Good evening everybody and welcome to another Thursday night members webinar. My name is Bruce Stevenson and I have the honour and privilege of chairing the first part of this session. We will later on remind you again, part two is going to be in August.

But in the meantime, we have part one. Don't think we have any new members tonight, so the usual rules apply. Any questions into the Q&A box and we will hold those over to the end and Beno has very kindly agreed to answer as many as we can get through.

So Beno is a graduate of the National Veterinary School of Toulouse in France. After one year of clinical pathology specialty internship in Toulouse, he moved to Canada. Initially as a rotating intern at the University of Montreal, then as a rotating intern at the Ontario Veterinary College.

He subsequently completed a small animal internal medicine residency and a PhD at the Ontario Veterinary College. Beno is a diplomat of the American College of Veterinary Internal Medicine. Prior to his appointment at the UCD School of Veterinary Medicine, Bonno worked as a clinician in small animal internal medicine department at the Ontario Veterinary College and the Ontario and the University of Montreal, as well as in private practise in both Ontario and Quebec.

His area of interest include haematology, immune-mediated disorders, bone marrow diseases, as well as urology and nephrology in companion animals. But now, welcome back to the webinar vet, and it's over to you. Good evening, everyone.

Thank you very much, Bruce, for the introduction. So, yes, as, it was already disclosed, this will be a two-part talk about feline neal obstructions. Tonight we are gonna focus more on clinical presentation, how to establish the diagnosis and the initial treatment steps, and then, in August, we will discuss more in depth, advanced treatment with subs and their management and monitoring long term.

Oops This is better. So obviously when we talk about ureteral diseases in, in cats, the main question that's gonna be up in the air tonight is to sub or not to sub, that's the question for these patients. We are going to discuss about the pathophysiology of these obstructions and their complication and consequences for our patients, and as I mentioned, the initial management, and we will see through the presentation that ureteral obstruction can be quite a challenging diagnosis.

Which requires, a good clinical sense and a good kind of history taking and physical examination skills, so really important to nurture these skills and not jump necessarily on conclusion based on your laboratory diagnosis. If we review the literature that has been published over the recent years, there are more and more reports of ureteral obstructions and their treatments in cats. And I think it's mostly because we are better at recognising them.

Maybe they are occurring more often, but for sure, the, the progress in imaging and mostly, like technically, the ultrason machine being better, and technically the veterinarians being better at using them have increased our ability to, to see these obstruction and diagnose them. When we look at the different etiologies, in a big retrospective study of 135 cats, stones were coming at the first place, followed by stretchers, and then combination of stone and stretch were present, knowing that the structure is probably secondary to the inflammation created by the stone being embedded in the ureter. Infection, such as nephrosis or polynephritis was also reported.

The obstruction is then either secondary to mucus, mucus plugs, blood, or sometimes stricture from the inflammation. And then there are some more anecdotal and case reports about some more exotic cause of ureteral obstructions. So we have these dry solidified blood clots, circumcaval ureters that are kind of wrapping around, the, the vena cava, iatrogenic ligation of the ureter as a complication from abdominal surgery, .

Retroperitoneal fibrosis that has been described in cats with renal transplant, and then ectopic ureters can be associated with ureteral obstruction because they can be structured, and finally neoplasia. If you have an obstruction of the ureter, you're gonna have a backflow of urine into the kidney and an increase in the intra-kidney pressure that will result in acute kidney injury and that's what we call a pressure nephropathy or a pressure nephropathy associated AKI. The eases are I've been increasingly identified and I already said that, you know, I think it's, it's due to our ability to technically see them better.

It's been increased by 30-fold, so it's very, very significant, when, they have been looked back over 12 years, in, in the early 2000 retrospective studies, it's probably similar to what we see nowadays. I don't think it's changed that much since the early 2000s. And virtually all of these stones, like 87 + 11, we are near 100, are calcium oxalate or calcium-based stones, and that's very important because these years, these 12 years prior to 2000 are years.

There was a tremendous effort in changing feline food and preventing struvite stones, acidifying the food, and that has, and it's been recognised in other, other publications that has kind of skewed the stone formation toward calcium-based stones. So in the upper urinary tract of our cats, virtually 100% of the stones are calcium oxalate or calcium-based stones. That has been shown as well in the second publication from Canal in 2007, with 98% of these stones being calcium oxalate and again that same increase over 20 years, so it's, it's, it's quite significant and I think it really corresponds to what I see in my practise and what you might have also, .

Identified in in your practises. Calcium is, you can't dissolve calcium, so the medical management in terms of dissolution is not indicated for these patients. And when you look at the location of the stones throughout the ureter, 75% of these stones are in the proximal third of the ureter, so quite close to the kidney.

20% are in the mid portion of the ureter and 5% only are in the distal third of the ureter. That will become important when we talk about medical management, but as you can imagine, the furthest from the bladder of the stone is the hardest it might be for the cat to pass that stone into the bladder. When we look at the structures, most of them that have been described are congenital and they are identified in young cats.

They can be ureteral, so at any kind of level along the ureter or they can be at the urethrouric junction. Personally, that's the ones I've seen the most, so there is like a narrowing between the pieic cavity in the kidney and the opening of the ureter. Hydrogenic strictures have been reported either from inflammation following urethral thiasis removal.

So back in the days when you would go in and remove the urethral stones, then one of the main complications with that, there would be a structure that would develop at the site of the surgery. We suspect that previous stones will lead to inflammation and be associated with grannulation tissue and that could lead to a stricture. So if you identify a structure and the stones are in the bladder, for example, it's, it's a nice story to make to think that the stone went down and might be got caught at some point in the ureter.

Inflammation, so ureteritis, infection, neoplasia have also been reported. Stretchers, hydrogen stretchers following, tying the ureter during space surgery has also been reported. The dry soified blood clots are kind of a newly-ish recognised problem.

It's been exclusively retried from the feline upper urinary tract. It's never been reported in dogs, to my knowledge. These cats have a history of hematuria and then develop a ureteral obstruction.

They have no radio opaque material when radiographs of the. The men were performed or any kind of mineral opacity on ultrasound, although there is still an obstruction that has been identified and once they were sent to the Minnesota Uy centre or the Davis UI centre, they were determined to be blood, so like a big clot. A structure can lead to hematuria, and then some of these blood clots, might be secondary to that as well.

The circum caval ureters have been described, mostly in postmortem studies, and it's a dorsal displacement, sorry, of the ureter, dorsal to the vena cava, as you can see on the picture on the, on the right of the screen, and so that will create kind of a A loop around the vena cava and in humans it's been shown to create a pinch of the ureter and be associated with hydronephrosis. We don't have that very well characterised in, in veterinary medicine. There are only two studies where it's been reported and the frequency seem to vary quite between 1516 and 32%, .

Probably over time, the pinch might become a stricture or a complete occlusion, and that will lead to the clinical signs and the need for treatment that we will recognise in these patients. Regardless of the underlying aetiology, we have patients that will present an obstructive nephropathy, and we know that obstructive nephropathy is something that will progress through 3 phases and will progress relatively fast. So the first phase will increase, will lead to an increase in pressure in the tubules and that will then in return lead to decrease in the GFR because as you remember, most of your GFR.

Driven by an equilibrium between the pressure in the capillaries and in the Bowman capsule and then the tubules. So if the tubules are filled with urine and there is no way that the urine can go down, then the pressures. Will prevent further urine to be transferred.

There will still be some transfer of fluid due to the exchange that are still happening between the solutes. During the first phase, we will also will have a vasodilation through mediation of prostate glandin E and nitric oxide because the kidney is gonna try to maintain its blood flow despite that increase in intrakidney pressure. And finally, there will be inflammatory cells that will be kind of cold on the site of the inflammation and will be identified in renal tissue as early as 4 hours after ral obstruction in, in research models.

These cells will lead to tubular damages, necrosis, and will start to create the real damages that are associated with AKI. The second phase occurs around the same time as the cell infiltration. The renal blood flow will start to decrease despite the, the, the hardware from the kidney to try to maintain that blood flow.

However, as I said, because of the exchange in solutes, there will be still some, urine that will be produced and excreted, so the pressure will continue to increase in the ureters and the tubules. The complete extent of the damage will depend on at this stage the degree and the duration of the obstruction, and obviously if you have a kidney that was already kind of damaged, for sure, you might be able to pick up on changes for azotemia, for example, faster than any a cat that had perfectly healthy kidneys before anything. And the third phase is the phase where the loss of renal function will be occurring, and we know that.

In again, an experimental model, 40% of the renal function was lost within 24 hours after the initial insult. . If you don't resolve the obstruction, this vicious circle will continue with decreased renal perfusion and increase teral pressure, more necrosis because you have less blood flow and you have like this pressure on the cells, and then the presence of the inflammatory cells, the cytokines will lead to fibrosis, remodelling, and eventually progression towards more like definitive changes that will lead to chronic kidney disease, in the long term.

The kind of physical examination description of the big kidney, little kidney presentation where you can palpate very asymmetrical kidney in the cats, thought to be associated with that remodelling, where the, the, the kidney where you had pre, previously the stone and the stone might have passed has had so much changes that now is like smaller and fibrotic and the big kidney is actually the kidney that is the normal size and the most normal of the two. In terms of management, there are a few options here, and the medical management has been described and attempted and historically what we would always, always go with. Fluid therapy to try to force the diuresis can be attempted although you can imagine that if the obstruction is really complete, the risks are to make things worse and transform your obstruction and your my dilation into hydronephrosis.

So you have to be quite cautious with your fluid therapy. Alpha antagonists, have been reported and they are helping to relax the smooth muscle of the ureter. And kind of lift any sort of spasm that would be secondary to the inflammation and the presence of the stone.

Processing has been historically used. Tamsulosin is increasingly used in North America. I'm not too sure for the UK, we can't have it very easily here in Ireland.

The Tamsulosin is kind of the go to drug now for human with ureteral obstruction and more and more, the go to drug for big centres in North America. Steroids, I would probably not jump on steroids at initial presentation, but if you manage to prove that you have an inflammation, a ureteritis, that might be of interest, diuretics again, interesting in, in the sense of trying to kind of increase diuresis, but you have to be cautious and, you know, know that they can worsen the picture if you have a complete obstruction and a complete inability of the patient to produce any urine. The success rate of medical management is fairly low and it's reported to be 13%.

And I would say my experience is even less than that, but maybe I'm a bit biassed because I work in a centre where we can place subs quite quickly. As you remember, in a few slides, a few slides ago, I, I was saying that the location of the stone was variable and most of them were in the proximal ureter. And so again, if they are stuck there, it's very hard for them to move and to, to be eventually passed.

I have had two patients who To pass the stones in, in my experience, and both were very, very close to the papillae. So with a bit of a forced er and a good dose of alpha, antagonist, sorry, we managed to, to get these patients to pass their stones, but it's, it's a fairly low rate, of success. Surgical options, historically we were performing ureterotomy, so going in, in a laparotomy approach, identifying the ureter, doing an incision on the ureter, removing the, the stone or whatever was causing the obstruction, and then enclosing that as we discussed before, it was associated with risk of stricture at the site of the .

Of the inflammation and of the stone, reimplantation, so cutting the ureter and creating a new, ureterostomy, in the bladder has also been described. However, these, the surgical options were associated with quite high post-op complication and quite high post-op mortality if you think of a surgery with 21% chance mortality is, you know, fairly risky. So due to that, it was not really, really, satisfying and other options have been attempted.

The first one that was historically attempted was to place a stent. So a stent would be placed, usually in an antegrade phase, so going downwards from the PLA cavity pushed down into the bladder. However, in cats, they appear to be quite challenging because the cats ureters are narrow and they are fairly, fairly strong and they have a good peristalsis.

So to place the stent has been, has been quite difficult and they were still associated with mortality. So more recently, we have had the apparition of the sub, so the subcutaneous ureteral bypass, it's it's an implant that will be placed and stay in the patient for Ever in theory, it's composed of a nephrostomy tube, a cystotomy tube, and a subcutaneous port with a little multifunctional, functionable membrane to allow for sampling, and It will basically bypass the natural ureters and allow for patency between the kidney and the bladder. The urine will choose the path of least resistance and go down the circuit down into the bladder, and, and that will restore a normal function in terms of urine production and urine flow from the kidney to the bladder.

If we look at the clinical presentation of this patient, there is no sex preference in any of the studies that have been published so far. The median age is 9, but if you look at the actual age of the patient, it's a very wide range from very young patient we've discussed about congenital structure to very old cats that can develop neoplasia or or stones. Most of these cats are domestic shorthair, however, some breeds have been reported a bit more commonly than others.

Samese, Russian Blue, Persian, ragon, Burmese. The clinical signs are quite vague and very non-specific. Cats present for like a poor appetite, chronic weight loss, vomiting.

Some cats will present with PPD. Few cats will have urinary signs with hematuria dysuria, and very few cats will have oliura or aura associated with this obstruction. I would say personally my Go to, kind of clinical presentation where I'm like, oh my God, that might be a ureteral obstruction is my cat has been hiding from me for the past two days.

It doesn't want to move from underneath the couch because I think it's really painful and it's a really painful condition in humans as well. So the behaviour of the cat is actually quite different than the normal behaviour of these patients, before. All of these signs that are in the slide are more associated with the, the AKI that that is resulting from the disease, but I think they also have moments where they're in pain and they are just like a cat, so they are hiding or kind of like hunched and crawled into like a bowl in their bed and they don't just don't want to move on and do anything.

Surprisingly, despite it being an acute kidney injury, the median duration of the clinical signs is 2 weeks, and I think that comes from the fact that the obstruction might be partial, might be kind of a stone that's going in and out of the ureter, for example, . And most of these cats will present more than one clinical signs at the time of presentation. The physical examination is also non-specific and we will find a renal symmetry in 82% of the cats, so that's the big kidney, small kidney syndrome that we discussed earlier.

60% of these cats will have a heart murmur, depending on the studies, but half to more than half of half of them will have that heart murmur. And we think it can be kind of due to the concurrent anaemia. Or it could be secondary to some cardiac dysfunction, secondary to the uremia.

In some patients, it's been shown to be associated with fluid overload if they have been aggressively resuscitated, because of the obstruction trying to force the dialysis, and they have just been overloaded, and not that often due to structural heart disease. But it's very important to remember that cardiovascular monitoring is very important in critically ill feline patients. Remember that cats with fluid overload will first have pulmonary edoema before they develop any other sort of decompensation signs, unlike dogs that will have peripheral edoema and, and other signs associated with fluid overload.

About a third of the cats were dehydrated and, 2/3 were appropriately hydrated, and so 6% were overhydrated. However, these ones were patients from a referral hospital, so they had been seen by a vet, and that vet had placed these cats on an IV and tried to heavily them based on the creatinine values. As most of cats with renal disease, they can present nausea, hypersalivation, uremic ulceration, and then when you palpate their abdomen, the bladder might be empty or might be normal depending on their ability to pass any urine.

On biochemistry, obviously, we will have an azotemia, and that has been consistent in the vast majority of these cases. The median creatinine one of the retrospective study was over 500 millimo per litre. However, that can be very valuable and you can see in the brackets that the lower end was 106, which is a normal creatinine value.

BUN was also quite increased, although again in the brackets, you can see that the lower value was normal. Potassium, very variable, but hyperkalemia is quite common and it makes sense as a sign of AKI and decreased urinary output. So you expect your potassium to be high on the right hand side and the top, you have a creatinine from a patient here in in Dublin at the very top, and you can see the potassium was 5.53, for a creatinine of 800 and its phosphorus was actually decreased.

The bottom picture is a blood gas from a cat that I saw when I was a resident in Canada, whose potassium was 9 on presentation and requires some treatment before we could do anything else with it. So the phosphorus is rarely increased, so you can see the median is 1.7, which is very normal.

It can go high, I think if it's been going on for a long time and these cats have started to have like chronic remodelling, decrease, decrease excretion of phosphorus, decrease urine production as well. And then interestingly, a quarter of the cats in one of the retrospective studies from AMC. Showed ionised hypercalcemia, which fits with, calcium oxalate stones, and that hypercalcemia will have to be investigated and treated in a second time once you have stabilised the AKI and treated the obstruction.

In parallel to your biochemistry, you will perform a haematology upon presentation. Anaemia is quite common. The median PCV in, in the same AMCB retrospective study was 27%.

As we mentioned, these cats can have a hamic murmur, but it's rarely reported that they have transfusion triggers and we need a transfusion, but I would still be prepared because The surgery, they can bleed at the time of surgery or if they are very anaemic with the anaesthesia, they might become a bit unstable and need a transfusion during the procedure. But in that big retrospective study from Bentanal in 2018, there was no cats that had need for transfusion in their cohort. I've, I've had a couple that needed transfusion either during the surgery or right after.

Then ideally, once you have your blood, you want to collect some urine, . The urine again, nothing pathognomonic. Most of the urine will be diluted due to the decrease in renal function, presence of blood, presence of white blood cells, presence of epithelial cells due to the damages in the tubules, crystals can be.

Present, they don't always match with the stone that you may find after all. And as you can see and I find that very interesting, the presence of bacteria and the, the positive culture if we go to the next, point is not that high and so. I, I don't think, you know, jumping on an antibiotic when you suspect ureteral obstruction is, is necessarily the first thing to do because in the end, between the, the retrospective cohort, we have a 25% to 3 only of the patient that will have infection.

So you have time to send your culture and, and wait for it and if you don't do it, we will do one at the time of the procedure. And then obviously we are discussing about stones obstruction, so the big chunk of your investigation is going to be diagnostic imaging. There are reports of radiographs, ultrasounds, and CT in the literature.

However, I would say that if you suspect an obstruction, a CT is highly, highly not recommended. Contraindication, like azotemia and moreover, azotemia secondary to a renal obstruction is a contraindication for a CT with contrast and honestly, a CT of the urinary tract without contrast has no interest. So I would say with the good old radiographs and ultrasound, they are very good, and they will give you a good hint on what's happening with your patient.

. Yeah. Contrast can be administered directly into the PL cavity to do ureterop pyelogram, and that is the gold standard to see the obstruction. This is what we perform at the time of the surgery just before treating them just to confirm, but we put the contrast in that PLE cavity knowing that if we prove it's obstructed, we are going to place this up right away, .

I would feel a bit less comfortable to do a CT scan, have that contrast accumulate in the PLA cavity, and then. While the CT is under review, the patient is recovered, you might have to transfer your patient to another centre for the surgery. So I would advise against it and to just, stay with your radiographs and your ultrasound.

It's unlikely that the CT is going to give you any further indication, for people who think that we can calculate the GFR with a CT. Yes, we can, but if you have an obstruction, you can't interpret it. So really, really stick with the classics.

On radiographs, 98% of the stones that are identified are calcium oxalate, which means that they are radio opaque stones to be visible, they have to be over 2 millimetres, but as you can see on the right side, they are quite easily identifiable. I really like radiographs for urinary cases because they can give you an overview of the entire urinary tract. I kind of cropped the image there to kind of remove any personal information, but the radiograph was actually going a tiny bit further, on the right, because you want to have the entire urethra in your radiograph up to, up to the sphincter.

So for a female up to the vulva. And for a male you want to make sure that you, you get the penis, same for dogs and they, they help you to see if you have nephrolis, which was the case in that cat, ureteralis, which is also the case in that cat, and bladder stones that are also present in the in the cat on the images. Prior to anaesthesia for the procedure, you might want to do pre-anesthetic chest radiographs.

They will help you to see if you have changes in the cardiac silhouette and if you have any signs of fluid overload. Again, I, I will say that multiple times, but cats are really prone of pulmonary decompensation as their first manifestation of fluid overload. Ultrasound, I usually like to do both, and I think it's been shown in a study that they increased, doing both radiographs and ultrasound increases the sensitivity to detect stones and determine the nature of the obstruction.

Stones will have a shadowing, as you can see on the top image on the right. In 4%, it's been shown that the calculi was not evident on radiographs, probably because it was too small, but could be seen on ultrasound and surgery. Reversely, 3% of the cases had no calculi that could be identified on ultrasound, but was then subsequently identified.

Find on radiographs and surgery, and there is 1% where no calculus could have been, seen on imaging, but was still confirmed at the time of surgery. That's a study from New York. So, when they say surgery, it means that at the time of surgery, they did a contrast study with the urethropyelogram, and they confirmed there was a stone, before they placed the stud, so.

So I think it's very interesting and it kind of justify for me the fact that I really want both in this patient. I will start with the radiographs and and move on to the ultrasound usually afterwards. You can do it in whichever order you you want because you want both and you want both to be reviewed.

For the cases with dry solidified blood clots, it's important to remember that they are not visible on ultrasound and they are not visible on radiographs. So you will see an obstruction or an obstructive pattern with distension of the ureter, distension of the periodic cavity, but we, you will not see the material in the, urinary tract that is creating the obstruction. Similarly with strictures, you don't always see the stricture, you can suspect it, but sometimes it's hard to see exactly where it is.

The other thing that you can assess with the blood, with the ultrasound is the renal blood flow, how good is the profusion of the kidney. You can look at the parenchymal ecotecture, see if you have a good corticomeduar distinction or if you suspect that the cat might have CKD because the, the kidney looked remodelled already. You can look at the size of the renal pelvis.

Is it normal? Is it increased? Is it hydronephrosis like on the top right image?

It's very, you know, variable, what you, what you can see on ultrasound, and it's a lot of very valuable information that you can get from it. You will look at the urethral signs. So I'm not a ratiologist at all, and, and obviously I don't perform these, these images myself, but if I do a quick scan and I see the ureter, that means it's big if I'm able to see it.

So, depending on, on your level, of, of confidence and your, your ability to see them or not, I would say if you can see them easily, it's probably big. And if you can't see them, they might be normal. That's kind of where I am in archaeology.

On your training, you might, you might be a bit more detailed and a bit better than me in assessing these ureters. Inflammation like ureteritis will be displayed as a thickening of the ureteral walls, and you can sometimes, see if you have a good machine, increased peristalsis as well with like contraction of the ureter. Ectopia can be suspected if the ureter go beyond the bladder and the pelvis and you kind of lose the ureter into the pelvic cavity.

Mm And the pelvic bones. Finally, the ultrasound, and unlike the the radiograph will be more detailed if there is infiltration of the tissue, any neoplasia, any invasion of local regional lymph nodes. If there is any effusion, you can also, sample it.

But if you just look at stones, the sensitivity is not very good, and that's why if you increase both radiographs and ultrasound, that sensitivity increases above 80%. So now the question is, does size really matter? Like can ultrasound predict an obstruction based on the size of the periodic cavity and the size of the kidney?

And for a very long time we thought that yes, this is one of the very first study that described pieic cavity and pieic obstruction in cats, ureteral obstruction in cats and I, I, I do like that paper very much. It's a very good paper, but I think one of the conclusion is a bit too drastic for me because they said that if you are If you have a pure cavity that's above 12.5 millimetre, which starts to be very big, you can say for sure it's obstructed.

Great. But what if it's below that? Because we see a lot of cats with like a pelvis of 3467 millimetres.

How can we interpret that? And the problem is like, you have a major overlap in between all of the categories of of disease that will lead to, pelvic distention. So if you look at obstructions.

Sorry. In, in dogs and cats, it's the number 5 and, in the list. You can see that they, they, they go the highest.

And yes, in both species, above 12.5, there is nothing else that will lead to pelvic, with that high. But if you go below that, and especially for the cats, you can see that.

The, the median of the pelvic distension is 7, and at 7, you have an overlap with pyelonephritis, renal diseases, and miscellaneous. So I think it's important to remember that the distention is not pathognomonic and is not the cutoff that you will use to decide yes or no, the cut needs a procedure. A more recent papers has also looked at ultrasound and the diagnosis and management of cat with ureteral obstruction.

It was another retrospective study and that study compared ultrasound. To pyelograms, so injecting directly contrast product into the pelvis and looking at its diffusion into the ureter. And they proved that once more, the pyelogram is much more sensitive and it's a superior task to the ultrasound alone.

So it's invasive and it's risky. So you have to do it only if you're ready to treat the patient, but As a general practitioner, or for me as an internist who don't place the sub, I have to interpret my ultrasound and. The ultrasound gives me information, but it is not the only deciding factor for an intervention.

So if you look at ultrasound of renal pelvis in proximal ureters and cats, viruses chronic kidney disease, pyonephritis, and ureteral obstruction as a prospective study in a third paper now, you can see that 2/3 of cats with CKD will have pelvic dilation. And 84% of cats with pyonephritis will also have pelvic dilation. So yes, it's always present in cats with ureteral obstruction in their cohort.

I do not always agree. I think some of them are barely, distended, but anyway, in their cohort, it's, it's always present, but it still overlaps with all of the other categories and so it's impossible to determine. If it's obstructed or not, if you have a dilation of like 457.

Mhm. In terms of stats, they didn't get any significance between pyelonephritis and ureteral obstruction. So again, difficult to make a definitive cutoff, but they confirmed the old cutoff of 12.5 or 13 millimetres, but we know that some cats are obstructed.

And are way below that. And again, if you look at the whisker boxes, the median for the urethral obstructions, which are the two, the two most right columns, are low, and the median, which means that that's 50% of the obstructed population overlap with the pattern nephritis, and overlap with the extreme of the chronic kidney disease cats. So, now your turn to play.

On the right side of the slide, you have 3 pictures from the same cat, that was seen by Doctor Dun in the University of Montreal. You have a kidney picture, you have a urethral picture, and a left kidney picture, . That's kind of aiming for the pelvis.

Do you think based on these images, that the cat is obstructed or not obstructed? Right, folks, you know how to play this game. It's anonymous, so please don't be shy.

Give your opinion. But simply just click on the answer that you feel best represents, the, the correct answer. Is the substructed cat, or is it not?

Yes or no? And, Those questions will, or the answers will come through to me. We will let this run for maybe another 10 or so seconds while we allow people to answer.

And then we will relieve or reveal the answers to Beno. And I think you, well, let me end the poll and show you what everybody thinks. Perfect.

100% obstructed. I agree with you. So as you can see on the pictures, sorry, close this, .

Oh yeah, perfect. As you can see, you have a massive hydronephrosis on the top right picture. You can see the stone, it's labelled and it has a nice measurement.

You can see actually. You can see the shadow here underneath the stone. So it's quite nice, and you can see a distended ureter and you can see a very distended proximal ureter at the junction between the kidney and the ureter here.

So that cat was obstructed, went to procedure, had an obstructed obstruction confirmed on the pyelogram. And it was a unilateral obstruction. Its creatinine at the time was 316.

Same game, different cat. So on the top right, yeah, top right, the two first pictures are, the kidneys and the bottom picture is, the bladder and then some cystic structures. Do you think that cat is obstructed or not obstructed?

Right. Same game, guys. Click on the answer that you feel is the correct one.

Please don't be shy. It is anonymous, so, it's only yourself that you have to answer to, and I have no doubt that Beno will talk us through the correct answer and why that answer is there. So, I'm just gonna give you another 5 seconds to answer.

We have got a little bit slower answering coming through in this one, Beno, so it's not as obvious as the first one. Right. Oh, this is a close call.

Let's show you what the results are. There you go. OK, so let's say fifty-fifty, and I agree with you and that's the problem with looking just at the picture of The ultrasound.

So if I go with the 50%, who said no, I think they looked closely at the kidneys and they were like, this looks like a normal kidney. Actually quite a happy kidney. You have a nice corticomeduar distinction.

You have no dilation of the PLA cavity. When you look at it in transverse, you can see the PLA cavity here, and it's like normal, in terms of size, no distention. It's a happy kidney.

And then we have the bladder, and then we have these and that. These are two. The two kind of view of the ur that has been cut in transfers, .

And the obstruction for that cat was quite distal, and it was obstructed bilaterally and the right and left here actually are indicating the right and the left ureter that were both quite distended. Sorry, so he was obstructed. A pyelogram confirmed the obstruction, and the serum creatinine was 662 at the time of presentation.

So, you know, again, the big picture has to be important, but the ultrasound is not necessarily the only way to get an answer. Last one, obstructed or not obstructed, you know the game and you can answer the question and I will talk you through right after. Right, 3rd one's a charm.

Let's get answering on that. And, it's been really good to see so much participation. But no, that's really nice because it shows that everybody is still engaged with what you are talking about and, are happy to give opinions.

So that is absolutely fantastic. Another 5 seconds and then we will close this poll. And reveal the great reveal of who got it right and who got it wrong.

Obviously anonymously. So don't be shy. Right, let's show you what the people think.

There you go. Perfect. So I'm sure some of you have played the odds of I can't always present obstructed cases, but I actually do.

So the people who voted yes were right. Again, a difficult one. Kidney looks normal, not so good corticomeduar distinction, so maybe some CKD there.

A very, very, very mild dilation of the, pic cavity and a ureter that is visible, but not that distended, maybe on the high end of normal, but nothing crazy and definitely no stone, in sight. However, based on the clinical presentation and the creatinine of over 1000, that cat was suspected to have an obstruction and went to procedure, had a pyelogram that confirmed a bilateral obstruction and sub were placed. So as you've seen through these three cases.

It doesn't always look like what it is, and it's important as a clinician to get the whole picture. So assess the history of your cats and how they present it. If you determine that there is an azotemia, try to figure out if it's chronic, acute, and if it's acute, go through your differentials of, you know, other cause of acute kidney injury like toxics, infectious, etc.

. But keep your mind open, even if you don't see the site of the obstruction. If it feels like an obstruction and if it looks like an obstruction, even if you don't see the stone, it can still be an obstruction. So be cautious with that and don't be afraid to contact, you know, a referral centre, a place where you know they play subs and discuss the case with them as soon as you can because every minute counts to kind of save as many nephrines as you can.

Now we're going to go through a case that I've seen, back in Canada. Yukiko was a 4 year old female spayed rag doll cat, and she has been hiding from the owners for about 3 days. Like the owner said, she's under the couch, she doesn't want to come out, she doesn't want to eat.

She barely goes to the litter. Box, the owner find a pile of vomit once, and, she's actually not sure when she actually saw the cat going and pee. Last, for her, the cat hasn't moved in 3 days.

It was otherwise a healthy, happy cat. On presentation, she was quiet but responsive. Her coat was well kept, her body condition was good.

Muscle muscle, condition was good as well. She was mildly dehydrated, pale pink mucous membrane, but it's a cat, so it's always hard to interpret. And then she had a very mild heart murmur, and the rest of her auscultation was normal, and on abdominal palpation she was mild uncomfortable, and she has bilateral, symmetrical, smooth kidneys and no palpable bladder.

On admission blood works, we identified a severe, azotemia with initially a creatinine that could not be measured, and then a creatine that was measured over 2000 for a urea that is over 100, so massive azotemia. And a very severe hyperkalemia. So, you can see here the potassium is 8.7.

So we decided to confirm the hyperkalemia because there are some confounding factors just to be sure. And that's the blood gas that I showed you earlier, and you can see that the potassium here was 9. So it's really important to to confirm the hyperkalemia because now it's important to treat it because with the potassium of 9, there is not much anyone would want to do with your cat in terms of procedure.

So we initiated an insulin dextrose protocol, where we gave the cat a bolus of dextrose, as well as a bolus of insulin, and then we placed the cat on dextrose CRI. The insulin is gonna help shifting the potassium with the dextrose inside the cells and decrease the extracellular load of potassium. And then the dextrose that you add in the CRI helps the cats not become hypoglycemic from the insulin injection.

But also provide more dextrose for an endogenous insulin release and continue that shift of the potassium into the cells. And you can see that I don't remember if it was one hour or two after the infusion was started, we have already decreased her potassium and it's down to 6.9.

In the meantime, while she was receiving all of that, I was very worried about anuria because I couldn't palpate her bladder and the owner just didn't remember when she went to the, to the box, last. So we performed some radiographs that you must be familiar with now because they have been kind of the background of most of the presentation. And if you remember well, we identified nephroliths, ureterolith, and Cystolith, you can also see in the radiographs that the bladder is empty, like the bladder is here.

And it's like a flat pancake with some stones inside and there is no urine that is reaching the bladder. We went from the ultra the radiograph room to the ultrasound room, and she was a bit nicer than the 3rd case because she was fitting the description of a distended pure cavity. Like this starts to be a marked, distention.

Like here, we have 1 centimetre, so it's probably close to 1 centimetre of distension. There is a loss of cortical medular distinction, but with that degree of distension, like You know, the mediaite kind of squished against the cortex and so it's harder to interpret the corticalmela distinction. And then they could identify a stone and a distended the other.

So we went for surgery, we placed the sub, which we'll discuss the surgery about next time, but 12 hours after the placement of the device, her creatinine had been cut in half, and then 3 days after the surgery, her creatinine was normal at 109. We removed the stone from the bladder and we sent them for analysis. They were ammonium urate stones, coated with calcium oxalate shell, which has been described in ragdoll to have, ammonium urate and she was later, when she was stable, investigated for liver disease and she had no liver diseases.

So, A successful case where we managed to, to, you know, deal with the AKI quickly and correct the azotemia quickly and preserve as many nephrons as possible. So as you've seen through that presentation, feline neurral obstruction is a challenging diagnosis, because the clinical presentation, the clinical physical examination is unspecific. You have a cat that is unwell with severe asthmia.

The sensitivity of the ultrasound alone is only 77% for stones, so remember to combine it with your radiographs to increase the sensitivity to 90%. But also remember that not all obstructions can be seen on imaging, and if you strongly suspect one, refer it to a centre that places subs that can do further workup for you. It's a presumptive clinical diagnosis based on the presentation, the clinical pathological data, the imaging findings, and your clinical feeling and clinical assessment of the entire case.

As I've said a couple of times during that presentation, time is Naron and remember that there is a 40% loss of function after 24 hours. So it's important to act and act quickly. Medical management is extremely limited, 10, 13% success rate, so I usually don't really advise to push it too far, and to refer these patients where they can be actually treated with the surgery.

And placing the subcutaneous ureteral bypass is, I think, considered as a new gold standard treatment for these obstructions. It's an emergency surgery. So for example, here in Dublin, we don't do it overnight, but we would do it the following morning.

If a cat comes in the afternoon, it will go probably the following morning, and if it comes over the weekend, it will go on Monday morning, unless it goes, bad over the weekend and needs the intervention much sooner. And on the right, you have a little table from the University of Montreal. They have a study that's ongoing, which is the our study column.

It's not my study, it's theirs, so I, I thank them for their results. But that study plus the Behn study in 2018, at, the AMC in New York, and the Kopakni study from the Davis University where they placed both subs and stent, showed that you have a very significant decrease in creatinine. After the compression of the kidney, these are obviously American units, but I think just the, the figure speaks for itself, with the column on the left being twice, if not more higher than the one on the right.

And one last patient, this was 0. It was presented to the ECD recently with a creatinine of 879, same workup, and we concluded that an obstruction and after his sub again his creatinine went back to normal, and we are now close to a year and a half post-surgery, and it's still doing very well and his creatinine is still normal. So thank you very much for your attention tonight.

Again, this was the first of two talks about foetal ureteral obstruction. Today was more like clinical presentation and diagnostic tests. Next time, we will cover, the surgery of subs and the long-term management of this patient.

If you have any questions, I would be more than happy to answer. Beno, thank you very much for that incredibly interesting, presentation. And I, those three cases with the, the same question were striking in their reinforcing of what you were talking about of you've got to get the big picture.

Because otherwise you can, you can miss these things. Yes. And I think it's a, it's a very, it's, it's more and more recognised and I think it, it's something that's worth being aware of, because you will come across these cases in practise and, and, and, I think it's very important to, to know that if you suspect an obstruction, keep it in your mind until, until you can cross it for sure off of your list.

Yeah, and, and, you know, time is of the essence. Time is nephrons, as you correctly said. So, it's not something that you, especially in that, that last case you were talking about or the, the one, with the cat had been hiding for 3 days.

I mean, that's already far into it. We don't want to, as clinicians, take another day or two to start making diagnoses, because it's, it might end up just being too late. Although the response of that creatinine was quite spectacular.

Yeah, and I think kidneys are an amazing organ and, and they, they can, you know, we always say the liver can regenerate, the kidney can't. It's true if you arrive too late, but kidney can regenerate up to a certain degree if the, if the obstruction is lifted or if you have an AKI for whatever other reason, you manage to support them and get them out of the phase of inflammation and tubular damages and tubular obstructions. So yes, time is of the essence and I think it's important to, you know, sensitise the owners that there are things that can be done.

It is not cheap and, and that will be one of the discussion next, next time. But, but things can be done for these cats. The other thing that is important is the pain management.

So if you have an obstruction and you have a very important increasing pressure in the, in the renal capsule, that's very uncomfortable for the patient. So it's important to treat them and treat them early so that they feel as comfortable as possible. And I think that's very important as well.

Yeah, having, having suffered from from kidney stones and urethral stones myself, I can vouch for the pain. It's not fun. It's really not fun.

Folks in the chat box, Kyle has just dropped in a link, for, as a reminder to part two, which I'm sure is going to be just as fascinating as this was. And, for those of you like me that have a, a little bit of a surgical bias, and, are a, a closet surgeon, I'm sure the, the surgical techniques and that will be absolutely fantastic, to see and to understand. Although I don't.

Know that we in general practise will ever get to do these. We can only be envious of Beno and his colleagues for getting to play with all these things. But it, it really is nice to be able to see and understand what is done when we refer these cases through to the specialist.

So, click on that link if you're interested in part two, if you've enjoyed part one as much as I have. And, that will just help to remind you, when part two is, is ready to be, enjoyed. But no, I haven't got any questions that have come through to us.

I think, everybody was fascinated and, and, and really enjoyed it. And you were very clear on, on your interpretation. So thank you so much for your time tonight and sharing your knowledge.

And I know I can't wait for part two. Thank you for having me and I will be there in August for the rest of the story. Fantastic.

Folks, thank you for your time tonight and attending. Thanks to Kyle in the background, my controller for making everything run smoothly and from myself, Bruce Stevenson, it's good night.