Thank you very much. Welcome, everyone, and, it's good, it's good to be back on, on the webinar that. So, we're going to talk about the, approach to jaundice today, and, I thought we'd, the plan would be that we take a, a, a reasonably case-based approach.

I'll, I'll introduce you to a, to a case and look at how we, we approach, a clinical case of jaundice. And then we'll finish up, the last 1015 minutes or so about the treatment of, specifically hepatic jaundiced. So here is our case.

This is Molly, a 5 year old female neutered Labrador, and Molly has been presented to you, with a relatively short history, of, of, vomiting. Which she's been treated with mropotent, so she's not vomiting now, but she certainly has a decreasing appetite, and when a Labrador is turning their noses up at food, you know, it's serious. She's lost some weight in this time.

She's polyure polydipsy, she's lethargic. You can read it all there, and as the title of this talk, may. Suggest you lift up the gums and lift up the lip, and there are those bright yellow gums, which I think for many of us really sort of is a very concerning sign.

Of note, she also had some circular erythemat to scaling lesions on the ventrum. We're not going to talk too much about those. I think these were a superficial pyoderma, .

So, when I see a dog with jaundice, the first thing I start doing is asking questions about other signs. So, as well as obviously the appetite and the vomiting, one examines carefully for evidence of asciTS, one looks at other mucous membranes. One last about questions about whether the dog's behaving.

Abnormally, so any evidence of encephalopathy, and of course polyure polydipsia. So it's rare that you see a case of jaundice that doesn't have other signs. And I think these, these, it's important to remember that, not to just get panicked into seeing the jaundice and and going ahead, but to record all the clinical signs there.

So first point, when we start to look at a dog with jaundice. We, we want to just quickly revise, how a dog ends up, having, having jaundice. And it's basically, down to the bilirubin metabolism.

Bilirubin is, is formed from the hemolytic deregation of red blood cells. This happens all the time in a dog. Old red blood cells are destroyed and in the various reticular endothelial cells of the body, the haemoglobin is converted to bilirubin via biliverdin.

Now, What happens then is that the bilirubin is loosely bound to, to albumen and it has to be carried around. Bilirrubin is, totally insoluble in, in water, really, and needs to be, carried from those reticular endothelial cells to the liver. And albumin takes a, a very important, part in that.

That then can go on to a chemical covalent bonding of bilirubin with not just albumin, but, but many other proteins in the body. So, so the, the collagen in the sclera of the dog's eye can become a biy protein. And the half-life of those bili proteins reflects the half-life of the original protein.

So in terms of albumin, you're looking at a half-life of 2 to 3 weeks. So once you have a jaundiced situation, that jaundice, once those biy proteins start forming, can last an awful long time. The bilirubin bound to the albumin is taken to the liver where the bilirubin is bound to dig dilycurinide.

Now that makes the bilirubin soluble in water, and that's how the bilirubin gets out into the bile and then into the GI tract in that soluble form. It used to be fashionable to try to tell the difference between bilirubin that was loosely bound to albumin and the free bilirubindiglyurinide in the blood, to try to tell the origin of the bilirubin according to the, what's called the Vander Berg test. This, this does not work as we'll see later because of, overlap between the various signs, but we, forms, but we, we, just mention that, that those are the, the two forms of, of bilirubin.

Once in the gastrointestinal tract, then some of this bilirubin is reabsorbed, but much of it passes out into the faeces in the form of stercobilin, which is a large component of the, the colour of, of faeces. A small quantity of the reabsorbed bilirubin. Is, excreted through the kidney.

And in this form, urobilinnogen, is, is, part of what gives urine, it, its colour. And about 20%. Of the bilirubin is normally excreted by this route.

So finding urobilinnogen in the urine of dogs is entirely normal, and it's not to be worried about that if you, when you're doing your dipsticks, you get a positive, that is not an indicator of jaundice. Billirubin can accumulate for a number of reasons, as we'll see, in, in, in the Blood. And when bilirubin accumulates in the blood, then it's termed jaundiced.

Anything greater than about 7 micromoles is, is abnormal. At 17, you can see it when you spin down the blood, and at 35, you can actually see it on the mucous membranes and that, that level will lead to discoloration of the sclera and the formation of bili proteins there, in, in the, in the eye. We don't detect low levels of bilirubin just, just on clinical exam.

So if the dog has a measurable bilirubin of, say, 15 in the blood, but is yellow, that would indicate a very significant improvement because it would indicate that at some time in the past that this dog had high levels of bilirubin in the blood, but it's now getting better. Billirubin is one of the few things that we measure in a routine biochemical profile profile that has been shown in clinical situations that have prognostic significance. It has prognostic significance in liver disease, in biliary tract obstruction, and indeed in hemolytic disease.

And the higher the bilirubin and the more that it's going up each day, the more worrying, it is. Laundice, the accumulation of bilirubin in the blood, it comes down to three causes hepatic, post-hepatic, and pre-hepatic. The hepatic causes can be inflammatory, infectious, degenerative, all causes of liver disease that we're going to talk about.

The pre-hepatic can be immune-mediated hemolytic processes or non-immune-mediated hemolytic processes. And finally, the postipathic causes are caused by an extra patic bile duct obstruction. Now, this can be absolute complete, total blockage of the, common bile duct, for example, by a tumour or a, a gallstone.

Or they can be functional, that, that there is delayed emptying, within, and from the gallbladder, but that some is coming out. And that's quite an important distinction as I, as I'll come on to show you, that we need to make. So when we're faced with a case of jaundice like Molly, this is what we need to, to, to try to decide which one of these 6 things is going on.

And the basic approach to the jaundiced animal is to look first of all for the prehepatic causes, then for the post-hepatic causes, and finally then look at the hepatic causes partly by ruling out the pre and post-hepatic causes, but then also specifically investigating those hepatic causes. So let's go with that in mind now. Let's go and look at Molly's blood results, and when I see a dog with jaundice, the first thing I do actually is to look at the haemoglobin.

Some of you may have looked at these results and gone straight for something else, but the first question is, can we rule out the pre-hepatic? And, and for these purposes, we want to look at the measurement of the red cell mass. In a set of automated results like this, the pack cell volume is derived from the haemoglobin, so you shouldn't really be using pack cell volumes in this circumstance because it's a derived indices.

What the most machines measure are the haemoglobin and the red cell numbers. And that's why if you ever go to a doctor and they talk to you about whether you are anaemic or not, the medical profession have talked about haemoglobin for a long time. Most of them don't look at pack cell volumes because they're derived in the disease.

And if you are measuring a pack cell volume on a micro hematocrit, thing, then actually it's, that, that has been shown to be a, one that is more prone to operator error. Than putting it through a machine. So for all those reasons, I, I try to encourage people to look at the haemoglobin first.

And clearly in Molly's case, the haemoglobin is nice and safely in the reference range. Therefore, in Molly's case at any rate, this is not a prehepatic cause. But we should just, just discuss prehepatic jaundice.

This is a Scully, who did have a pre-hepatic jaundice. You can see here the, the, the pale mucous membranes, the haemoglobin was only 4 grammes per litre. And, If you are not familiar and you're struggling to use hemoglobins, then a simple trick is to multiply by 3.

So that would have given you a pack cell volume of about 12%. And, when we looked at the blood on the slide there, we did a, in saline or glutination test. You can see it's positive.

It's fairly easy to see what's going on here. This is a case of immune mediated hemolytic anaemia. Immune-mediated hemolytic anemias have to be ruled out, but the jaundice associated them, is, is relatively uncommon, and I think it's worthwhile emphasising that most dogs with hemolysis are not jaundiced.

The, the reasons why some of them become jaundiced is not clear. As well as the immune mediated causes which one would diagnose using the presence of spherocytes on the blood smear and a positive insaline autoglutination test, and I should remind you that how to do an in saline or glutination test is to take one drop of EDTA blood. And mix it with 2 drops of saline.

I sometimes people hear people saying they took one drop of blood and 2 drops of saline, and it always worries me slightly that they may have got the dog, dog's blood fresh out of the syringe, and it isn't that we should be very careful. It's one drop of EDTA blood. I see that mistake made in a few of my students, who don't know how to do in saline or to glutination until they're taught the proper way.

Non-immune-mediated causes of preapatic jaundice would include, some, rather uncommon poisons like onions, and, and paracetamol if there's, there's been a deliberate overdosage or an accidental overdosage by, by the owner. And, and in certain countries, not in the UK, then some forms of Babesiosis are more or less associated with jaundice. But most cases of bubesiosis don't produce jaundice, some do, and some forms of irbezia are more prone to hemolytic jaundice.

So having looked at the haemoglobin and said, OK, this is not a pre-hepatic cause, I think a lot of people then go and look at the liver enzymes and looking at that, you know, 84,560 on the alkaline phosphatase, beat that if you can. ALT 1000. Well, those are really high.

However, I have to say the role of liver enzymes in the approach to drawing this is a big fat zero as far as I'm concerned. Those liver enzymes don't help you at all. And the reason why those liver enzymes don't help you is because there is very significant overlap between the various causes of liver pathology, biliary causes, so extraopathic bile duct obstruction leads to hepatocellular damage, leads to vascular compromise.

Vascular compromise leads to patocellular damage and ultimately it can cause biliary problems as well. There are big overlaps here and things move very quickly. So an obstructive jaundice can produce high levels of both ALT and a phosphatase and GDT and AST and equally, liver diseases, can, can, of course, cause, problems, and equally, of course, a vascular components for hypoxia caused by anaemia can start to cause problems.

As well as that primary causes, there are secondary causes. The primary disease can lead to all of these things going on within the liver, the tissue hypoxia, the endoxpoxemia, and so forth produced by the prime primary disease causes liver damage. And if you look at the list of primary diseases that cause secondary hepatopathies.

Then right there is anaemia and biliary stasis as being particular causes of secondary hepatopathies and therefore, liver enzymes don't help you distinguish between the prehepatic, the hepatic, and the post-hepatic causes of jaundice. So what is the role of biochemistry in jaundice? Well, those specific tests for liver damage or hepatic enzymes tell you that the liver is being damaged, and if they don't go up, then that would suggest that it may be a rule out for, for, for liver damage, except in cases of end-stage cirrhosis, one can help that.

But as I said, most cases, it, it goes up, so it doesn't really help you. The role of biochemistry in jaundice is primarily for those non-specific tests for liver function to try to assess how much functional impairment. High liver enzymes tell you nothing about the functional impairment.

If you take Take a, a, animal, I'm not suggesting you do this, but if you were to during a bitch bay, take a piece of liver, up through the, get, get up their lung incision admittedly, and squeeze one part of that liver really firmly. Create a bruise on the liver, and then, finish your bit spray and then measure the liver enzymes afterwards. They will be absolutely astronomical, despite the fact that there's no effect on function whatsoever.

That dog will survive that, no, no problem. Not suggesting you do that. That test has been, done experimentally on, on mice and so forth.

And, and it's been shown that these liver enzymes can go up massively, even more than Molly, has gone up, in cases where there is very specific focal liver damage. So what we're interested in is liver function and the tests for that are albumin, globulin, urea, cholesterol and glucose. And you, in failing liver, you will see low urea, low albumin, low cholesterol, low glucose, and sometimes you will get a low globulin.

That really depends on which globulins are affected. Gamma globulins are not produced in the liver, but alpha and beta are. So we can get low globulins in, in animals with a substantial liver impairment.

And of course, then we can also look at specific lung function tests. So bilirubin is a great liver function test, but we can also talk about ammonia and bile acids. So, if we're not going to look at, at that, what we're going to look at are the functional, functional, measures.

So we will look at bilirubin. And the extent of the bilirubin increase is pronoxtic and is significant in terms of the liver dysfunction. So bilirubin of 277 here is extremely high, and that indicates a fairly substantial liver impairment, if this is a liver disease.

The albumin is normal. The urea is, is. It is low and normal, the glucose is normal.

There, there's a lot going on here, which suggests that Molly for all the high liver enzymes, does not have significant liver impairment, in terms of actual function. Why don't we look at bile acids? Well, the reason we're not looking at bile acids in a jaundiced patient is that it goes through exactly the same enteropathic recycling as bilirubin and therefore will be affected by the same things.

So when you have high bilirubin, you will almost certainly have bile acids. And the real problem is that most of the bile acid measurements rely on a change in colour or turbidity, which is affected by cholera as well, and that means that high bilirubin on its own will cause falsely high bile acids. So we can't trust bile acid measurements in dogs with bilirubin, and even if we could trust them, they probably wouldn't tell us very much.

It might be worth just considering ammonia in this, in this context. A ammonia does not go through that enteropathic recycling. It's produced by the enteric bacteria and cleared in the liver to become urea.

So it has a slightly different pathway and because of that may be more relevant in terms of assessing whether an animal has an encephalopathic problem or not. The trouble with ammonia is that it has to be measured very quickly. You have to measure it within 30 minutes, and that unfortunately means that, you need an in-house method of measuring this.

There are ammonia slides available on some dry chemistry tests, but when these, these have been tested, these have often been found to be wanting. They lack both the sensitivity of, of diagnosis to pick up, moderate increases, and the, the, the methodology seems to be less than robust. One alternative to that is that there are little, ammonia metres out there.

This one, pocket chem, is, has been shown to correlate with the sort of reference method of measuring ammonia in a, in a very good study by Rob Goggs, out of the Royal Veterinary College. And these, these little metres, are relatively cheap to buy and relatively cheap to run. So if you work in a large small animal hospital and you're seeing patients with lots of liver diseases coming through, then this is actually quite a, a, a useful, a useful little thing.

So in, in Molly's case, because she was jaundiced, we, we did run the ammonia, and that is slightly high, and that would suggest that there is a degree of encephalopathy going on there. Having looked at these biochemistry now, I think most people, having established that this is either a pre-hepatic jaundice, sorry, having ruled out a prehepatic jaundice and have now decided that it's either hepatic or post-hepatic jaundice, will now go on to do ultrasonography. And, to, to do this, we want to look at, the, particularly at the gallbladder and at the common bile duct for evidence of the extraathic bile duct obstruction.

Of course, the problem with ultrasonography is you do need an ultrasound machine and you do need a bit of experience. . It is very, very, very easy to find the gallbladder.

Most people have an ultrasound. This is the first thing that they find. Having found the gallbladder, I think it's worthwhile taking a little bit of a look at it fairly carefully in a dog with .

jaundice. This case here has quite substantial thickening of the gallbladder wall, and you would, on that basis, be, of course, quite worried about chalangia hepatitis, in, in this. So spend the time looking at it.

It's important not to overinterpret, things. we can see here the, A, a gallbladder here with a, what appears to be a, a large amount of material in it. This is a very common finding in, in, in many dogs and really is of very little significance at all.

On the right here, however, we actually have, some mineralized content within the gallbladder, and you can see that here producing this very sharp shadowing beyond it. And this was possibly, maybe more significant, but this is actually from a dog that was incidentally found to have this. So these are incidental gallstones, that, that we find in, in dogs.

And we, as we go through, we, our ultrasound, we're doing more and more ultrasound, we're finding these, as not uncommon findings. And in a, a normal dog, I wouldn't worry too much about this, but if this dog was jaundiced, I would worry that this might be causing some sort of obstruction. On the bottom here, on the left, we have a mucous seal, again, not, not sludge.

It's not dependent. If you turn the dog around, move the dog around, this, this will not change place. And a dog with jaundice, this would, this would be a, a very, important finding, that may well indicates that, that one has to, to, to start thinking about, some sort of surgical removal of that as it's clearly going to cause an obstruction.

In many cases of extra hepatic bile duct obstruction, however, and this is a case of hepatic bile duct obstruction, then all you see is a large gallbladder. In fact, the gallbladder may not even be particularly large. There may be acoustic enhancement beyond.

You can see the acoustic enhancement beyond here, but that's all you see. So when we see something like that, then the next stage is to find the common bile duct. And this is where a bit of experience and, and, and, and, training helps a bit.

It is possible to find the common bilelock in most normal animals, but, it, it is, something that, that takes a little time and patience. And once you've actually, done it once or twice, you'll be a lot more confident about finding the common bile duct, routinely. If you have a jaundiced patient, it's absolutely essential that you find the common bile duct by tracing from the pancreatic, from the gallbladder, apex.

And tracing it down and we're really looking for a common bile duct to be less than 3 millimetres. This was the common bile duct of that dog that I showed you last with the enlarged gallbladder, and you can see here that it's 6 millimetres across. There is clearly an obstruction there, and, and this, and this is a good evidence that this is an extrahepatic bile duct obstruction.

If you do find a large common bile duct, then don't rush into surgery. Many of these obstructions are functional, and that particularly rate relates to pancreatitis. And we do not want to start operating on those animals.

The anatomical obstructions, the ones where they're actually obstructed by a, tumour or a, a stone, or would, require surgery. So we have to make this distinction between functional obstruction and anatomical obstruction. And it's not necessarily that easy.

Getting a, a really experienced specialist sonographer may help, but even then, my experience is that they can't necessarily tell the difference on first presentation. It is therefore a decision that is made over time. Make that decision, we monitor the bilirubin.

If the bilirubin is rising dramatically each day or there is evidence of free fluid, then we intervene. So it is a question of monitoring this. So monitoring the size of the gallbladder, monitoring the common bile duct, monitoring the builder Rubin, and we will do it probably twice a day for the 1st 36 hours, 48 hours, and then once a day.

Functional obstructions can become anatomical obstructions, so we need to monitor them. But the moment the bilirubin in the blood starts going down, You know, you're in the clear, and you can then just manage these cases and medically. So.

That clearly means after checking the common bile duct, you have to check the pancreas. If you can't see the pancreas easily, then actually it's probably going to be fairly normal. Inflamed, enlarged, hyper surrounded by hypoechoic, fat, the pancreas is reasonably easy to spot.

A normal pancreas may not be quite so easy. It does take a bit of time, therefore, to get the experience because you have to scan dogs with pancreatitis to see these changes. And once you see those, then you can clearly see that in these cases where you have a pancreatitis, the obstruction is likely to be functional and therefore likely not to require surgical intervention.

This is an example. This is cholangio hepatitis, stroke, pancreatitis in a, in a Cornish Rex. Billirubin arrives at 178, for some reason somebody measured bile acids, 242.

I would totally disregard that. I don't trust that at all. We can see that the liver enzymes for a cat, are really quite high.

We can see the high globulins. There's lots going on here. But this was a functional obstruction.

The next day, the bilirubin was 160, the next day, it was 80. And, and it's that sort of change that we want. If this cat had gone from 178 to 220 the next day, I would be starting to say, this cat may need surgery.

Lastly, of course, in a jaundiced animal, it's important to look for liver masses and not to confuse those with, with a, a gallbladder. This here is a liver mass, not the gallbladder with a necrotic centre. Identify the gallbladder, then look for the liver mass.

What did we find in Molly's case? We found nothing. Really very little there.

Normal a paddock portal vein there with normal arborization, very vague changes perhaps in, in, in, in the parenchyma of the, of the liver there, but really nothing. There, there was no evidence of biliary tract obstruction. There was no enlargement of the gallbladder, no enlargement of the common bile duct.

So I'm now fairly confident on the basis of this ultrasound, having ruled out the pre-hepatic, having ruled out the post-hepatic that Molly has hepatic jaundice. So what next? Well, for me, yes, you could go on and do more blood tests at this stage.

Yes, you could do, do, do some more ultrasonography, but I would actually want to do some radiography and particularly if I wasn't too sure on my ultrasonography skills, I would want to get some radiographs. Radiographs tell you a lot, not just about the liver, but about any other problems that are going on. Remember that the liver is primarily an organ that gets a lot of secondary damage.

So I think it's important to know about, other problems. I think it's important to look for some of those focal mineralizations, and, milder scis and so forth if we've not got the ultrasound to back it up. Problems are, of course, if the dog does have substantial obscis, then you're not going to see very much, and in thin cases, you're not going to see very much.

So this is a radiograph that really probably should not have been taken. It was clearly obvious from the abdominal swelling this dog had fluid, but it shows you how difficult it is to assess anything that where there is a SciTES. This radiograph is more valuable.

This, this shows you the size of the liver, which from the gastric axis is clearly quite, quite small. People who, who do a lot of ultrasound can tell you something about the size of the liver, but unless you're doing quite a bit of ultrasound, ultrasound is not a very good way of assessing liver size compared to radiography. Yes, this dog's got a very large mass.

This is, this is a hepatoma, and, and this would be one reason for taking a radiograph for a dog with an enlarged abdomen, which you weren't sure of, and you wanted a quick assessment, particularly if you didn't have ultrasound. So particularly if you don't have ultrasound, I would encourage you to do radiography. But even if you, have ultrasound, then it is worthwhile doing radiography to look for other diseases, take the chest radiograph, looking for nets and so forth, before we start rushing in there and focusing too much on the leather.

I think people, are, are sometimes forgetful, in, in having done one form of imaging, not to do the other. This is quite a nice little radiograph here showing that that sometimes these gallstones are visible. This is a cat, but we've got plenty of dog films that show the same thing.

You do see this in the cat as a, as an incidental finding on occasions, and, and to be aware of that. So what happened with Molly? Well, with Molly.

We had a bit of a surprise. This was not visible on the ultrasound. And we saw this Normal leather Normal bladder, normal spleen, spleen slightly enlarged because Molly was, was sedated for, for, for this.

No evidence of ascites, no free fluid there. GI tract doesn't look too bad. There's, you can see a gas-filled coal on there, but nothing too, too, too remarkable.

So for our first question, I thought I'd ask you. What is your next step for Molly? More radiographs, more ultrasound, more blood tests, exploratory laparotomy, liver FNA, or liver biopsy.

Right, folks, you know how this works. Simply click on the answer which best suits your opinion. And we will give you 45 seconds or so to get that done.

And then we can reveal those answers and see if Ian's predictions were correct. It's an interesting one, yeah. Come on, folks.

There's a couple of you that are still sitting on the fence. Remember, these are anonymous. Nobody will know what you voted except you.

5 more seconds. Right, I don't think the others are gonna vote. Let's end the poll and reveal those quickly to you.

Can you see those in? Yes, I can. So, 48% of you have gone for exploratory laparotomy, 28% more radiographs.

Nobody wants to do any more ultrasound. I, I actually mentioned that, that we couldn't see this on ultrasound. So one option would be to go back to, to the ultrasonographer or, or, or have another look with ultrasound and say, can we really see it?

It would be a fair thing. And it's reasonable to talk about FMAs and, and liver biopsies, but, but I, I think, if you have something like that on, on a radiograph, I, my, my own view is, can we close that down now? Can I close it, I can close it, yes.

My own view is that, one should, really make sure you know where it is before you dive in there and do surgery. And you only know it in one plane. You don't know where that foreign body is.

You might guess it's in the stomach, but you don't know whether it's long or short. It could be a long steel tube that you are looking at, in, in cross section. It, it, it just is, is sensible.

Whenever you have a radiograph that shows what you think is a foreign body, is to go and take another radiograph in the orthogonal view to make sure you know what you're dealing with. So now we know that, this is, a round foreign body. It is, probably metallic, and, is, not, not, in, in any dimension, that large.

So my next question. Having said we should take another radiograph before we do an exploratory laparotomy, is what now? Right, same questions, different poll, .

Let's click on these answers and . All righty. Let's end that poll and share those results.

Right, so 78% of you, have gone for, now you really want to chop it out. Now you really want to take this, this, foreign body out, because you've seen it. a few of you want to do some more blood tests.

nobody wants to do a liver FNA and, one of you wants to do liver biopsy. Well, OK, so let's see what, what I, what I, what I did, . I think the first thing to say is, how do we link?

This foreign body to the presenting problem. How does this metallic foreign body turn into a massive hepatic jaundice? A few of you might be thinking, oh, maybe it's some sort of toxic metal that's been corroded by the stomach acid.

It's zinc or, or, or something like that causing a, well, zinc causes hemolysis, so that doesn't work, no. So, so how? You've seen something, but how do you relate it to the jaundice?

And the truth is I can't. I can't easily. Do that.

And if, and if, and if I'm right that this is, this, this foreign body is causing the jaundice, then that it should be causing jaundice by a toxicity. So, so the liver will be toxic. So surely making sure that that is what's going on before we dive in there might be a, a, a good idea.

But before we do any of that, We have to be sure of one thing. Hepatic jaundice is associated with a high risk of coagulopathies. The liver makes coagulation enzymes.

You've all rushed in there and done exploratory laparotomy, but in reality, I think more blood tests and making sure that we really do have. A good clotting parameter. OK, I know some, some of you may have been smart enough to have spot that on the slide earlier on and said, yes, I knew that these clotting parameters were fine.

So, fair enough, in that case, yeah, you, but the, the, the, the, the answer would, would not be to do. Blood tests, but I think the best answer is to do more blood tests to look at the clotting times, either by doing a whole blood clotting time, an activated clotting time, or by doing a prothrombin time or an activated partial thrombo and an activated partial thromboplastin time. Note the fibrinogen on this animal on Molly is quite low.

So although she does not have a coagulopathy at this time, the amount of fibrinogen in her blood is quite low, and I would be a little concerned. I'd certainly be making sure that I had some fresh frozen plasma around before I rushed in there and did any surgery so that if I started to have a bleed that I could supplement. But I say again that the issue here really is How do you link that to the foreign body to the jaundice?

And I can't. So, actually, having got those results, I then went and did an FNA of the liver. Which nobody voted for.

I'm very disappointed, but nobody, nobody supports this. But anyway, that's what I did. And that's what I found.

Now, some of you may look at that and say, inconclusive. Well, that's, that's shows you what a rubbish, rubbish FNA it is. I, I would dispute that because actually, I don't think that is inconclusive.

That's what the cytology said, but they didn't know the picture. I'm in charge of the case. I've got the whole picture.

I know what's going on here. I'm asking the question, Is this toxic damage to the liver? I know now it's not.

There's regenerative changes. There's mononuclear cells. There's inflammatory infiltrate, including some lymphoblasts.

Now, that's starting to look a little bit more worrying that to me. And therefore, I think if we are going to go in and remove the foreign body, that we should be doing a liver biopsy. And that we should be telling the owners that small metallic foreign bodies generally pass without incident.

Through the intestines. That metallic foreign body is not obstructing anything. It is of a size and a shape that would be expected to pass through the GI tract without event.

And therefore, in fact, I think it's very unlikely that the liver. So what would I do next then? Well, clearly, we have to get a proper sample of the liver.

We could repeat the FNA if we wanted to. We could cut a true cut biopsy, or we could go to surgery. Given that there is the foreign body, I think now, now you can do an exploratory laparotomy.

Having done the blood tests, having done the fine needle aspirates, now you can actually turn around to the owner and say, look, the foreign body is not the big issue. It's not likely to be the big issue here. The liver still is, and that brings us to the hepatic jaundice, things.

So if we're going to do a hepatic or, biopsy, we're going to check the clotting time first. We're gonna make sure that when we, do this, we're going to check the patency of the gallbladder with gentle pressure. We're gonna aspirate bowelpha culture at the time of surgery.

We're going to take the liver biopsy. It's a relatively simple technique. Take 2 or 3 small, small snips.

You don't need very much. You need, one, put into a, a clean, dry test tube, plastic sample tube for copper analysis in these chronic cases, if you want, you want a couple of bits in, into formally. you don't need, as, as one pathologist, this is not stakes strong enough.

You really don't need a big bit, tiny bit, that is all, all you need, and, it should be fairly straightforward. So what do we find at Molly's surgery? Well, we found a very bad liver, but we also found the foreign body, and the foreign body was some 2 pence pieces.

Quite why she had the 2 pence pieces, I don't know. More sadly for Molly, This was the histopathology, and as you can see here, large numbers of lymphoblasts. This is hepatic lymphoma.

And I'm afraid, therefore, the outcome for Molly was very poor. He panic lymphoma is not something that responds well to chemotherapy, and the owners elected to have a euthanas. And we were able to give them 10 pence off the bill.

So that was a sad outcome. Not all cases end like that. Unfortunately, a large numbers of hepatic jaundice cases do end like this.

This was another case of ours with hepatic jaundice, and you can see here the cirrhosis that so often occurs, but not all hepatic jaundice is bad. Some is relatively good. This is, this is a cat with hepatic libidosis, common cause of jaundice, hepatic jaundice in cats, high bilirubin there, very high alk phosphor cat there, high ALT, and the aim in these cases is complete liver regeneration.

If you, take a mouse and you chop out half its liver. That mouse will regrow its liver. In a week.

It's a phenomenal organ. It can regrow. The heart can't regrow.

The brain can't regrow. The kidney end stage differentiation to glomerulite, you're born with all the glomerui you will ever have in your life. The liver can regrow and in acute hepatic jaundice, we are aiming for complete cure.

We are aiming to get all this liver regrown. We don't even have to conserve the remaining function. So when we see an acute hepatic jaundice, our first thing is to support them.

I say 2 times maintenance there. I would regard that as minimum, 3 times, 3 times maintenance quite easily. It's keeping them well hydrated, that keeps them diaries, that keeps the kidneys working in these cases, that keeps the hepatic perfusion good, and, and, and that gets rid of the toxins via alternative routes.

Other options would include antibiotics, and we'll come on to talk about which ones in a moment, and vitamin K. Other things like ursodeoxycholic acid, steroids are not beneficial in these cases and should be avoided. They're, they're not necessary, or they positively make things worse.

In, in severe cases, blood transfusions, would work in hemolytic jaundice. But of course, this is hepatic jaundice, and you really don't need to do that, that, that at all. use toile down at the bottom there, is.

It is of course always an option with hepatic jaundice because the prognosis is relatively poor. But I think in cases of where you identify a hepatic libidosis and cholangio hepatitis, we really shouldn't be reaching too quickly for that. We should give these dogs and cats time.

They may take a week or 10 days to, to come around, but they, they do come around and they don't need a huge amount of intervention. They need rest. They need fluids, they need, some basic treatment.

When I see a case of acute hepatic jaundice or acute post-hepatic jaundice, you really don't have time to get cultures of the bile back and, and so forth, to make their choices. I, I think you should, should start antibacterials in these cases, even if the, cause is not bacterial, then these animals are, are, are highly immunosuppressed by the jaundice. So I think it is reasonable to give antibacterials to these critical cases.

And in the case of, a dog or with, severe, potentially severe liver dysfunction, it is reasonable, to go for, penicillins, with or without fluoroquinolones, depending on how much you feel that this is, related to sepsis or, or to, to, severe cholangio hepatitis. I appreciate that's, that's, on an antibiotic prescribing thing. obviously, we don't want to be using fluoroquinolones willy-nilly, but they are one of the few drugs that are relatively safe in, in liver disease.

Metronidazole, certainly, the, authorised dose of 20 mg per kg is, is too much for a dog with liver disease. I would go to, to half that. And I have to say I have used a lot of metronidazole at 10 mg per kg in liver disease without any evidence of metronidazole toxicity.

Other ones like tetracyclines and, and potential sulfonamides, erythromycin, are, are liver excreted, and, and are best avoided, if you have those on your shelf anyway. Vitamin K is important for these acute hepatopathies, although physical evidence of bleeding, as, as in this cat here, is relatively rare, and clinical pathological evidence, that is to say, prolonged clotting parameters are certainly not. and I think it's important that we, supply vitamin K and particularly supply vitamin K if we're contemplating doing a hepatic biopsy.

We really don't want to, to, be doing anything, without getting some vitamin K, on board. If we're talking about more chronic hepatic jaundice, then, then there's a group of other drugs that we can look at. The first and most important one is food.

They, they're making sure these animals are getting nutrition into their liver. And to do that and to that end, we have to support the animal's appetite. And, and it's, I think it's the anorexia of hepatopathies that really is the, the, the killer blow, to these animals.

If we can keep them eating, they stand a much better chance. And we need to maintain that by, dealing with the nausea associated with, with, with jaundice. So, so moppotent would be a good way.

And pharmacologically adding in things like mirtazapine as, as appetite stimulants. But quite often in these cases, we need some sort of, tube feeding. So a, a nasal esophageal tube and a cap with hepatic lippidosis here, or if We're doing a panic biopsy, then, yes, absolutely, take the chance to sit down an esophageal tube at the time of doing that, that, panic biopsy.

Of course, both of these are contraindicated if the dog or cat is vomiting, so you do need to make sure you get the vomiting under control. Part of that also would involve treating the GI ulceration associated with liver disease. and here's an interesting, thing that I think a lot of people forget, but omeprazole has exactly the same effect on hepatic enzymes as cymetidin.

And, and, and I think that, as we, we sort of move away from using ranitidine in dogs onto omeprazole and, in many cases, it's worthwhile remembering that, that ranitidine has less effect on empatic microsomal enzymes and omeprazole, and therefore may be a more logical choice, albeit that the effect on, on, GI acidity is, is not as good as with omeprazole. Scraphate is quite useful. It binds to, various things that are like bile acids and pepin and so forth, that will be causing some, some problems.

And, it may be quite useful, but it does cause constipation in these animals and it does increase the aluminium, of course, which is toxic to the kidney. What do we feed? Well, we want, a high energy diet with lots of good quality protein in there, and, maybe, some carbohydrate fibre, that's a bit of controversy there, and certainly low fat.

And rather relying on home cooked diets because those are often short in micronutrients. What I like to do is is to take a baseline hepatic diet like hepatic support diet, but if you want the Hill's equivalent, which is LD, that's fine too, and add protein, both hepatic support diet and the Hills LD are relatively low in protein. and, and in these cases of hepatic jaundice, we need to supplement the protein.

So, so adding in then to that baseline diet, some, some good quality protein in the form of a white fish could be chicken or, or, or, or, or, or whatever, but, whatever that, that, that, that, they'll eat, would be probably my, my preference. Alsoodeoxycholic acid is a, a, a known choleretic. It's been shown to be a choleratic in the dog, and, it, it reduces the, damage done to, the liver in, in many different, situations.

It's contrary, it's said to be contraindicated in exopathic bile duct obstruction, but I would suggest that that's contraindicated in anatomical. Bile duct obstruction. We commonly use it in the jaundice associated with pancreatitis, and I've never seen a problem with it.

So I'm, I'm not sure that it would be, all extra paddock bile duct obstructions, just the anatomical ones. And this is probably the things and, and the dose for this, is, is really quite wide. the, the formulary state's 15 migs per gig, but there are publications looking at 50 Migs per kg.

in dogs, as being, being effective as well. So, we, we don't want to hold back on this stuff, at all. Antioxidants, a variety on the market, they, they, they, they theoretically do lots of good things.

In reality, there's been very little evidence that shows that they actually achieve any or all of these things. Still less actually make a difference to clinical outcome. And I feel in, in the case of a, a dog that is, is jaundiced, these are probably, OK to add in.

They're fine if, if, if the dog will take them and you can afford them. But if your, your, your client has of limited resource, these are the first things to cut out, because of that lack of published efficacy. You may want to think about steroids.

They're anti-inflammatory. They're choleratic. They promote the, the, the, the flow of bile.

They, act as an appetite stimulant. So, you know, in, in the short term, there are many benefits, to, to, to a small dose of steroids. But once you've given them, stop.

They're water retentive, they're ulcerative, they're suppress the immunism, and ultimately they are hepatotoxic. So a very small dose of steroids is one thing. Giving lots and repeatedly giving lots, not such a good idea.

And, and, we always hear let no thing die without the benefit of steroids. Well, that's very much how I feel about steroids and jaundice. If, if I am struggling, then I will give them, but I understand that in, in, in doing so, that I, I'm accepting that I am now, heading towards death, and, and, and, and this is a last-ditch attempt.

So that's a quick run through some talk about how we manage hepatic jaundice. We've talked about the three types of jaundice. We've talked about the, approach about the importance of measuring the haemoglobin, about doing, Good quality ultrasound if you can.

If you can't do ultrasound, at least do radiography and then about doing a biopsy before we go on to, to, to, to judge what the outcome of this condition will be. And if we can't do a biopsy, then think about fine needle aspects. We've talked about the treatment of hepatic jaundice, about the importance of nutrition, about the importance of monitoring.

And remembering that the liver can completely regenerate, and in those acute cases, we can get, see, see them through as long as we have some patients, and, a client who is willing, to, to, to support the treatment, for, for a week to 10 days. OK, then. So I hope that was useful.

I hope that helps you to take something back to, to your practises, to think about it. If nothing else, thinking about doing those orthogonal X-rays before you jump in there to an exploratory laparotomy and linking the foreign body to the actual clinical signs that the animal is. Showing.

And I'd be happy to know to take any questions. I should say a big thank you to Gwinne Hammond, our ultra sonographer for supplying me with some of those images and Trish Ward for some of our help with them as well. And also Rory Bell for a couple of the images as well.

And with that, I'm happy to take any questions. Thank you very much. I, thank you so much.

It was absolutely fabulous as always. Very clear and concise and, It just makes it seem so simple. And when you're in front of that patient, it's not always that easy.

When you were talking about the foreign bodies, Catherine asked if that were a copper foreign body, could that explain the, toxic damage to the liver? No. No, I, I, I mean, there are many dogs that have eaten copper, from bodies because it would pass through too quickly.

It has to get obstructed, and that was not going to obstruct. Copper, at that level, you would have to actually get acid degradation. Of that, and you would see that, on the radiograph probably.

And even if you, you didn't, the amount of copper that would then be absorbed is relatively limited, you know, to, to get copper poisoning, would actually require either the injection of copper or an inability to process copper. We hear about copper toxicosis in dogs, but that's because they innately can't cope with the copper. Copper in the GI tract.

You know, it isn't just freely absorbed. And even if it did what the bits get in, the body can deal with quite a bit. So it would need to, need, I, I'd really struggle to see how that would cause I, I'm, I'd be much more interested in, in some of these NICAD batteries, and, and some people have suggested that could be a NICAD battery.

I've used this radiograph on several occasions and, and some people have said NICAD batteries. And, and, and I don't deny that. So, so, you know, it may be, this is a toxic one, but that's why you do the fine needle aspirate.

To make sure that you can link the foreign body to the signs, the jaundice that came in. And, and if you can't, then just stop and think, is that foreign body actually causing a problem? OK.

Another question from Catherine. She says, is CSL an appropriate fluid choice in hepatic jaundice? Is it any true that the liver, diseased liver cannot metabolise this?

Yeah, one of those things that, intensive care people were talking about 15 years ago, I think they were saying you can't, you know, serious liver disease, the liver might not be able to metabolise the lactate, so wouldn't produce bicarbonate, so in fact, would actually make the matters worse. This was a theoretical discussion between intensive care people that became almost mantra that you couldn't use lactated ringers in liver disease without any evidence that any dog had ever been harmed by lactated ringers, it became, you don't use it. When they actually looked at it, they, they found none of these dogs had a problem metabolising the lactate.

If a dog liver is so bad that it can't metabolise lactate, the dog's dead. and, and, and, and, you know, it's just so easy to metabolise lactate that, that you, you can just do it. And, and there are other sites in the body that can metabolise lactate as well.

So, there's no reason not to use lactated, ringer solution in, in a dog with, with, with hepatic disease, never mind jaundice, hepatic disease. it, it, it, I, I regard it as, as being one of those things that escaped out of academic institutions without, without too much. Caveats that this was only a discussion we were having and not a, a, a real thing.

But so no, I, I, I have used, and continue to use lactated ringers in these, in these cases. It's one of those where, as you say, the, The powers that be and we all respect and look up to researchers and professors and that, and when somebody comments, it becomes gospel. Absolutely.

And and and and it's a, it's a theory, you know, there's good, I understand the theory. There's, it's always this, this problem about making the distinction between what a bunch of academics are talking about and what actually translates into real clinical recommendations based on real outcome measures in the clinic. and, and unfortunately, we tend to snatch at these things quite quickly in the human medical field, there, there's, it's much more difficult to change the protocol.

and, and so, until there's good evidence and, and, anyway, that's, that's the situation. So yes, go ahead and use, Hartman's in, in, in liver disease with, with, confidence. Excellent.

Rebecca is asking what parameters would you use when deciding if you're going to give vitamin K? Would it be based on related to COAGs? To be honest, obviously if the COAGs are prolonged, yes, you give vitamin K, but I would give vitamin K to any dog that had an hepatic jaundice.

Because I know that that dog is really seriously affected, and we may want to do, a biopsy in the future, and we want to prevent the problem rather than having to treat the problem. When you see dogs which are haemorrhaging because of a lack of, clotting factors, it's, it's really is very late in the day to start saying, oh, maybe we should give some vitamin K. And vitamin K is relatively cheap compared to repeatedly doing COAG screens.

So it, it, it makes common sense to, to therefore give the vitamin K. It's unlikely you're going to, I'm not aware of any downsides to giving doses of vitamin K. I mean, it's not like you can cause hypervitaminosis K.

I'm not sure even if that exists. And it's it's better to do that than have to wash all the blood off your shoes as a surgeon. Well, yes.

Katherine has asked another question. She says, is there any value to the use of acetylcysteine in acute liver disease that is not related to paracetamol toxicity? Oh, that's a, that's an advanced question.

yes is the answer. And, acute hepatopathies, it's, it's doing the job of that an acetylcysteine. And, that, that is something that, that, again, we, we are looking at, I have to say, I mean, clearly, obviously in paracetamol poison there's a need.

Again, lack of good objective clinical trials, seeing that this does work, but it has certainly become de rigueur, if that's the word, in, in acute hepatic disease. To consider the use of that. Again, I have to say without any measure of outcomes.

So it's, that's a very current thing. Stinks the place out, and, not perhaps available to everyone, but, yes, I, I, I wait to see a good published trial showing that there's a significant difference in outcome. Maybe there is one out there and I haven't seen it, but, that is, that is certainly a possibility.

Well done, Catherine. Right up to date with that question. Folks, that's all we have time for for tonight.

It is my pleasure once again to thank Ian for a hugely insightful and very thought-provoking presentation. So Ian, thank you for your time tonight. Back onto my screen, there's one last slide that I picked up.

OK, you need to do that if you just click on your like you did in the beginning, it'll pick you up just a little thing I picked up which was quite amusing really in . This doing this presentation between Iris and Jaundice, I wonder, you know, what's the difference? And I thought I'd just leave you with the thought about why, why, why, where Itaru comes from.

That it's actually refers to a yellow bird. And it was believed that a patient with jaundice could be cured because the disease would transmigrate from the jaundiced patient to the poor bird. Yeah, there's, there's some not cutting edge medicine.

Folks, that's it for tonight. To my control in the background. Thank you very much.

And I, once again, thank you folks for attending tonight. Thank you and good night.