in her areas of interest gastroenterology, hepatology, and clinical nutrition. Penny is ECVIM past president and the former chair of the EVM Internal Medicine Diploma Examination Committee and former honorary secretary of BISala. Penny's research focuses on livers and pancreas diseases in dogs and cats, particularly chronic diseases and fibrosis, and she has published widely in these areas.
So welcome, Penny, and the floor is yours. Thank you, Victoria. I will now attempt to share my screen.
So, hopefully, everybody can see my presentation now. And it's an enormous pleasure for me to be able to join you tonight and to talk to you about the role of low fat diets in supporting fat sensitive conditions in dogs, because not only did I take a particular interest in nutrition when I was working at the university, but in addition, as we'll see as we go through this, fat, low fat diets are very helpful in a lot of the conditions that I used to, to see and that I did my research in. I'm really pleased to see so many of you here today, because I often find that, people are not so interested in nutrition.
Because you don't really appreciate that, diets can be as effective as drug therapy in a number of conditions. And I'm hoping that by the end of this lecture, you will realise that and you'll be, have an added enthusiasm for the nutritional management of your patients. So we're going to talk about, we're basically going to have a lot of case examples this evening, and we're going to talk about, situations where low fat diets are helpful.
And also we're going to talk about how you decide if a diet that you're recommending to a client is actually low fat. So we'll have to talk a little bit about dry matter versus wet matter calculations, but not too many equations this evening. So the case examples we're gonna talk about is delayed gastric emptying, gastroesophageal reflux.
We're gonna talk about particularly the use of low fat diets in chronic pancreatitis and when they might be used in acute, cases and also in those, enteropathy cases and if we have time, if we haven't been, chucked out by then, familial hypertriglyceridemia. We know that fat is an important nutrient. We tend, because of the messaging to humans about not wanting to eat too much fat, we tend to sometimes have a negative view of fat.
But it is very important, in dog and cat food as an energy source. We know that all animals can use protein, fat, or carbohydrates for energy, but protein isn't a, isn't used as an energy source in, in dogs and humans, only really in cats, because it's usually Needed structurally. And so, fat is an important energy source.
And as you can see here from this slide, it's much more energy dense than carbohydrate. As long as there's plenty of oxygen available, 1 gramme of fat will yield 37 kilojoules as compared to 17 kilojoules with 1 gramme of carbohydrate. So it's not always a bad thing, and there are parts, times in life where dogs need, increased fat levels, particularly when they're pregnant and lactating, growing animals, and also, animals that are very energetic and have very energetic life, life cycles.
The other thing to bear in mind is that if you do reduce the fat in the diet, we have to increase something else to maintain the energy intake. So typically you would increase the carbohydrates, you could increase the protein. You definitely can't have a diet that's low in both fat, carbohydrates and protein.
You have to get the energy from somewhere. So let's start with a case example, and this is Barney who came to us at the vet school many years ago before we were bare before the elbow, below the elbow, and we were still wearing white coats, as you can see. And you can see from this picture that this is Barney looking very skinny and miserable, and he's got a gastrostomy tube in place underneath this body bandage.
Barney was a 4 year old neutered male Labrador retriever. He had a 2-year history of eosinophilic enteritis, and he'd shown a very poor response to immunosuppressives, to prednisolone and azathioprine. And in fact, not only had he had a poor clinical response, but he developed a secondary fungal skin infection that is typical for dogs that are on immunosuppressives, so alternaria infection.
To make matters worse, he'd also recently had a large section of his small intestine removed because he'd been playing, catch the stones with the neighbour's children and swallowed a lot of stones and got intestinal obstructions. So he also had short bowel syndrome, so he had a lot of problems. He presented to us with anorexia, complete anorexia, weight loss, and severe diarrhoea.
And we had some discussions with the owner that the only way we were going to be able to deal with Barney at this stage was to take him off all his immunosuppressives, and because he wasn't eating, we were going to have to put a feeding tube in. And we actually recommended at the time that we fed him initially a human elemental diet, so a very basic diet which hopefully his gut would be able to deal with. We took some radiographs in Barney to make sure there was nothing else going on, and what you can see on these radiographs is you can see on the left hand side here, you can see this is his stomach.
He's got a very enlarged gastric shadow with some, little areas of, of, of bone which look like a gravel sign and his stomach looks as if it's full of fluid. So, This suggests delayed gastric emptying and in the other radiograph we can see poorly formed faeces in his colon confirming that he has a degree of of diarrhoea. We did an endoscopy to place his, gastrostomy tube, and we found, the remnants of some dried food that he had last eaten 13 days ago in there, and it did smell as if it was fermenting.
It was a bit like the smell you get in a horse with grass sickness, if any of you have, have, have smelt what you get in, in, in horses. We checked around his stomach and we biopsied the gastric wall, and it was completely normal, and there was no pyloric obstruction. So we may ask ourselves, why has he got such delayed gastric emptying?
Why has he still got food in there that he ate 13 days ago? Well, we need to look at the normal motility of the stomach and the normal feed forward and feedback, reflexes, that's the word I was looking for, of the stomach. We know that the stomach has a complex motility.
It, has com a combination of vagually mediated stretch during filling, and then at the same time, these contractions that mix and bake food. The pylorus, contracts 2 or 3 times a minute and lets out very small particles. And with an average diet, the stomach would be empty about 10 to 12 hours after feeding in a normal dog.
And it depends on the consistency and as we'll see in a minute, the fat and fibre content. And then in fasting in dogs, but not in cats and rabbits, we get these giant contractions, these fasting migrating motility complexes every sort of 1.5 hours.
It's very important that gastric emptying is carefully coordinated because this is the last time where you can really slow down the passage of food through the gut and to allow complete digestion of food. If food is going down through the gut too quickly, you'll get these feedback loops that are telling the stomach not to empty so quickly. So, if you get too much acid or too much fat in the, in the duodenum, and fat is the hardest nutrient to digest, then you'll get these feedbacks saying, delay your gastric emptying.
And the most potent of those signals is from the distal ileum, and this is what we call the ileal break. Because if you get undigested fat and protein going through into the colon, Not only is that a waste of precious resources, but also it tends to cause diarrhoea because the bacteria in the colon, ferment this to, to horrible things. So undigested nutrients, especially fat, reaching the distal ileum really delay gastric emptying.
And so what we thought was going on in Barney, Barney was because he had a combination of inflammatory bowel disease and now a short bowel, which means that he could not properly digest his food. He had a lot of undigested fat and protein reaching his distal ileum, and he had this profound ileal break. So this was a motility problem causing delayed gastric emptying.
It wasn't a physical problem, but it was his stomach just not emptying because he had undigested food reaching his distal ileum. He's an extreme example of this, but you find this in a lot of animals with any form of mild digestion, particularly severe inflammatory bowel disease, and it's particularly prominent we've found in in cats. So then I'm not going to ask you to vote because this will be too complicated, but this is a question for you to think in your, in your head.
What type of diet would you choose for a dog with delayed gastric emptying? Would you choose a dried, low fat diet, a moist, low fat diet, a dried protein restricted diet, or a most moist protein restricted diet? And hopefully now, having sort of said what we've said, we've said that maybe fat is the thing that is going to most delay gastric emptying, then in fact, I would definitely choose a low fat diet, and I would choose a moist or even liquid diet if things are as bad as with Barney.
Because we know that the consistency of the diet has a big effect on gastric emptying. So remember that the pyloris allows out very small particles, 1 to 2 millimetres in size. And so a liquid diet will empty much faster than a solid diet, maybe a tinned diet, and much faster than a dried diet.
And this has been proved in dogs by, putting barium in different types of diets and measuring how long it takes for them to leave the stomach. And ideally little and often. And as we've seen, fat delays gastric emptying, it also has the additional effects of increasing gastric acid secretion and reducing gastroesophageal sphincter tone, so it increases the risk of acid reflux.
And we're going to talk about that in a minute when we talk about reflux, esophagitis in dogs. So what happened with Barney, we fed him little and often with this human elemental diet, and initially we had to use prokinetics to help him empty his stomach, because after the first meal, 2 hours later, 3 hours later, we went to feed him a bit again, and we found all of his previous meal was still in his stomach. So, for the first day, it was very difficult, but after that, things started moving.
We used a low fat, low fibre, liquid human elemental diet. And then interestingly, this is how old Barney was. He was probably one of the first dogs in the United Kingdom to be fed HA diet, because we wanted a, a, to, to move him from this really elemental peptide-based diet onto a polypeptide hypoallergenic diet.
And Purina HA was just being launched in the UK, so we actually used that. We gradually transitioned him over and we soaked it to make sure that it was not just a dried food, but it was moist, to go through. And he actually did very well long term.
He never had fully formed faeces. His faeces were always like a whipped ice cream, Mr. Whippy Ice Cream, but he gained weight, his appetite improved, and he had a good quality of life.
So that was Barney. So what about the second case? The second case was Blue.
Blue was a 2 year old female bearded collie who presented to us with a 1 week history of gagging and wretching. We took a careful history, and it sounded reasonably typical of regurgitation, esophageal regurgitation, but with one or two unusual aspects. So it was usually passive, a variable time after feeding, and often on exercise.
So Blue would be going out for exercise, would put her head down, and just this food and lots of white saliva would come out. The thing that was unusual for regurgitation was that there was some distress, especially when Blue was swallowing. There was definitely some pain and distress there.
And then Blue would try and eat this again after regurgitating. So, it was typical of regurgitation, but with some distress, which alerts us to the possibility that Blue may well have a degree of esophagitis as well as, as, regurgitation. Thinking of the common causes of regurgitation, we've got oesophageal foreign body, megaesophagus, such as you can see in this radiograph, we can see this dilated gas-filled oesophagus here.
Vascular ring anomaly, gastroesophageal reflux, and esophagitis. And then perhaps the less common causes are oesophageal stricture, hiatal hernia, which is generally uncommon unless you have a lot of, French bulldogs in your, in your practise amongst your patients because they are predisposed. We can see oesophageal diverticular, perioesophageal masses, or gastroesophageal interception.
So we took a bit more history from Blue, trying to understand if Blue had a foreign body, was there any other predisposing factor, and we did discover that Blue had had a general anaesthetic 3 weeks previously, I think for a dental procedure as far as I can remember. She was also thin, but there were no other abnormalities on clinical examination and nothing else in the history. But the general anaesthetic definitely makes us worry about gastroesophageal reflux during anaesthesia.
Blue's thoracic radiograph didn't show any evidence of a megaesophagus, and I guess if we didn't have the suspicion of, a gastroesophageal reflux, we might have left it at that, but we were very suspicious that there may be reflux and potentially a stricture. Because of the history. So we gave Blue some barium.
Barium and liquid, really didn't outline the lesion very well, but suggested there was a lesion over the heart base. And then when we gave Blue some carefully, some food, because there's always a risk of aspiration with esophageal disease, we could see clearly a stricture here over the heart base. Now, if Blue had been a young dog, we may have been worrying about vascular ring anomaly because that can look very similar, but Blue is an older dog with a recent general anaesthetic, and we're very concerned with Blue that this is likely to be a stricture as a result of oesophageal reflux after a general anaesthetic.
We wouldn't do esophagoscopy in a case like this as our first test because there may be multiple strictures after anaesthetic, and we probably wouldn't be able to get past this first stricture in order to see the other strictures. And in addition, there's always a risk when you anaesthetize a dog with a megaesophagus that you can get aspiration pneumonia, but this is something we will be doing to try and treat the stricture. So we diagnose oesophageal stricture as a result of gastroesophageal reflux during surgery and clinically an esophagitis as well.
And I just put up this picture because we saw this case recently just to show you how severe strictures can be. This was actually a cat. And this was a severe stricture as a result of non-steroidals being used orally and obviously not being followed down with fluid or, or food, and one of these non-steroidals must have got stuck in the oesophagus.
And this was very challenging to treat. This is a tiny, tiny hole now left in that cat's oesophagus. So reflux is a risk with surgery.
It doesn't occur with every surgery, but it does depend, on the type of surgery and also the length of contact, and also whether the animal refluxes, duodenal contents as well as gastric contents, because if there's acid, and there's also proteases and by all sorts, then you're more likely to get damage. It's a small risk but potentially serious because strictures can be very difficult to treat and they can occur up to 14 days after, or from 14 days after an anaesthesia. And as we mentioned, they may be multiple sites.
We would treat an esophagitis if we were aware or suspicious, that there is an esophagitis early and aggressively. So, because there's a high risk of strictures and also aspiration pneumonia, if the animal's very ill, we may put them on fluids and electrolytes. Otherwise, we would give them acid secretory inhibitors, proton pump.
Inhibitors, omeprazole, sucralfate suspension, and in the acute phase, little and often low fat food. And why would we use low fat food? Because, as we saw earlier, high fat diets increase the risk of, gastroesophageal reflux because they reduce the gastroesophageal sphincter tone.
So in any disease where you have that reflux and you have an esophagitis, a low fat food will try and help to stop an ongoing reflux, from the stomach. I actually always remember that my mother-in-law had hiatal hernia and she was told not to eat things like fish and chips because, again, they would increase the risk of her refluxing with her hernia. So Blue had two bougies of her stricture.
It was in the days before we had the availability of these balloons to dilate the stricture, and sadly on the second procedure, Blue ruptured and got a severe mediastinitis and died. And actually, that, that isn't too unusual, depending on the study that you read, the reported mortality with esophageal strictures and the treatment of them is between 12 and 23%, which is quite a high mortality. So we should try and avoid these as much as possible.
And then after surgery, we fed as hard a possible low fat diet with, omeprazole and sucralfate paste. And we would avoid putting in nasoesophageal feeding tubes after, after boozes and after because the, if the oesophagus is inflamed, then these might increase the risk of, of repeat stricture. Just a quick word on proton pump, blockers.
These aren't currently licenced for dogs and cats, they are licenced for horses, but we do use them a lot. They're the most effective acid secretory inhibitors. The, the dose that we would use is at the bottom of this slide, and they're the drug of choice for any dog or cat with bleeding, bleeding ulcers or oesophageal reflux, and they're more effective if we give them twice a day.
But these are really the only cases where we use them. We still see a lot of cases of inappropriate use of proton pump inhibitors and there are risks of toxicity. You can get a rebound increase in gastrin in long-term use and gastric mucosal hyperplasia.
We can, because of a lack of acid in the stomach, we get, get, can get a risk of bacterial or fungal overgrowth. And in addition, because there's less acid going into the duodenum, which is not normal, that's not normal physiology, you tend to get effects on gut flora. You can get a quite marked dysbiosis, and they can cause diarrhoea and anorexia.
So, just a word of Caution. They're not an antiemetic. They're an antacid, and they're only indicated in bleeding ulcers and animals with gastroesophageal reflux.
If you think you have an increased risk of ulceration, you would probably be better off using an H2, blocker, which is, less potent, actually, if you have an increased risk, but without ulceration. And before we leave reflux, I've mentioned hiatal hernias a few times, and low fat foods are also are also very much indicated for those animals that get acquired hiatal hernias as a result of breathing difficulties, particularly those little boass dogs, because they're having to produce very large negative pressures in their chest in order to breathe in. Then some of these animals will actually suck the hiatus of the stomach into the chest and then they have a big risk of gastroesophageal reflux and low fat diets along with other treatments make a big deal of difference to these dogs.
So now, moving further down the gut, I'll introduce you to Missy, who was a case who was seen by Ben Harris when he was doing a residency with us at the vet school. She's a six year old neutered female Staffordshire Bull Terrier with a long history of a picky appetite, occasional vomiting and diarrhoea. Recently, her diarrhoea worsened, was light brown and watery, and daily with a reduced appetite.
Now at the time that she presented to us, she'd been fed a homemade diet made of cooked chicken, minced rabbit rabbit and raw minced beef, so probably not particularly low in fat. Clinical examination was actually unremarkable apart from subjectively perhaps slightly thickened gut loops on abdominal palpation but no abdominal pain. So her problem list was a long history of, of gastrointestinal signs and recently worsening diarrhoea, and we were thinking of differentials like potentially an infectious cause because she's on a raw diet.
It wouldn't be top of my list in an adult dog normally, but when they're on raw diets, we always have. To consider the possibility of something like salmonella, for example. It could be that she has a dietary allergy, it could be a form of inflammatory bowel disease, possibly neoplasia or extraintestinal disease such as pancreatic insufficiency or liver or renal disease.
So we did some blood samples, we took faecal samples, including for culture, including salmonella culture, which we have to ask for specially, and also some imaging. On her blood samples, you will see that the, the sort of most remarkable findings are that she has a significantly low albumin and globulin, so she has a low total protein. She also has a low cholesterol, and this, this triad in a dog with diarrhoea does suggest that you may have a protein losing enteropathy because you will be losing, if you lose lymph into the abdomen, this into the gut, this contains protein and cholesterol and also lymphocytes, so you often get a lymphopenia as well.
And she also has a low calcium, which may be just because she has a reduced protein binding because of her low albumin, so her ionised calcium may be normal. But if you have the capability, it's worth checking the ionised calcium because they've, it's also been demonstrated that dogs with protein losing enteropathy also have an increased risk of, of, vitamin D deficiency, so it could be due to that as well. And her ALT is moderately increased, which may be a reaction to whatever is going on in her gut.
B12 folate and trypsin-like immunoreactivity were checked at her own vets, and they were all normal. And her urine protein creatinine ratio was also normal, and it's, it's good to rule out, a loss in the, in the urine. Normally that would be just albumin, but occasionally dogs can have both protein losing enteropathy and protein losing, nephropathy.
And we took 2 faecal samples and checked for pathogens, both parasites and bacteria and didn't find anything. Abdominal ultrasound showed hyperchoextriations throughout her small intestine, which were suggestive of lymphangiectasia, and her duodenal and duodenal walls were mildly thickened. Her pancreas, kidneys, liver, spleen, and adrenal glands looked unremarkable.
So we concluded that her protein loss was in the gut. Her liver appeared, you know, unremarkable apart from this mild increase in ALT. We haven't got a biopsy to confirm that.
Her diet was high enough in protein, albeit it was, it was homemade, so it wasn't a dietary protein allergy. And her cabalamin was normal, but her calcium was low, as we were discussing. I'll just whiz through this slide through lack of time.
So what are we going to advise now? Are we're gonna try some presumptive treatment, perhaps with a single protein source diet, or are we going to biopsy and are we going to do this endoscopically or at the laparotomy? We were concerned enough in her case to, to rule out diffuse neoplasia, particularly lymphoma, that we had decided with the owner to do endoscopy after discussing the risks and benefits, because there's always a small risk with anaesthetic, especially with animals that have a low albumin.
She had a normal appearance to her oesophagus, stomach, and duodenum. We took multiple biopsies of the upper GI tract. She didn't have an ileal investigation.
Her stomach and gastric biopsies were unremarkable, but her duodenum did show a moderate lymphoplasmocytic enteritis and mild lactal dilation. And actually, our pathologists are very, loath. They're very unwilling to say anything about the lacteals in endoscopic biopsies.
So we felt that that was really quite something that they said there was mild lac dilation. So, we did have quite a, a, a strong suspicion now that Missy has lymphangiectasia. Protein losing enteropathy in dogs tends to be caused by either a severe lymphoplasmocytic or eosinophilic inflammatory bowel disease, lymphoma in particular, or other gut tumours, and lymphangiectasia, and we have seen it sometimes in dogs with ongoing chronic pancreatitis as well.
But of course it's possible to have more than one concurrent disease, so lymphangiectasia, for example, could occur secondary to inflammatory bowel disease or lymphoma. So, lymphangiectasia can be primary or secondary, and the diagnosis is challenging because a lot of pathologists want full thickness biopsies. But in Missy's case, the ultrasound was already suggestive.
There are some suggestive findings on ultrasound, and then the pathology was suggestive again. So, we made a presumptive diagnosis in her of lymphangiectasia, potentially secondary to inflammatory bowel disease. We would treat these cases with a low fat diet, and we may add steroids in if we think this is secondary to inflammation.
But the low fat diet is crucial because it reduces lymphatic flow, and since it's, it's loss of lymph into the gut from the lymphatics that causes the diarrhoea, this should reduce the diarrhoea. And we might use a single protein novel antigen in inflammatory disease. So in Missy we chose to go on an exclusion diet and we started with a homemade exclusion diet, venison and potato, which is actually relatively low fat because venison is a low fat meat.
So that was a reasonably good one to use in, in her. She had a marked improvement in appetite and her faeces was normal within 2 days, which was very dramatic. However, the long term with Missy wasn't so good.
At a recheck six weeks later, her appetite was poor over the last 2 days. Her recheck bloods, her albumin and globulin had improved, so the diet together, had actually improved, her condition considerably. Her calcium was now normal, which is really good.
Her urea was slightly high, we're not really quite sure why that was, and she did have an elevated snap CPL suggesting she may have concurrent pancreatitis. And I give you all these details because I'd love to have finished where I finished, but I just wanted you to know that actually she didn't do too well long term. So she only survived 6 months after we saw her.
She had a, a relapse after 3 months when she ate a dead fish. She had been changed effectively over to a manufactured low fat novel protein diet. She had a gradual deterioration after that first episode of bloody diarrhoea, and then her, her, proteins dropped again.
We started her on immunosuppressives, but she had an acute GI bleed and died three months later. And I'm afraid I can't tell you why, because she didn't have a postmortem. Even in referral practise, some of these cases are very frustrating.
We don't know if it was because she had a really bad inflammatory bowel disease. Did she have a concurrent pancreatitis that actually caused that final severe bout? Or in fact, was there perhaps a small cell lymphoma in her ileum that we hadn't diagnosed that was causing her, protein losing, condition.
And had we not, you know, treated her ideally for that. So we don't really know what went wrong with Missy. The problem with protein losing enteropathies in dogs is that the prognosis can be poor, and we always warn the owners of this.
And it may be because the underlying disease is severe, and it may be because some of those cases have a gastrointestinal lymphoma that we are not diagnosing. Also, the low protein itself, which has, secondary problems, can cause pulmonary edoema and cerebral edoema. And potentially because on occasions I think our, our immunosuppressives can result in ulceration as well, which can, can make things worse.
So for example, in this study that came out of the Royal Veterinary College, inhospital mortality for dogs with protein losing enteropathy, and these were obviously the more severe cases referred to a referral centre, but inhospital mortality was, you know, 21.5%, which is really quite high. What we do know is that low fat diets make a real difference in these dogs, and it can be an effective monotherapy in some dogs, and it was.
This is why I, I showed you, Missy, to begin with, it worked extremely well in Missy. So there was something else going on in her that caused that rapid deterioration, the, the, the, the second time around. But initially in just low fat diet alone without any immunosuppressives, normalised her proteins.
So we know that that that can work, particularly in animals with lymphangiectasia. You may have heard about ultra low fat diets and the use of ultra low fat diets in dogs with protein losing enteropathy, and these can work even better in these dogs, but ultra low fat diets are not manufactured diets, they are only made by qualified veterinary nutritionists, and because they're so low in fat, they have to be formulated very carefully. Because there is a danger with ultra low fat that you may have an animal that is, for example, deficient in fat soluble vitamins.
And it, this was, if you're interested, you can read this paper in Journal of Veterinary Internal Medicine. These were dogs that were referred because they had protein losing enteropathy that weren't responding to normal manufactured diets, and in some of these cases being put on a very low fat diet actually made the difference for those animals. And what do we mean by ultra low fat?
Well, where a low fat diet might be 17 to 30 grammes per 1000 kilocalories fat, ultra low fat would be, that should say less than, not greater than 17 grammes per 1000 kilocalories. And this brings us on to discussing what we mean by a low fat diet, and this is very important, before you get too sleepy, at the end of the session. When you and your owners are looking at the side of a bag or a can of, of dog food, you will see the fat percentage on the side.
So for example, for this Purina, EN gastrointestinal low fat, you'll find the moisture content is really quite low, protein 24%, fat 7.5%. Now, on a dried and carbohydrate, 51%, on a dry diet, we can look at the fat content, and that is the content, dry matter in that diet, so that gives us a realistic estimate.
And I always advised owners that if they were going for a low fat diet, they should go for something that's less than 10% dry matter. So, this would, this would fit very well with this low fat diet. There are some problems, however, and one of the problems is canned food.
So, if you look on the side of this, and this is not EN, low fat, this is just EN gastrointestinal food. If you look on the ingredients of this diet, the moisture content is 72.5%, the fat content is 4.9%.
So, owners will look at that, look at that and say, but that's less than 10%. So, therefore, in the, in this diet, this must be low in fat. And you're like, well, no, it's not.
Because, actually, 27.5% of that diet is water. So, you need to take that water away before you look at the fat content, because actually, the nutrients that the dog is taking are dry matter nutrients.
They're not the water. So, you need to calculate the dry matter fat content, and the dry matter is 100. Take away the moisture, which is 27.5%.
And then the fat is the fat content of that. So, it's 4.9 divided by 27.5 times 100.
And you might have to go away and think about this calculation, but it, I'm no good at maths, and it makes perfect sense to me. So, the actual fat content of that diet is 17.5%.
And going back to the previous slide, the other thing that is there to catch us out is we can only really compare diets by dry matter if they have the same calorie content, because dogs will eat to fulfil their calorie requirement every day, not because of the volume of the food. And most maintenance diets are the same calorie content, so that's fine. You can compare dry matter calculations in the supermarket and for most maintenance diets.
But beware diets that are marketed for weight loss, because they have a lower calorie content. So they might appear low in fat if you do a dry matter calculation. But if you actually compare on the amount of calories that the dog is going to eat each, each day, then they are not low in fat.
So, hence why, if we're doing this properly, it's not easy to do just looking at the label, but if we can look at the book, we can actually compare the number of grammes per 1000 kilocalories, as opposed to dry matter. But I have to say in the real world, in your clinics, what you'll be doing is these dry matter calculations. Just beware, don't think that low that low calorie weight loss diets are low in fat because they aren't necessarily, you really do need to compare those on a calorie basis.
So we're getting, we've, we've got a little bit to go now, but we've got 2 more cases, so I may have to shorten the last case slightly. But, we'll look at Tommy. So Tommy, because I can't finish without going into pancreatitis.
Tommy here has an arrow. This is Tommy as a puppy. He came to us actually when he was an adult.
The owner was incredibly fond of this, this dog. She, she loves her cavaliers. So Tommy came to us not when he was a puppy, but when he was 11 years old, male neutered cavalier King Charles Spaniel.
And he actually came to us for management advice because he'd already had a diagnosis of recurrent or chronic pancreatitis, which is very common in this breed, and he also had concurrent renal failure. And really the advice was, what should we be feeding this dog? Should we be feeding him on a low fat diet for his chronic kidney failure, or should, sorry, for his chronic pancreatitis, or should we be feeding him on a low phosphate diet?
There is chronic kidney failure, but renal diets tend to be high in fat because they're high in calories, because dogs with chronic renal failure don't want to eat, so, they tend to be relatively calorie dense. Tommy had a classic cavalier history. He had everything cavaliers get.
He'd had an MRI scan at 5 years old, which had diagnosed syringomyelia, which was mild with associated clinical signs. He'd been deaf since he was 8 years old. He had a heart murmur since he was 9 years old, which was mitral valve disease.
He had dry eye and recurrent ulceration, recurrent dental disease, and then his chronic renal failure diagnosis at 9 years of age. And then the vet had moved him to a renal diet which had triggered his bouts of pancreatitis, so hence the, the dietary discussion. On clinical examination, this is him as an adult asleep.
He was bright and tail wagging, which is extraordinary given all his concurrent diseases. He had a healing corneal ulcer in his left eye. He had no evidence of abdominal pain, but a grade through systolic murmur, and he had good femoral pulse volume.
And his blood results demonstrated to us an increase in urea and creatinine, typical of a dog with chronic renal failure, and he had an elevated phosphate. He also had an elevated calcium, which often happens in these animals with renal secondary hyperparathyroidism, and he had a, a moderately increased cholesterol but normal triglycerides, and his other electrolytes were normal. He had a mild increase in his liver enzymes, and his urine protein creatinine ratio was increased, and he had poorly concentrated urine, a negative culture, and normal systolic blood pressure, so relatively normal.
So what his haematology also showed a mild non-regenerative anaemia, again, typical of chronic renal failure, and he had a very low platelet count, but there were platelet clumps, and he had macroplatelets seen. So his count was probably higher than that, but it may still only have been about 50 because he's a cavalier, and he's got the giant platelets that cavaliers get. And these small numbers of big platelets in cavaliers, they've shown that it's present in about half of the cavaliers in the UK.
They have a lower activation threshold for aggregation, so these dogs will clot perfectly fine, which explains why when we go back here, there were platelet clumps within the haematology scheme. He's clotting absolutely fine. So this is normal, we're not too concerned about this.
So, I brought Tommy along as a case, just to demonstrate that we do sometimes have issues because we have dogs with chronic pancreatitis who tend to do really quite well with low fat diets. It tends to reduce the severity of their recurrences, and importantly, it reduces the pain in long-term management. But it can be difficult because if these dogs have concurrent Disease, particularly chronic kidney failure, which is common concurrently, particularly in cavaliers and cockers, then what do we do?
Do we put them on a low phosphate, renal diet and risk worsening of the pancreatitis, or do we put them on a low fat diet? The ideal would be if the, pet food companies would give us a low phosphate, low fat diet, precisely for these dogs. But in, in Tommy's case, we got a qualified veterinary nutritionist to actually, make him a homemade low phosphate, low fat diet.
So we were able to produce something that was ideal for both diseases. And then he needed analgesia whenever he had his flare-ups, and in the UK we often will use paracetamol for dogs, not for cats, but for dogs because we have a licenced product. And also tramadol, which is a of of questionable efficacy, but it's difficult to know what to use for home treatment in these dogs.
And he did have a good quality of life for another 6 months before he was euthanased for his renal failure. In pancreatitis, we believe that low fat diets make a real difference to the pain in both acute and chronic disease. This has been recognised in humans but is anecdotal in dogs, and there is no evidence actually that fat increases the severity of the disease histologically.
And so if you have an animal in the hospital that is being adequately analgesed with intravenous opiates, then normal amounts of fat are OK. So, if you wanted to, you could use normal fat level diets in your critical care cases, especially these liquid diets. Although we often still use the lower fat liquid diets that were available for these dogs.
And in a dog that's had a single bout of acute pancreatitis that's maybe been triggered by dietary indiscretion, We might feed a low fat diet while the dog recovers, but we wouldn't necessarily keep it on that low fat diet long term, whereas in the chronic cases, we would keep them on long term. The owner was was very kind and allowed us to postmortem Tommy, and at postmortem we were confirmed his syringomyelia, his mitral valve disease, he had meembryoproliferative glomerulonephritis and interstitial fibrosis in his kidneys. He had just a normal ageing change in his liver, nodular hyperplasia, but he did have quite marked evidence of pancreatic fibrosis and chronic pancreatitis, which is a, A classic finding in cavaliers, this, this is a Masson's trichrome stain on the right of a Cavalier King Charles Spaniel with severe end stage chronic pancreatitis, and the green is fibrosis, and the red is the remaining pancreatic tissue, and the white is actually fat in the pancreas as well, which, Which is not unsurprising in cavaliers.
And we demonstrated that cavaliers have a high prevalence of concurrent pancreatic and renal disease at postmortem, and we published a paper showing this in a number of dogs, and I will speed on for the sake of time. So cavaliers, certainly in the UK have a very high relative risk of pancreatitis, chronic pancreatitis, and we tend to underestimate the prevalence. They tend to be very good at hiding their clinical signs, and often you don't know if it's the syringomyelia or the pancreas that's causing the pain.
And because it's a largely fibrotic disease, transcutaneous ultrasound has quite a low sensitivity in these dogs. But again, just something to go away with. If you have any Cavalier King Charles Spaniel patients with diabetes or exocrine pancreatic insufficiency, it's very likely that they have underlying chronic pancreatitis, even if you haven't been able to demonstrate that with blood tests or potentially with ultrasound, just keep trying, keep measuring your, your pancreatic lipase during bouts and, and hopefully you'll get a positive.
Now, finally, time is short, so I'm not gonna tell you about the case example that I have, I'm afraid of a miniature schnauzer with hypertriglyceridemia, but I will shoot straight through, so Poppy will, to the slides that, that describe the disease, because otherwise we'll be here way beyond I'm allowed to be here. So, I had a lovely case of familial hypertriglycer. Emia in a miniature schnauzer.
When I first worked at Cambridge, we didn't used to see these cases in the UK at all. I still remember the first dog that came through the door with this. It was very common in the States, but now it's worldwide.
They seem to have, used quite a lot of the same dogs for breeding, and now we see it in triglycerides in, miniature schnauzers in the UK as well. It's also been reported in some other breeds, particularly Briards and rough collies in the UK and Belgium, and also Shetland Sheepdogs in the USA and Japan, and you can see it in a variety of other dog breeds and crossbreeds, as you can in humans. This is an interaction between the genes and the environment.
So these dogs have a delayed clearance of triglycerides from the blood after a meal. And generally speaking, when they're young, because their liver, which clears these triglycerides, is young and healthy, Then they're very good at clearing triglycerides, and you don't notice it. As they get older, this abnormality becomes more apparent because the liver senesces and is less good at clearing the triglycerides.
It's a bit like old livers are less good at clearing alcohol. Well, old dogs. Livers are less good at clearing triglycerides.
And, in, in some studies, by the time these dogs, these miniature schnauzers were over 9 years of age, over 75% of them, certainly in the States, are showing signs of this condition, which is a quite large number. So, it's something to really be aware of in miniature schnauzers. Fat, is usually emulsified in the, by bile acids in the small intestine, is digested by lipase, and then these chylomicron aggregates of protein and triglycerides and cholesterol are absorbed in the lymphatics, from there into the bloodstream.
And then endothelial lipoprotein, lipase releases these triglycerides into the tissues, especially muscle and adipose tissue, and the cholesterol is transported to the liver. As I've said, these dogs have a delayed clearance of triglycerides, and how badly they're affected depends on other factors. So how much is their liver senescing, how high is the fat in their diet, because if they're already on a low fat diet, you may not notice it, and then the older the dog gets, the worse.
And if you have a dog with concurrent endocrine disease, particularly hypothyroidism, that also causes hypertriglyceridemia, then they will also present younger. We know that this is genetic because there's a high risk in certain breeds, but candidate gene studies have, have so far not found the cause, and it's likely a polygeneticgenic disease as it is in humans. What we tend to see in those cases that have high triglycerides is this combination of, diseases.
So, we've mentioned these triggers. You tend to see bouts of acute pancreatitis. You get a vacular hepatopathy, and they're predisposed to gallbladder mucocele.
So you're typically, You see increases in alkaline phosphatase and ALT on bloods. And you may see signs of recurrent pancreatitis. So, obviously, for me, somebody who's interested in pancreas and liver disease, this is absolutely, and diseases of ageing, this is absolutely the kind of ideal, disease in these dogs.
And we treat this by giving them a low fat diet and identifying and treating concurrent diseases. So if the dog is hypothyroid, great, that gives us something we can treat, and we would give it thyroid supplementation and low fat diet, and that may be all you need to do, because if you're able to, to, to, to, to treat that, dog's other predisposing diseases, that may be all you need. However, if you're not getting on top of the triglycerides and you're still getting clinical signs, particularly of recurrent pancreatitis, which is really painful, then you should consider drug therapy.
Now, initially, you might use omega 3 fatty acids, and if they are not working alone, fenofibrate, and occasionally these dogs need ultra low fat diets, but really not very often. Normally all we need, in fact, in most of the cases I treated, low fat diet and omega 3 fatty acids worked. And you may say to yourself, why on earth, would we use omega 3 fatty acids?
Well, I'm just, this is a study that showed that low fat diet was effective in reducing triglycerides and cholesterol in affected miniature schnauzers. And then here's another more recent. Study that shows that supplementation of omega-3 fatty acids helps.
Omega 3 fatty acids actually stimulate the hormone sensitive lipase, which, which, causes fat, uptake into tissues. So that's, this is why omega 3s are actually helpful. And then more recently, fefibrate, which is used in humans with hypertriglyceridemia, has been demonstrated to be effective in dogs, but it's not licenced for use in dogs, and there's really no need to use it if those other methods work well in these animals.
And so, these dogs are classic of animals where you have an interaction, a breed, the environment, which is often diet, and then the age of the dog. So, I've managed, I think, by skipping a few slides, to finish about 5 or 6, minutes early. So, I'm going to stop sharing my screen, and I don't know if we have, any questions in the chat, but I think, as was, said earlier.
Earlier on, if you have questions, and you put them in the chat and we don't have time to answer, then, then we'd be very, I'd be very happy to answer them after this webinar. Thank you. Thank you very much.
Thank you very much, Penny. Thank you for finishing in time as well. But don't worry, we don't have a lot of questions.
We only have 2. And one of them was already answered as I see, so it was related to the manufactured ultra fat diets. So I can read the case.
So I'm in the US. I have a canine patient diagnosed with protein losing enteropathy. He did not respond to their treatments, including Purine AHA.
I switched. Him to a homemade ultra low fat diet and he responded very well. Then his diarrhoea and peritoneal effusion diarrhoea resolved, and I was very slowly switching him to Purina EN when he decompensated and developed the peritoneal effusion and profuse diarrhoea.
I promptly switched him back again to the homemade ultra low fat diet, and he improved. If there is any commercial ultra fat diet that could work. Yeah, no, not as far as I'm aware.
And I think it sounds like your dog needs that ultra low fat diet. And as long as you're happy that it's balanced, I think, particularly the vitamin D and the other fat soluble vitamins would need to be balanced, in that dog, and it might, it might even be worth, you know, checking his ionised calcium every now and again. Again, but as long as you're happy that that diet has been carefully balanced by a nutritionists, then it sounds like that's going to be what you, you're going to have to feed the dog.
They are really challenging cases, annoyingly challenging, those protein losing enteropathy dogs. So, yeah, yeah, I do, yeah, I'm not aware of one. Are you, Victoria?
No, unfortunately not. In the US we have a little bit different portfolio, but still we have the EN low fat, which has approximately 2 grammes per 100 kilocalories of fat, but still it can be not considered and that recent paper that I flashed past, they were all the ultra low fat diets were definitely all being made by a nutrition service, and I think that that may that study, I can't remember now, but I think that may have been from the states as well. So.
It, it implies there really isn't, there really isn't one available. I see someone has put in what omega 3 supplement would you recommend for hypertriglyceridemia, and it's a very good question. I would just see the vet school go and get whatever we had on the shelf in our pharmacy at the time.
But I think as long as the problem, you know, we could talk a long time about nutraceuticals, because I really do believe in nutraceuticals, and we have evidence for the omega 3 supplements in this case, but you need to make sure that you get a product because they are not, subject to the same, rigorous sort of, legal, testing as drugs. You need to make sure that it's from. Manufacturer that you trust.
So, I would, often it's good to get them from a trusted veterinary nutraceutical manufacturer. Occasionally people will go and get them from, you know, their own chemist, from a human nutraceutical manufacturer. But I, I would want to know that this was somebody that was trustworthy so that you knew that what they say is in the supplement is actually there.
The other thing if owners are going and buying it, is to make sure that they don't go and get themselves, any form of fish oil with extra vitamin D in it, because then you run the risk of vitamin D toxicity in, in dogs if they're, if they're giving it themselves. So, ideally, give them a veterinary one that you've got that you know, does not. Have, you know, excess vitamin D in it.
That's a long answer to a short question. Yeah. And it's different in different countries.
Now, I work, now I live in France. I've become recently very aware that the nutraceuticals available in France are different from the UK, which is surprising because we're very close, but, yeah. That's true.
And we also have two questions regarding the, if, what do you think is the low fat diet with phosphate binder work for a dog that needs low fat and low phosphate? It's a very good question. I'm glad you asked that because I didn't address that.
It may do or it may not. We, we, you can try. The problem is is that most normal dog diets have quite a lot of phosphate in because it comes in with the protein.
And so, we have an English saying, it's like whistling in the wind. It may be that it's going to make very little difference. It's worth trying.
And if it works, great. But normally, phosphate binders work better if you use them already with a phosphate restricted diet. So, yeah.
Yeah. Thank you. OK, questions are coming and coming.
Where does one go to find a veterinary nutritionist? I think that's a good question to answer. So, what you can actually do is you can go onto the EBVS, the European Board of Veterinary specialisation, website, and you can look for a specialist in nutrition, because I think it's really good to get a European specialist in nutrition or an ACVIM specialist.
So I don't know if you can do. The same in America. You could probably look at the ACVIM or the European College of Veterinary Nutrition and see who they have.
I mean, I've, I know of two in the UK, so, actually 3 now. but, but it, you know, it's finding out who in your country is a, is a veterinary nutritional specialist, and I would look for American or European nutrition specialists. There's quite a lot of them around now.
Yeah. OK, thank you. So the time ran out, I'm afraid, but we can collect the questions and then send the answers, I suppose, the next day, as well as I wanted to mention that you can collect your CPD certificates and you can have the recordings, like in 24 hours.
So within that we have to finish our session. Thank you very much once again, Penny. It was very interesting.
Yeah, I would listen for this, for 2 hours at least. So it's very, very interesting. Thank you very much.
Thank you everybody for coming on an evening, or not an evening for all of you, but thank you. OK, thank you. Bye-bye.
Bye.
