Many thanks, Bruce, and thank you, to everybody for tuning in to listen to this talk on, approach to the chronic cough from the basics to beyond. OK, so this talk is going to guide you through my approach to how I investigate these patients who present with chronic coughs. And what I'm going to talk about is based on anecdotally, what I find works and my experiences, but also some of what is out there in the literature as well.

And I'll highlight those, different papers at different points throughout the talk. So, let's get started because it's really quite a lot to get through and some of it I will skip over to some degree, and you might want me to expand on it in the questions section. But let's start out by defining what a cough is.

So a cough is an important reflex that protects the respiratory system from inhalation of foreign materials and secretions. The cough can be a normal physiological process, as we know, but it may also be associated with a pathological change, which is what we're interested in tonight. Coughing can be associated with pathology of any part of the respiratory system, the cardiovascular system, or any other disorder which exerts pressure on the airways.

And we'll talk about how we can start to differentiate these different groups of diseases as we go through the talk. So coughing can be an acute, transient and self-limiting process, such as the doctor presents with kennel cough. And it could be a acute presentation that's really quite sort of severe, requiring lots of medical therapy, investigation, and even hospitalisation.

An example of that might be a severe, bacterial pneumonia in a puppy. We're not going to talk about these acute cases tonight, we're more interested in the chronic guys. So, coughing can present as a chronic presentation and it can require multiple investigations and lifelong therapy.

An example of that would perhaps be chronic bronchitis in the dog. However, some chronic disorders may present with a much more acute decompensation. So an example of that might be, for instance, the West Highland white terrier that has a history of interstitial fibrosis, that's been on treatment for quite a while, or maybe not, it's just been coughing for quite a while, and then it suddenly presents at the practise with signs of right-sided congestive heart failure in quite a bad way, because it's now developed core pulmonale secondary to its underlying lung problem.

So not all chronic presentations presented in a chronic manner, some of them can have acute flare-ups. I think one of the things that I always like to point out to people at this point is how we manage our clients' expectations, because ultimately we want them to keep coming back and keep paying their bills, so we've got to keep them satisfied. And I think one of the things that we have to do is be aware that this patient has presented because the owner, perceived effect that the cough is having on their pet's quality of life, OK?

So we have to bear that in mind because when we're treating these guys, often owners will only see. Their perhaps perceived improvement in their pet's cough, and they don't understand that some of the other things that we're doing with treatment might be treating things that are going on within the dog that they might not be able to see the effects of. So you have to make them aware of that from the beginning.

We also have to make them aware that with chronic coughs, you know, these patients can require quite a lot of different diagnostic procedures, so ultimately they're going to cost in some cases quite a bit of money to investigate. And something I think it's very important to make clear at the outset is complete resolution of the cough is not always possible. So for instance, chronic bronchitis or feline asthma, we certainly aim to improve cough severity and frequency, and we definitely want to manage that chronic disorder to make sure that it doesn't continue to get worse and we get other complications, but ultimately, making them aware that, you know, in some cases, we're not going to stop, stop this cough altogether is quite important from the word go.

So I think one of the first stages in the workup is to be able to differentiate those patients that are primarily presenting with respiratory tract disease versus cardiac disease. And I'll talk, sort of at length throughout this talk about the different ways we can do that and why we need to do that early on. So unfortunately, we have to talk about physiology at this point, so please bear with me.

It's pretty basic stuff, and there's a few things that we need to point out here, really. So the lower respiratory tract is protected from inhaled matter by filtration in the, in the nose, because of all of our little fine bones that are in there, and adherence to that mucus lining. The mucus lining itself is produced in the goblet cells and the submucosal glands of the conducting airways, and these are the airways from the nose down to the terminal bronchioles.

And this mucus lining has two basic properties. One, it's quite viscous and tenacious, so, inhaled particulate matter and organisms get stuck in it, which allows our functioning cilia to waft this mucus up the airway into the larynx where it can be coughed up, expelled from the airway, and then swallowed. But also the mucus itself does have antimicrobial properties as well to help fight infection.

We sometimes see patients that are sneezing in combination with their coughing, we'll talk about that a bit more later on, and basically patients that do that generally are sneezing to also help them eliminate matter from their airways. The larynx is a very important part of, coughing, and we know that the larynx closes to prevent macroscopic contamination of the airways. So we'll talk later on, that'll help us understand why patients with disorders of the larynx can quite often cough.

It's also important to be aware that we talk about increased mucus production and bronchoconstriction in a lot of pathological disease processes as being detrimental. But we also have to remember that they are also, important, physiological responses to certain diseases, that allow us to eliminate inhaled material more effectively by increasing the effectiveness of the cough reflex. So not all increased production and bronchoconstriction is bad.

So you have to bear that in mind as well. So what about the cough reflex itself? So cough receptors are found in the epithelium of the larynx, pharynx, and the conducting airways, OK?

And within the conducting airways, these cough receptors are most densely packed at the bifurcations, OK? When we look at the density of cough receptors, as we move down the airways, we notice that they are the highest density, higher up in the airway, and as we go down, down, down through the respiratory tree, we get less and less cough receptors, OK? And actually, in our respiratory bronchioles and alveoli, we don't have any cough receptors.

So that's maybe something that not everybody is aware of, that a lot of our patients who are coughing, it's because of stimulation of receptors, you know, in the upper airway, not necessarily right down in the lower airway. And as a result of that, I think a simple thing to always remember in, in our coughing patients is that disorders of the pulmonary parenchyma itself, and of the alveoli do not stimulate a cough to the same severity that airway disorders do. OK.

So for instance, a patient with chronic bronchitis will cough a lot more than a patient, say, with a bacterial pneumonia. So these cough receptors can be stimulated by mechanical or chemical stimuli. And these receptors, when activated, send afferent information via the C fibres to the brain stem initiating the cough reflex.

So the cough reflex is pretty, is pretty simple to understand. It's initiated by a phase of deep inspiration. And then there is a compressive phase where the glottis in front of the larynx closes, and that causes a significant increase in the airway pressure.

Eventually this airway pressure gets high enough to knock the glottis back open, and there is a rapid expulsion of air, from, from the upper airway out of the larynx along that pressure gradient, OK? Really. So whenever I've got a patient that's booked in to see me for a chronic cough, I always like to open up their record before they've even walked into the consulting room and have a look, you know, at the signalment, and have a little think about the presentation to help me start to think about, a list of differentials and help me refine them as early as possible.

One of the important things that we've got to remember with these guys is that they certainly may be booked in as a patient with a cough, but actually, we need to be very careful when we're taking history from our clients to make sure that that patient actually is coughing, as it's quite common for clients to mistake things like vomiting or regurgitation as a cough, especially if you're productive. I'm sure everybody's got an experience, of seeing a pet that's been booked in for a cough, a very productive one, and the onus is the vomiting, and, and you witness it, and actually it's a dog with kennel cough. It's just coughing up a huge amount of froth, from the lungs, OK?

So we have to be very careful in how we, we question our clients, when we're taking a history. We can also have the confusion that there are other clinical signs that can also be seen in patients that are coughing. So it's not uncommon for a patient to choke, gag or wretch, particularly as they are bringing up mucus from the lower airways and it stimulates the pharynx.

So that's really not uncommon, but again needs to be differentiated from vomiting regurgitation. That being said, I've also seen a few patients, over the years that have coughed so severely that they actually do end up vomiting as well. So sometimes I will ask a client to record an episode of their pet coughing, so they could be 100% sure that's what what the patient's presenting for.

And if they're unable to get a video, I'll just pull up YouTube on my phone and show them a few. Examples, you know, of coughing cats, that are easily, Available on YouTube. Let's just start to think about some of the differentials that will be causing chronic cough in our patients.

So there's a nice comprehensive list here with common in the middle and uncommon on the right. So just to briefly go through a few of them. Certainly I see quite a lot of patients with brachycephalic obstructive airway syndrome that are coughing.

And that also might be because they also have concurrent gastroesophageal reflux. So that's something that's really commonly seen in these patients. Bit of brachycephalic.

Laryngeal paralysis obviously can cause a cough, and we tend to see that in our older large breed dogs such as Labradors, and they're quite easy to diagnose because they quite commonly present with quite marked strider. I'll talk about that a bit more later on. Tracheal collapse is something that we really quite commonly see in our older terriers, particularly Yorkshire terriers, and they have that characteristic goose honking type cough.

Kennel cough itself is generally not a chronic, the cause of a chronic cough. It often causes an acute cough, but actually that can, set off, an inflammatory reaction that causes a more chronic cough because of chronic tracheobronchial syndrome, essentially a form of, chronic bronchitis. We may also see patients with inhaled airway foreign bodies who present with a chronic cough.

And often these guys, when we're taking a history and and asking about when the cough first started and, and how it's changed, they often have had, a very acute initial bout of coughing. When the airway foreign body was first inhaled, for instance, a day when a young springer spaniel has been running around in long grass, may have inhaled a grass horn, and then often the cough subsides a couple of days later, and then 23 weeks down the line once that foreign body started to establish a focal pneumonia, the cough then starts to become chronic. Chronic bronchitis is something that we very, very commonly see in older terrier types, and also in cats as well.

So that's one of the most common, diagnoses that, that we probably will be making these patients. Ear xenophilic bronchone neuropathy is, is one to be on our radar. So these are patients who have severe ear xenophilic infiltrates within the lungs, but no evidence of underlying parasitic diseases.

And they are, seen quite commonly in huskies. OK. Bronomalacia is something that we'll touch on a little bit later on.

Lung worm is something that obviously is on everyone's radar, these days with the amount of marketing. Around that, so we're gonna talk about a bit of lung worm testing later on. Pulmonary fibrosis, obviously Wesley lung disease, very, very common in that breed, I think every Westie I see it.

I assume it's, pulmonary fibrosis until proven otherwise. But bear in mind it's not only Westies that get it, I have diagnosed it in cats, and also Staffordshire Bull terriers are a little bit overrepresented with that as well. Pulmonary neoplasia certainly can cause a chronic cough, but it's also quite surprising in some of our patients that I'm sure we've all radiographed that have really advanced pulmonary neoplasia and have no cough at all, but perhaps are tachypneic or even dyspneic presentation.

Cardiac disease we'll talk about a little bit later in more detail, so I'll skip over that. Plural space disease certainly can cause a chronic cough, but I suppose it more commonly presents as dyspnea. And then at the bottom we've got esophageal disorders.

So again, I'll touch on that a little bit later on. But we're generally talking about patients who have, regurgitation secondary to their esophageal disorders, that develop recurrent aspiration pneumonia. OK, Brill.

So as I said, we are sat in front of our computer, just about to open the consulting room door and bring in our client with a chronic cough. Before we do that, let's have a look at the patient's signalment. And the reason for that is that common things occur commonly, OK?

Westies get Westie lung. Siamese cats get asthma, OK? So what I do is have a quick think about the age of the patient, older patients are more likely to develop neoplasia as their causes of cough.

Younger patients more likely to get bacterial and parasitic lung diseases. What's the species of the patient, you know, what's the breed of the patient, as I talked about, there are lots of different breeds that are overrepresented with certain conditions. Is there any previous history of cardiorespiratory disease or any medications that could have precipitated, this chronic cough?

What's the patient's analytic status and are you in a lung worm endemic region? I'll also ask, when does the patient cough, and it's quite common for patients that are coughing because of our large airway disorders to do that during excitement and exercise, and often when they're at rest, they don't cough so much. And it's quite common for patients who are coughing because of forminent congestive heart failure to do it after periods of being, lay down or asleep.

How long has the patient been coughing, I think, is quite important because the longer our patient has been coughing, the more likely we are to have complications, of that cough, such as the development of core pulmonale, secondary to chronic lung disease or tracheobronchial malalaia, which we'll touch on a little bit later. How severe is the cough as well? We want to be able to sort of grade that cough on day one, so that as we're treating it, we're able to monitor treatment response with a reduction in the grade of that cough.

also, we, we know that certain types of, airway diseases, you know, will make cough coughs that are more severe than others as well. How frequent is the cough and is it progressive? Is it getting progressively worse or staying about the same?

Is the cough associated with eating or drinking this is something I always ask because if it is, it may be that patient actually has pharyngeal or laryngeal disease. And then one of my favourite questions to ask, is this cough? A harsh hacking type cough or a soft moist type cough.

And the reason for that is that in my opinion, the harsh hacking type coughs, which are the kind of, Sounding cough are often associated with airway diseases, whereas the soft moist type coughs, which are a bit more of a are often associated with more pulmonary parentchial diseases. And I apologise there if those impressions are terribly awful, but hopefully, I'm also going to ask my clients, has your pet had a had a episodes of fainting or any vacant episodes, because this could be indicative of syncope or presyncope, which is when a patient doesn't quite faint because of a lack of oxygen to the brain, but just goes a little bit weak and starry eyed and vacant. Because if they have, any evidence of syncope or pre-syncope, I'm instantly going to be thinking, you know, maybe this is a cardiovascular problem.

Or at least a severe lung problem that maybe could be causing right-sided heart failure, OK? Some patients who actually have syncopal episodes during coughing are classed as having tussive syncope, and that's something that we quite commonly see in older terriers, with mitral valve disease. Often during periods of excitement.

Does the patient have dyspnea or exercise intolerance? Again, that'll give us an idea about the, the severity of the underlying problem. Are there any ocular nasal signs?

Do we need to start investigating the nasopharynx as well? And does the patient have a strider or stor? So strider is that sound that our, Labradors with laryngeal paralysis make, which is sort of a, an inspiratory wheeze, kind of a.

Type sound and strider, whenever you hear it, is generally associated with upper airway obstruction, but particularly of the larynx, although I have heard a Labrador with a tracheal mass presenting the strider once. Sturter is that sort of noise that our brachycephalic patients make, that sort of snorting type noise, and that's associated with nasopharyngeal pathology. OK?

When we observe our patients in the consulting room, we're gonna have a look and see if they have increased inspiratory or expiratory effort. And again, this helps us localise the disease process as patients with significant inspiratory efforts often have upper airway disease, and patients with significant expiratory effort often have lower airway disease. We're going to ask if our cats have outdoors access, as they're more likely to have infectious diseases and certainly we'll need retroviral testing.

And we'll ask if there are any other pets in the household, and if so, are they coughing. What is the air hygiene like in the household as well? If the owners smoke, I'm not saying that that's going to cause the chronic cough, but certainly, we'll want to improve their hygiene as the treatment plan for any patient with chronic, cardiopulmonary disease.

We might ask if there's any building work going on at home, because that unto itself could certainly, be associated with, aspiration pneumonias and foreign bodies. Or irritation of the airways with, with any underlying chronic cough. And we'll also ask about previous, responses to medical therapy, OK, or any other, concurrent medical disorders that might change the way we investigate or treat these patients.

So now I'm just gonna quickly touch on this question, which is a little bit controversial, but it is do patients with cardiac disease cough? And the answer is yes, and unfortunately, no, not really. So what do I mean by that?

Well, when you open up textbooks and you look at the clinical signs of congestive heart failure, very commonly says coughing, OK? Whereas we actually know now from a few studies, but one of which being this one from Leukaferisin here in 2013, that actually a lot of patients with congestive heart failure do not cough. They are actually much, much more likely to have tachypnea.

Or dyspnea, or exercise intolerance than they are to have a cough in their history, OK. So certainly if the patient's coughing, it could have heart failure, but if it's not coughing, it does mean it does not have heart failure, if that makes sense. So that's heart failure.

What about heart disease? Well, yes, there are patients with heart disease who do cough. And the reason why they cough is because of cardiomegaly causing airway compression, particularly of the left main stem bronchus which rides.

Just over the left atrium. Rather than because they have pulmonary edoema. So we'll talk about that in a little bit more detail later on.

But essentially, a cough is a much more reliable of res indicator of respiratory tract disease than it is of congestive heart failure. OK, so just bear that in mind. We're gonna move on to the physical examination now, and I always say that a good physical examination in combination with a sound history.

And patient observation can often give us a very good idea about the severity of the patient's cardiorespiratory problem and perhaps where that problem might be originating. So normally by the end of the physical exam and history, I think we should all have a pretty good idea about whether this is cardiac or respiratory in nature and therefore be able to set them off down the right diagnostic. Path.

So how do we do that? Well, we'll start with a really systematic nose to tail approach, being very thorough, not overlooking any findings. Don't jump to conclusions in every case, pattern recognition can be a wonderful thing sometimes, but it can catch you out occasionally.

And record all findings. It's very common to look back through clinical notes of patients that have had a chronic cough and not see a record of that patient's resting respiratory rate, or of its heart rate, or of its heart rhythm. I'm absolutely sure people are checking these things, but by recording them, it can actually give us a lot more information, when we're looking at how we investigate these patients and also how we monitor their response to treatment.

So I'm gonna go through this really quite quickly cos a lot of it is teaching grandma to suck eggs, but if we see a patient with a chronic cough and pale mucous membranes, that may be consistent with forward failure or left-sided heart failure, OK? Bear in mind that if our patient is cyanotic at presentation, then they will generally have an SPO2 of below 78%, which is pretty scary, but somehow they managed to adapt to that in the chronic setting, you know, to cope with it. Cyanosis, however, does not occur in patients with moderate to severe anaemia, so be aware of that, and that's because they don't have enough haemoglobin in their bloodstream to become deoxygenated to turn their mucous membranes blue.

And I think a good, sort of general rule of thumb, is that cyanosis is more common in advanced primary respiratory tract disease plus or minus pulmonary hypertension, than it is in congestive heart failure, OK? Not true in every case, but generally sinus patients think they're perhaps more likely to have respiratory tract disease, particularly if they present with a chronic cough. If we see prolonged capillary refill times in association with pale mucous membranes, and again that can be, an indicator of forward heart failure.

We want to carefully palpate the neck and throat, and again this is something that's often overlooked, and we want to be sure that there's no evidence of masses or foreign bodies causing breathing problems. I've seen a couple of dogs that are presented with a chronic cough and have had large thyroid tumours, OK, that haven't been noticed by the clients. Then we'll generally perform a tracheal pinch, which is fine, but we need to be aware of its limitations.

So I was certainly taught when I was seeing practise that a tracheal pinch equals can cough, and there is no doubt they have the most notable tracheal pinches. But all the tracheal pinch does is tells us there is inflammation and irritation within the trachea, and that means they have. Some disease within the trachea and or lower airways, and it means no more than that, OK?

So I'll do it to see that there seems to be airway inflammation, but I won't jump to conclusions about the cause of that airway inflammation. We then want to check the lymph nodes because obviously, if our lymph nodes around the head and neck area are increased, it could be consistent with, infectious diseases, but also could be consistent with neoplasia. And then we're gonna palpate the patient.

So we're gonna palpate the lean muscle mass and do a bodily condition score and record them. So I tend to use this scoring scale for assessing lean muscle mass, the A, B, CD scale, or I'll just write a comment such as mild, moderate, or marked loss of lean muscle mass. Why is this important?

Well, there's a few reasons. One, we know that lean muscle mass correlates pretty well with disease severity and therefore prognosis. So it's a prognostic indicator.

But also you tend to find That patients with advanced cardiac disease quite commonly develop cardiac chexia and lose lean muscle mass. Whereas actually, a lot of patients with quite advanced respiratory disease don't lose their lean muscle mass, and actually a lot of my chronic cough patients are a bit overweight. So we're also going to do their bodily condition score, and I use the scale of 1 to 9 on, you know, too fat, too thin, or ideal.

So we're going to write these down and we're going to record them every time and we can monitor them, because certainly that Yorkie that's presenting, and been diagnosed with tracheal collapse, that's, you know, bodily condition score of 8 out of 9, the mainstay of that PET's treatment is going to be weight loss. It's going to be far more effective than any medication we're going to give it. So please do not overlook your bodily condition score.

We're then gonna continue to palpate and we're gonna squeeze the cranial thorax of the cats to do a cranial rib spring. So if you just squeeze the ribs with your thumb and index finger on each side of the rib cage in front of the cat's heart, it should have a little bit of springiness to it. If you lose that springiness and it feels really solid, it could be because that patient's got a mediastinal mass as the cause of its chronic cough.

We'll then block the abdomen and check for ascites, and the reason why we're doing that is that patients with chronic respiratory tract disease can develop right-sided heart failure secondary to it. And one of the signs of right-sided heart failure is ascites. We're then gonna palpate the apex beat of the heart, and check for precordial thrill, which would grade, any murmur that's there is a grade 5 or above.

And then we're gonna palpate the pulses to check for pulse rate, pulse quality, and synchronicity with the heart. We'll get on to that in just a couple of slides. I also do this, and this is sometimes overlooked, I think as well in practise.

I'll check the jugular veins in any chronic cough patient again for signs of right-sided heart failure. So one of the things that we might see with this is distension of the jugular veins. Or we might want to check this patient and, and, and see if we can cause these jugular veins to be distended by using a test called the hepatojugular reflux.

So this is a video here. . Now, if you just look at the jugular groove here.

OK, you can't see the press now pressings there, can you see that raising it'll disappear in a se? Maybe on the side here. OK.

So the hepatojugular reflux is a test where you get somebody to palpate the cranial abdomen and squeeze the cranial abdomen in the area of the liver. And what you can see is distension of the jugular veins secondary to that. And if that's positive, that indicates elevated central venous pressures and probable right-sided heart failure.

You may also see jugular pulsation with right-sided heart failure, as in this patient here. And the pulsation is often most prominent if that patient has got right-sided heart failure in association with tricuspid regurgitation. OK?

We're then going to auscultate the heart using a very systematic approach and in dogs we're going to listen to all three valves on the left side of the heart, and then in coughing patients, don't forget to listen to the right side because if they have pulmonary hypertension and tricuspid regurge, that's the side that you're going to hear it the most clear. In cats, I tend to just listen along the sternum, as that's often where heart murmurs are loudest, but I do also rock the stethoscope up the side of the chest as well, a little bit in those guys. But in cats, I, I think it's very hard to to auscultate the individual.

Valves, so I'll just say the cat has a cradle or recording, sternal heart murmur. We're then going to listen to the heart rate and also the heart rhythm whilst palpating the pulses, and we're going to think about what our patient's normal heart rate should be. Why is that?

Well. If our patients have irregular heart rhythms, they are much more likely to have cardiac disease as the cause of their cough than if they have a regular heart rhythm. OK?

We also have to bear in mind that patients with heart disease can have normal heart rates and even, you know, sinus arrhythmias. However, when a patient progresses from heart disease to heart failure, one of the first things that happens is they lose their sinus arrhythmia. So if you hear a sinus arrhythmia in a patient with a cough, you can be almost certain they've not got congestive heart failure based on that alone, OK?

That's because of an elevation in the sympathetic tone when you go into heart failure that abolishes that. Patients with heart failure also generally have high normal or even elevated heart rates, and plus or minus arrhythmias. However, cats can do their own thing.

Cats can have normal, low or high heart rates with congestive heart failure. Brachycephalics are also a bit of an exception to this rule, and that's because they have naturally very elevated vagal tone because of their obstructive airway syndrome. So it is possible for a brachycephalic dog to have heart failure and still maintain a sinus arrhythmia, OK?

Patients generally who have primary respiratory tract disease as the cause of their chronic chronic cough will generally have a normal heart rate and often a really pronounced sinus arrhythmia. So get used to checking heart rhythm in these patients quite intensely. I'm pretty much gonna skip through, murmurs other than say, If we hear, well, heart sounds, should I say, if we hear a gallop rhythm in a cat, that's highly indicative of primary heart disease.

When we hear murmurs in dogs. We have to be aware that not all murmurs mean heart disease because they could be physiological murmurs. And we want to grade our murmur as well, because it can tell us quite a bit about how important that murmur is, OK?

And bear in mind, you know, that some animals have more than one murmur. So, for instance, mitral valve disease patients have a left-sided, systolic apical murmur. But 30% of those guys will also have tricuspid regurgitation and a concurrent right-sided murmur, if it's quite a loud regurge.

Those general rules of thumb, and small breed dogs, their murmurs correlate well with disease severity, if we suspect they've got mitral regurgitation. So generally you have to be above a grade 3 out of 6. in a small breed dog, to have a heart problem that's severe enough to be in failure.

So generally, if you've got below a grade 3 heart murmur and you're a small breed dog, you know, you probably don't have heart failure, but you could still have, cardiomegaly, which could be causing a cough. Large breed dogs, it's different in that the grade of the murmur does not correlate so well with disease severity. And actually, a lot of large breed dogs suspected of having DCM have very, very quiet murmurs or no murmur at all.

So any murmur in a large breed dog that you suspect may have DCM is significant. Cats again can be very tricky, because their murmur grade does not correlate very well with disease severity. And it's quite common for younger cats to have physiological murmurs that, you know, not because of underlying heart disease whatsoever.

One thing to bear in mind is that with cats, murmurs do become more significant with age, however. So we're then going to auscultate the larynx and trachea for any evidence of upper respiratory tract obstruction, and then we're going to auscultate the lungs. So we're going to listen for wheezes.

So wheezes are sounds that are made because of narrowed airways, because of diseases like asthma or chronic bronchitis, and if you hear them, they're great, but I very infrequently hear them. A lot of my cats are lower airway disease. I certainly can't hear any significant wheezes on them.

So I think the lack of a wheeze definitely does not exclude things like feline asthma. Or chronic bronchitis. We're then gonna have a listen to the lungs and see if there are any evidence of inspiratory crackles.

And if they are soft inspiratory crackles, they may be associated with pulmonary edoema, pulmonary haemorrhage, pneumonia, or other parentchimal disorders. When we hear loud crackles, they're generally associated with either pulmonary fibrosis or severe chronic bronchitis. And I often say to our interns that when you hear pulmonary fibrosis with a stethoscope, it almost sounds like somebody's scrunching a packet of crisps, as you're auscultating that patient.

So that's something that could help maybe point you in the direction of pulmonary fibrosis, even when you hear it. Just bear in mind that dogs with cardiogenic pulmonary edoema, i.e., congestive heart failure, often have very normal lung sounds.

Again, the textbooks say these guys have crackles, but I think to have a crackle, to have crackly lung sounds with pulmonary edoema, you often have to have a huge amount of edoema in your lungs, you know, and certainly in the initial stages of pulmonary edoema, it's actually built up fluid within the interstition. And it's not even in the airways itself. Even when it does get into the airways, we know that the alveoli don't have any cough receptors, so it's only when the pulmonary edoema is sufficient enough in volume that it spills out into the upper airways that it actually stimulates a cough.

So we'll then listen to both sides of the chest, both ventrally and dorsally, because we know certain diseases have certain distributions such as ventrally in patients with aspiration pneumonias. Any dull lung sounds also will indicate to us plural space disease. And then we'll record the patient's resting respiratory rate.

And this is quite useful because we know that, in a large retrospective study that was done on dogs at home, that when they're asleep, if their sleeping or resting respiratory rate is below 30 breaths per minute, it's very, very, very unlikely that they have congestive heart failure. So, you know, a normal resting respiratory rate, you probably will be able to exclude. Congestive heart failure is a cause of that patient's cough.

Fab. So we've done our physical examination and we've taken our history and at this point we should have a pretty good idea about whether or not we're dealing with primary cardiac or respiratory tract disease. And this is important to be aware of as the diagnostic pathways are really quite different.

So patients suspected of having cardiac disease, want to have, a echocardiogram, if possible, ECGs, systolic blood pressures, and perhaps, radiographs of the chest performed consciously or under light sedation. Whereas patients with primary respiratory tract disease would probably go, gonna go down the route of general anaesthesia for really nice inflated thoracic radiographs, followed by bronchoalveolar lavage plus or minus bronchoscopy. Let's go through our individual tests that we can select for these patients.

So firstly, blood work. Unfortunately, there is minimal diagnostic yield. We may see ear xenophilia in some patients with parasitic disease, ear xenophilic syndromes, or even feline asthma, but it's not that common.

And neutrophilia is, is quite commonly seen in many inflammatory diseases of the lungs, but it's unfortunately very non-specific. We may also detect hyperglobular anaemia in patients with chronic infectious inflammatory or neoplastic diseases as well. So a little bit on lung worm testing is it is very topical and it's something that I think we should be doing in all of our patients with a chronic cough.

Certainly the oldest technique is to perform a bareman flotation. So that's fine to do, but if we're going to do it, we certainly need to pool our faecal samples over 3 days because a single faecal sample is only 50% sensitive for lung worms, it's not very good, and it goes up quite considerably by pooling 3 consecutive samples. A berman floatation is not only good for checking for lung worm as in angiotroylus, but it also allows us to detect other types of pulmonary parasites as well, so it is quite nice for that reason.

We could also consider doing a wet mount. So, we've done this a couple of times in our clinic in a patient that we've suspected has, parasitic lung disease, and we just run a cotton wool swab around the inside of the rectum, roll that on a glass slide, drop a saline in a cover slip, and have a look at it under the microscope in-house, and you might be able to detect larvae of parasitic diseases in that. So that's really nice when you do that and you get, a nice immediate results on a test that's very, very cheap.

We're probably going to commonly in practise, be using the Angio Detect snap by IDEX, and this is a point of care Eliza snap, and it has a pretty good sensitivity of 85% and a very high specificity of 100%. So that basically means if you test that patient and it's positive on the test, it definitely has lung worm. If it's negative, there's a 15% chance that it still has lung worm.

OK? What other tests can we do? Well, there are a few other ones, and certainly, if I don't perform, you know, bronchoalveolar lavage, for whatever reason, I'll certainly do, some blood work, to test for, lung worm.

But something that we should perhaps be considering in our patients, a little bit more these days is PCR for angiostroos posaurum. So this is detecting. DNA of, of the, the parasite, and that can be performed on bowel fluid or even faeces.

And we know that PCR is, is actually at the moment, the most sensitive way of detecting angiostrongylus visorum. And that was demonstrated in this nice little paper, . From 2018, where there were seven cases of confirmed angiostrongylus on PCR and of those, in fact, only two of them were positive on an angiodetect test, and only 3 of them were positive on a Bearman flotation.

So generally, myself, when I'm doing a bronchoscopy and bronchialveolarvage, I'll perform PCRs to screen for stronglus. So a little bit onto radiographs, which we're gonna be doing in all of our chronic cough patients I'm sure, is it's most important diagnostic test after auscultation. It allows us to assess severity of pathology, and also, which lung regions are affected.

One thing to be aware of is the quality of the radiographs are obviously proportional to the accuracy of the radiographic interpretation. So spend time getting really nice films, OK? In dyspneic patients, we really want to avoid radiographs until they are stabilised, and once they're stabilised, we certainly want to use minimal physical restraint and no chemical restraint.

So just to let you know the way that I tend to do radiographs on these patients, if it's a patient with a cardiac disorder, I'll really try my best to do the radiographs of just physical restraint, or if I have to, I'll give them a cardiovascularly safe sedative combination. If, however, it's a patient that I think's got primary respiratory tract disease, I'll go straight to anaesthesia for really nice inflated views. I think we need to do a minimum of 2 views, orthogonal views in all of our patients, but we may do an additional lateral in patients that we think may have metastatic neoplasia.

And always remember as well in patients that we think may have upper airway causes their cough, to include the neck as well. And also include both inspiratory and expiratory views if we're suspicious of tracheal collapse, because different regions of the trachea will collapse during different phases of respiration, OK? Make sure that the legs are pulled forward on our lateral films and that the neck is not flexed, because that can often cause a sort of sigmoid flexure in the trachea and cause it to look artificially narrowed or as if there is almost some sort of soft tissue capacity causing deviation of the trachea.

OK, so keep the head nicely extended when we're doing our laterals. Make sure that we don't overinterpret interstitial patterns, we'll get on to them in a sec, and they're really quite commonly seen in obese patients, or patients that have had the film taken on exploration, or those that are a little bit underexposed. We'll talk about this next point in a couple of slides.

Yeah, and I think another reason to take radiographs at this point as well is, is, is clearly to monitor patients, for progression of their cardiorespiratory problems. So, progressive cardiogale and heart disease, or perhaps, resolution of lung patterns with other primary, pulmonary preable diseases. So this is what I, fondly named the chabdomen, and this is what I don't like to see when I'm investigating a patient with a chronic cough.

So it's a radiograph that's half abdomen and half chest, hence the chaabdomen. You know, let's get really nice, well centred and well culminated, . Thoracic films and then separate abdominal films if we need them.

So we're going to look at all these different things when we're assessing our radiographs, airways, plural space, vasculature, cardiac silhouette, media sinum, chest wall, diaphragm, and extra thoracic structures. And we're going to be particularly interested in lung patterns. So just to quickly go through those, because they can be quite confusing and sometimes overlapping, and just as a little hint, if you're ever unsure about what you're looking at, you can call it a broncho interstitial alveolar pattern, just say it's got a bit of everything.

So an alveolar pattern occurs when the terminal airways are filled with fluid, so the alveoli, and that's commonly seen in patients who have exudates within the lungs, such as pneumonia, patients with quite severe haemorrhage, because of trauma, neoplasia or coagulopathies, or patients who have edoema, whether that's cardiogenic or non-cardiogenic. Bear in mind though that in the early stages of edoema, as I said earlier, it starts out in the interstitial space, so you'll get an interstitial pattern. And as pulmonary edoema worsens, it spills out into the alveoli and you can start to get alveola patterns.

And we may see alveolar patterns associated with neoplasia, and particularly if there are regions of inflammation or haemorrhage, surrounding masses. We'll also see alveolar patterns in patients with lung lobe collapse or atolecttasis in patients with lung lobe torsion, so are deep narrow-chested breeds or pugs. And the way to describe an alveolar pattern is that it looks like a fluffy, homogeneous soft tissue opacity, and it may be focal, multifocal, generalised or even confined to a single lung lobe, such as in patients with right middle lung lobe aspiration pneumonia.

And one thing to always look out for is a bronchogram because it's absolutely classic of this pattern. So this is a patient with an alveolar pattern and complete consolidation is lung lobe, and here we have a really nice bronchogram, OK, so you have these air filled airways and you can't see the walls of the bronchi as they're completely surrounded by soft tissue density because of the fluid infiltrates, OK? So if you see a bronchogram, that equals alveolar pattern.

This is a cat with congestive heart failure, and what we can see here with the red arrows are regions of pulmonary edoema, so these fluffy coalescing soft tissue opacities. We've actually also got a little bit of a pleural effusion here identified by our yellow arrows, and this cat quite helpfully has got a bit of cardiogaly which is not always common, as highlighted by the green arrows. Whenever we're looking at heart and lungs, we always have to bear in mind that on a thoracic film, we have to look at everything else as well.

And this patient has quite a nice alveolar lung pattern in this region here, because of its aspiration pneumonia, which is secondary to its megaesophagus. So, this is a patient with a megaesophagus. You can see the dorsal and ventral walls of the oesophagus filled with air.

It's really nice when you pick these guys up. So bronchial patterns are because of enhancement of the bronchial walls and typically cause a doughnut and tramline type appearance. And that can be caused by chronic bronchitis, is inophilic bronchoneneumopathy, pulmonary parasites, bronchopneumonia, and sometimes neoplasia.

One thing that I would say is that these, findings can be much more subtle than you'd expect. This is really obvious in this cat, with chronic bronchitis. You've got lots and lots of nice doughnuts, and tram lines, you know, throughout this film, really easy bronchial pattern.

But actually, a lot of dogs I find with chronic bronchitis have really subtle bronchial changes. So I think a lack of bronchial changes does not mean that patient does not have chronic bronchitis, if that makes sense. So then we've got this weird type of pattern, the interstitial one, which is tricky, and we either have nodular interstitial patterns.

Which are generally caused by neoplasia, abscesses, granulomas, cysts hematomas and foreign bodies, or we may have what we call the unstructured, pattern, which causes just a diffuse, ill-defined ground glass appearance throughout the lungs, but it's superimposed on our normal structures. So what do I mean by that? Well, this is an interstitial, unstructured pattern here, and there is increased radio density throughout the lungs.

They're not as black as they should be, but we can see all of our airways, OK, and we can see all of our vessels. So this is not an alveolar pattern, because with that you would start to lose the vessels and you wouldn't see our airway walls if it was an alveolar pattern. So that's sometimes a helpful way to differentiate unstructured interstitial from an alveola.

Look for those. So this is a nodular interstitial pattern, and this patient unfortunately has quite advanced metastatic lung disease. And then we get the weird and wonderful things.

So this was a patient with a chronic cough that had an upper airway foreign body, which was easily removed. This is a little cat with a pericardial peritoneal diaphragmatic hernia here with some of its gastrointestinal tract herniating through into the chest cavity. So if you ever see an indistinct diaphragm, it may be because this patient has one of these and also a concurrent pleural effusion, as we can see here.

This was an unfortunate dog that had the world's largest chest mass. So this is all chest mass here, compressing the trachea right up against the ventral and vertebral bodies and compressing the lung fields to this tiny region here. And on the dorsoventral view, we see the mass again.

And the trachea is really deviated over to the right. So in all patients, the trachea does deviate a little bit to the right at this level, but it's never as far pushed over as this, OK? This is a Labrador that presented with a chronic cough because of a tracheal mass here.

And this is a patient with quite classic tracheal collapse in this region here, OK? This was a little British bulldog that presented with dysm and a previous chronic cough, and this poor little guy has really quite pronounced tracheal hypoplasia, with significant narrowing at this level here of the trachea compared to the thoracic inlet, although it is quite an underexposed film. Really, so we've talked about primary lung patterns.

What about radiographic changes associated with cardiac coughs? So what we're gonna look for is not pulmonary edoema, because we've already said pulmonary edoema very infrequently causes a cough, but what we are going to look for is a left atrial bulge on the right lateral view and cardiomegaly, OK? We're gonna assess the cardiac shape and look for elevation of the trachea.

So here is a classic example of a patient with a cardiac cough. We've got a generalised cardiomegaly, when you do the, the vertebral heart score, it's, it's significantly increased in this patient. But what you can very clearly see here is a huge left atrial bulge.

So the back of the heart here is actually the left side of the heart on the right lateral view, and it should curve up nicely to this point and continue to curve over like this up to the carina. And in this patient, we've got a huge left atrium here and you can actually quite clearly appreciate that this left main stem bronchus here, which is overlying the left atrium, is completely squished at this level here and you can see it tapering to a fine point. And if you've ever performed bronchoscopy on these patients, you will see that there is almost complete collapse of some of these airways, certainly as bad as 80% collapse.

And that is why a lot of patients with cardiac disease cough because of severe irritation of that airway, because of compression. And that is something that unfortunately we, we can't do a huge amount about. So I always make my clients aware of that when their patient's been diagnosed with a cough because of cardiac disease.

You know, this cough is unlikely to go away, OK, and it is not a good indicator of pulmonary edoema and heart failure. Here's a really nice DV of a dog with a 4 chamber cardiogaly as well. And then here's a cat who has pulmonary edoema here because of this fluffy alveolar and titial pattern.

And then the cardiogaly that we appreciate in cats is much more subtle. So this cat's heart is only slightly enlarged by this slight bulge here, which is the left atrium, and it gives the cat's heart what we call A sort of kidney bean appearance, OK, because of this little notch in here. So cats don't get that significant left atrial compression of the main stem bronchus.

So cats, you know, do not cough because of heart disease or heart failure. If a cat is coughing, it's because of generally lower airway disease. This is a cat with really significant cardiomegaly and actually this one probably did have a degree of compression of the railway, but again was not coughing at all at presentation.

OK, if we see this on our dorsoventral radiographs, this is a pericardial effusion. So this can be differentiated from cardiomegaly because their cardiac silhouettes are incredibly round or globoid. So when you see this on a radiograph, you need to pop the ultrasound probe on to check for fluid, OK?

Very, very round or globoid heart shapes. Just briefly want to mention fluoroscopy. It's something, that very few practises have access to, but if you have a patient who has got, dynamic airway collapse, which means the patient's airways are intermittently collapsing during different phases of, inspiration expiration, a fluoroscopy can, demonstrate that really nicely.

So all of my patients that I'm suspecting to have tracheal collapse, I do a fluoroscopy on, and I can look at that patient's whole trachea from top to bottom and watch all the different regions, for any evidence of dynamic airway collapse. And in a paper from 2007, they found that radiography was more sensitive than sorry, fluoroscopy was more sensitive than radiographs for the diagnosis of tracheal collapse by about 10%. I also use fluoroscopy in patients that I think are, regurgitating and having a chronic cough secondary to that.

So I'll do a barium swallow on those guys. Let's not forget to examine the larynx and the pharynx as well, just in case there is severe pathology there that could be causing our patients to have, a cough. And sometimes we will use flexible endoscopy to have a good look up behind the soft palate to check the nasopharynx, particularly for grass blade foreign bodies in cats, for instance.

Very briefly on cardiac biomarkers, essentially, they're not of any use, in my opinion, in the investigation of chronic cough. OK. NTPro BMP and troponin, I think, don't need to be performed in these guys, unless they, have been diagnosed perhaps with, with right-sided heart failure because of core pulmonale, for instance, or we suspect you've got very advanced DCM.

OK, so not very good as a screening test for patients with a chronic cough. Very briefly on CT, just to make people aware that it is out there and it is really very useful in these guys and certainly for me. It's, you know, my first choice method of imaging these patients.

So all of my chronic cough patients will generally head straight to CT rather than radiography, just because it's more sensitive and more specific. So for instance, a pulmonary mass on the radiograph has to be about 7 millimetres in diameter for it to be visible, whereas it only needs to be 1 to 2 millimetres for it to be visible on a CT. So it is much, much more sensitive, OK.

These can be performed under sedation, but generally we prefer to do GA, on patients that are having CT of the thorax, and we can give them contrast agent IV as well, which can really nicely highlight areas of inflammation or neoplasia. So just a few interesting images. From patients that I've done CTs on recently.

So this was a dog, and, we did the CT because the lung, patterns that were on here, you know, were, were quite clearly alveolar ones, such as down here and around here. What we couldn't see were, the odd little pulmonary mass that was hidden within these areas of alveolar infiltrate. OK.

This was a little, patient who had an interstitial lung disease. And there was no evidence of these little bully on its radiographs, however, very clear on the CT. And it's quite important to pick these up because this patient is at risk of these rupturing and developing a spontaneous pneumothorax.

So by seeing them, we can prepare the client, you know, for that eventuality. Note also how much bodily fat this patient has from the skin here right down. And this is really typical of patients with chronic respiratory tract disease versus chronic cardiac disease to be quite overweight.

Here are some enlarged bronchial and sternal lymph nodes which again are really, really hard to identify on radiography, but very clear on CT. Here's a Labrador that was unfortunate enough to have a ginormous carcinoma within its thorax displacing the heart here. OK, and this patient lived with this unbelievably for 6 months without removal.

So I said not to fall too much into pattern recognition. This is a CT of a cat that has interstitial fibrosis, very unusual. This was a little puppy that had a disorder called cituitus inversus.

So actually, all of its, thoracic and abdominal organs were on the wrong side. So this dog had a right middle lung lobe pneumonia, but that right lung lobe was actually on the left side of this dog. And that was an unusual one.

Because in this case, it was also associated with primary ciliary dyskinesia, which basically means it's silly didn't work, so that's why he got repeated, pneumonias. This was a working German Shepherd that presented with a pyothorax, and whether we see that in patients, that, that have had a chronic cough, we start to look, particularly in dogs for migrating foreign bodies, and this was a foreign body here in the lumbar muscles, that we went in and removed. So I'm just wrapping up, by touching a little bit on bronchoscopy and then I'll briefly go through bowel.

So, I think most patients, honestly, who, you know, we get a definitive diagnosis on, would benefit from bronchoscopy and definitely bronchoalveolarvage. So, I find bronchoscopy really useful to identify, certain pathological changes such as dynamic airway collapse, but also pulmonary haemorrhage, not so much pulmonary parasites, but it's possible. It can also be used to grade the severity of disorders such as tracheal collapse.

But obviously it does have to be performed under GA so these patients have to be stable and it is also really, you know, useful for being able to remove. Airway foreign bodies using bronchoscopy. However, if you don't have bronchoscopy, it's not the end of the world.

We can perform blind balance in any patient in general practise, although we just have to just be aware of the potential risks and complications. So these are just a few bronchoscopy images from the last perhaps two months. So this is a patient with really severe mucus hypersecion in its lower airways.

This was an ophilic bronchneumopathy. This is what airway collapse looks like, so that's about 80% collapse of the airway, if you appreciate that compared to this one. And that was a patient with dynamic airway collapse, so it would open and then close, open and then close.

This is a patient with a pneumonia. This is a patient who was coughing because of a laryngeal cyst just sat in front of the larynx here. This is a mass in a dog's nasopharynx, and this is a dog that was coughing because of post-nasal drip.

So this is the nasal pharynx and a purulent discharge coming down that and falling into the pharynx and stimulating a cough from the larynx. It just sort of shows you that some of these things really, you know, are very hard to detect with other imaging modalities other than bronchoscopy. This was a really cool case of a cat that was referred to me for removal of an airway foreign body, and after vigorous attempts in the bronchoscope to remove it, we finally got it out and it was actually one of the cat's own teeth, one of the molars that had become so decayed that it had come loose and the cat had inhaled it.

Pretty weird and wonderful. This is a patient with tracheal collapse, and I just included this because it highlights again how perhaps. You know, radiographs can misguide us in, in some of our patients.

So this patient's radiograph, even though it is quite under exposed, I was referred to this film, it does look like really quite, severe tracheal collapse in this region here when we compare it to the rest of the trachea. But actually on CT the collapse is only mild, and again on bronchoscopy you can hear, sorry, you can see that there's only about 25%. Reduction in, in the sort of, size of that lumen.

So again, only very mild, collapse when we've looked at it, on CT and bronchoscopy. So a little bit on blind bowels and we'll hopefully be very near the end of the presentation. So these, you know, although not in my opinion, the gold standard to do blind, they're much better to be done via bronchoscopy.

Certainly I've done them a lot before in general practise, and they can be performed pretty easily with minimal equipment. So what are the contraindications to blind bowels, these are important to be aware of. So the patient has to be stable for general anaesthesia and for you to be able to perform the lavage of the airway.

We ideally want to be sure that they've not got a coagulopathy, that they've not got a partial tracheal obstruction or pulmonary hypertension. We perform these under general anaesthesia and they're maintained with either volatile anaesthetic gas or total intravenous anaesthesia. And we place our patients' internal recumbency with their head elevated and the neck outstretched.

We then have a mouth gag in place to keep the mouth open, and I tend to use a 6 to 8 French, 30 to 60 centimetre long soft urinary catheter. We'll have 500 mLs of warm saline and, 5 or 20 mL syringes, and we'll have a selection of microscope slides, EDTA tubes, and plane tubes available. Very important to remember, any cat that we are performing a bronchoscopy or a bain or even a tracheal wash, they must be premedicated with tebutyle.

So that's a beta 2 agonist that causes bronchodilation, OK? And the reason for that is that when you put anything into their lower airways, they will bronchospasm, just like their larynx does, and that's why we obviously. Apply local to the larynx for the same reason.

So make sure we're doing that. And if at any point during, you know, performing a blind bowel, the cat really starts to, to, to cough a lot, and it's SPO2 starts dropping. We might give a little bit more of this medication as well.

Just bear in mind it will increase the heart rate, so don't panic if you see that when it's administered IV, . So we're going to have a patient anaesthetized and we're going to pass our urinary catheter through the ET tube and down into the lower airways until minimal resistance, hopefully not hesitant, is felt. As soon as it feels like resistance, you just stop advancing the urinary catheter.

And if it's a small animal, less than 10 kg, we're going to instil 95 mLs of sodium chloride, or about 10 to 20 mLs in a, in a larger patient. We're gonna instil that into the airways and then immediately aspirate. And stop once negative pressure is achieved.

If you keep sucking on that airway, and it's negative pressure, you are against the airway wall and you could damage it, OK? You can also perform coupage during aspiration to help improve yield. So a good bowel sample, we should retrieve about 50% or more of what we put into the patient, and it should have a frothy appearance as well, and that means that we've got right down into the alveoli, as its name suggests, and that means you've picked up alveolar surfactant if it's frothy.

You hold it up against the lights and shake it a bit and there should be some debris floating around. And then these samples we put in an EDTA tube to be sent for cytology, a plane tube to submit for culture and various PCRs for infectious organisms, but also we want to make an air dried smear immediately as well, because these cells can degrade really quite quickly. So I tend to spin down some of the sample in an Eppendorf tube.

I'll remove the supernatant, resuspend the pellet, put that on a glass slide, make a smear and quickly dry it. And there's a lot of labs as well these days that do really nice PCR packages, so it'll be called the Extended feline PCR package and have lots of different PCRs for lots of different infectious diseases and parasitic diseases. Be aware of the complications of the bowel, however, which include pneumothorax, haemorrhage, bronchospasm, and potential iatrogenic infection.

And then just finally, briefly to touch on echocardiography, this is obviously the gold standard for assessing cardiovascular disease and the only way to definitively diagnose many cardiovascular problems. It's also the only way to diagnose and grade pulmonary hypertension, which we see in respiratory tract patients, other than using invasive blood pressure measurement. And we also may use thoracic ultrasound for imaging of thoracic masses as well.

So the mediastinal mass that we pick up in that coffin cat, we might use ultrasound to assess it and allow us to perform fine needle aspiration of that mass. So this is just one case, just to demonstrate how significant the right-sided cardium megaly can be in a patient with core pulmonale. So here's a huge right side to the heart.

So this is the right ventricle here, OK, on this right parasternal short axis view, and this is the left ventricle here. So really the right ventricle should only ever be 1/3 of the size of this left ventricle, and as you can see in this patient. It's several times the size of the left ventricle, so very, very enlarged, you know, and, and very easy to spot actually.

This is the same patient looking at it on the right peristeral long axis view, and we've got the right ventricle here, bigger than the left, big right atrium here because this patient's disease, but it was actually a brachycephalic dog and also had something else, and it was this a heart-based mass. So this is something that we quite commonly see as an incidental. Finding in brachycephalic dogs and is not commonly pathological, unless it actually starts to cause, a pericardial effusion.

So that just helps highlight again, you know, echocardiography is just so sensitive for looking at the heart and the greater vessels. So, you know, perhaps, you know, consider it in, in more of our chronic cough patients. Final slide, and this is basically the Fruzamide response test.

It's something that I very, very infrequently use, but I know other people do sometimes use it, particularly if you've not got access to echocardiography. In that patient that you think has got congestive heart failure, you can't be 100% sure, from the radiographs. So basically, you administer rozamide at 1 to 2 mg per gig, twice daily for 2 to 4 days as a trial treatment.

And you then have them back to perform follow-up radiographs and you compare them A and B pre and post furosemide, to check for response, OK? And if there's a significant improvement in that radiograph, that patient had congestive heart failure, you know, for sure. Bear in mind though, that when we do the rosemide response test, We don't monitor, the improvement in cough frequency in response to furosemide.

It has to be the radiograph. And the reason for that is that rosemide actually has mild anti-inflammatory properties in the lungs, and patients with primary respiratory tract disease can transiently improve on furosemide even though they don't have congestive heart failure. Fab.

So that's the end of the talk, and I know it's been a bit of a whistle stop tour, but I've tried to cover everything from start to finish and what we tend to do in these patients, in what order and why, but I think the the most difficult challenge in these guys is is differentiating sometimes cardiac from non-cardiac disease, OK? But the vast majority of patients can be worked up to, you know, really reasonable, to, to a good degree, . With sound clinical approach and very basic equipment, and child treatment certainly can be useful in those not willing to investigate, but are not always ideal.

James, thank you very much for your insights tonight. It it really has been a, a, a fabulous covering of the situation, and, and what we can expect. Folks, unfortunately, we have run a little bit over time, so we don't have much time for many, many questions.

Two quick ones for you. How common are tracheal masses? Pretty infrequent.

You can also get cysts within the trachea, but I've seen 3 in the last 10 years, so pretty uncommon. OK. They're malignant as well, unfortunately.

Oh dear, oh dear. The other question is quite a long question just to summarise, prednisone makes more susceptible to picking up lung worm or to developing problems with lung worm? As far as I'm aware, no.

And I presume they mean at immunosuppressive doses for other, disorders. I don't know if there's any evidence in the literature of that, but it's certainly not something that that I've seen in practise. Excellent.

And I suppose we, we bear in mind if we're treating a patient with prednisolone, for instance, for chronic bronchitis, we're using anti-inflammatory doses, you know, 0.5 to 1 mg per gig, twice a daily, not immunosuppressive doses anyway. And often those patients as well will try and wean on to inhaled steroid therapy.

Great. Folks, that's all we have time for tonight. The other questions that have come in, Dawn will email through to James and ask him very nicely if he would mind responding to those.

So we will get back to you and with some answers on those. But James, thank you so much once again for your time. Folks, thank you all for attending and listening tonight to an absolutely fascinating talk and some really good pointers for us to pick up.

Born in the background. Thank you for making everything happen seamlessly and from myself, good night.