Good evening everybody and welcome to Monday night's sponsored webinar. Tonight's webinar is proudly brought to you by Breathe Easy, and we would really like to thank them for their sponsorship of tonight. It's going to be a fascinating talk.
I have seen some of the slides, beforehand and, I have listened to our speaker Phil Hadrad before and you are in for a treat. So thanks very much to Breathe Easy for their sponsorship of tonight. Just a little bit of housekeeping from my side.
My name is Bruce Stevenson and I'm going to be chairing the webinar tonight. If you have any questions for our speaker, simply hover your mouse over the screen. There's a little black control bar that pops up with a Q&A button.
Click on that, type in your questions. They will come through to me and we will hold those over until the And so as not to disturb Phil. Phil Padredge is a DBM and he went to New York School veterinary medicine from 1981 to 1985.
Following that year, he did an internship in small animal medicine and surgery at Santa Cruz Veterinary Hospital. The following two Years were spent doing a residency in small animal medicine at UC Davies. And then from 88 to 90, a fellowship in pulmonary and critical care medicine also at UC Davies.
1990 to 2000 saw Phil as the associate Professor of medicine, Immunology, molecular medicine at the University of Chicago. Phil's research regarding the molecular mechanisms involved in human and feline asthma was NIH supported for 10 years during his tenure at the University of Chicago. He's the author of more than 80 peer-reviewed manuscripts and book chapters in the fields of human and veterinary pulmonary medicine, including published manuscripts in the Journal of Immunology, British Journal of Pharmacology, and American Journal of Respiratory and Critical Care Medicine, amongst others.
He is the past author of respiratory medicine for the veterinary clinics of North America and he's acknowledged to be the first person in our profession to actively promote and research the use of inhaled medicines to treat our veterinary patients with respiratory diseases. Phil was also the original official veterinarian for the NPR-based radio station, Dog Talk, the radio show. Phil, no stranger to the webinar vets and welcome back.
It's over to you. Well, thank you so much for the lovely introduction. It's a pleasure to be with you this evening and I wanna start by thanking everyone who's tuned in for the talk tonight.
We're gonna talk about canine inflammatory airway disease, more specifically about the diagnosis and the treatment. When we think about taking care of patients with non-infectious airway disease, we typically consider corticosteroids as one of the mainstays of therapy. In a moment, I'm gonna talk about a little more about why that actually is so appropriate, more specifically to the respiratory system than others.
But I think we can all agree that in the dog especially, chronic use of corticosteroids has a whole number of potential side effects when given systemically by oral or the intravenous, I'm sorry, or the intramuscular subcutaneous root. And we're pretty aware that dogs given steroids chronically have a tendency to have behavioural changes which may or may not be directly related to increased hunger and thirst. They certainly do drink more, they certainly do eat more, they certainly do gain weight.
They're more likely to have propensity for skin and urinary tract infections. And again, because of the effect of steroids on insulin sensitivity, their certain glucose is certainly can go up. So those are long-term concerns we've had with the use of corticosteroids in dogs for as many years as we've been practising.
Now the interesting thing about, I hope it's interesting for people tonight to consider is that Any condition in the respiratory system that is amenable to steroids, any disease from the nose to the trachea, for which you would consider using systemic steroids, is a disease we can consider using inhaled corticosteroids and we'll discuss in a minute why that's true and why that's advantageous. Two points to make as we start. The first is, as we go through each of the disorders in the respiratory tract, we'll wait till the end of the lecture to talk about the specific doses of drugs to be used, that's OK.
And the second is that typically in a talk like this, it's fun to use videos to demonstrate the disorders we're actually talking about. But by the nature of a webinar and the fallibility of using an internet connection, we won't be using videos just this evening. When you think about the respiratory tract and you actually start from the tip of the nose and go to the lung, you can consider common diseases that we see in the nasal cavity would be chronic non-infectious rhinitis.
If you move back into the throat, the posterior pharynx, we see dogs that have what we call reverse sneeze, and if you'll forgive me when we get to some of these disorders, I'm gonna try to mimic the sounds that are made, so please allow me to do that. When we get to the larynx, one of the common diseases, of course, that we see is laryngeal paralysis. When we get to the trachea, a common disorder, we see tracheal collapse.
When we get down to the bronchi, one of the most common reasons for dogs to cough as they get a little bit older is the disease called chronic bronchitis. And finally, the one condition we won't speak of tonight, but which is completely amenable to inhale steroids, we typically call eosinopillic pneumonia or some variation off of that. If you stop for a second to think, well, why is the respiratory tract so specifically amenable to corticosteroids and then inhaled corticosteroids compared to other organ systems, the answer is pretty straightforward.
The respiratory system is line from beginning to the distal terminal bronchioles with mucosa. And the function of the mucosa, of course, is a protective barrier for the things that the respiratory tract is insulted by. And when I say insulted, of course, I mean none of us and none of the patients that we take care of are in rooms that are sterile, that have 14 air changes per hour.
Actually, we are as mammals, chronically insulted every day by bacteria, viruses, fungi, protozoa, etc. And yet, we're alive and we stay healthy. And a great reason for that is that the respiratory system is lined by mucosa and the things in the mucosa that protect us from all those other infectious and results.
I won't take too much time of your, of your evening to go through any histology, but just to make the point that the sepophilia is a very serious barrier against inhaled particulate matter and inhale infectious agents. And one of the things that it does in addition to being a barrier is have goblet cells that make mucus. So, the mucus traps the things that come into the airway to prevent it going down into the lung.
And in addition to that, there are serous cells that make a watery fluid with digestive enzymes, and immunoglobulin A also get secreted into the mucosa to help protect us and the patients that we take care of from these various bacteria and viruses, etc. This is just one picture of an epithelia, and if I can use the If I can use the pointer, I'll show you if this is the underlying stroma. Where I'm showing you the pointer up here, it's where epithelia should be.
I apologise. This is where normal epithelia should be, but it's truly disruptive because of all these neutrophils that are invading. So the point I'm making is that the infectious agent is the initial insult, but once it's cleared, the resulting damage is all from the inflammatory response of the body, which is why corticosteroids and then inhaled steroids become so effective.
It's because we're really dealing with the secondary long-lasting inflammatory response. There was a vet clinics in North America that was published some years ago by Doctors Conan Rro, and they, in their abstract, they really put it very succinctly, so I'll read this to you. Every breath holds the potential to introduce infectious organisms and irritating particulates into the respiratory tract.
Despite this continuous exposure, the lungs stay sterile. Further potential pathogens are distinguished from monoculous particulates, thus sparing respiratory tract from damaging inflammation. And that's really the point of the rest of this talk, to, to really appreciate the fact that a lot of the problems we see in the diseases I'm gonna talk about and that we see in our practise, have as much to do with the inflammatory response as anything else.
If we start from the nose, let's consider chronic rhinitis. When we see dogs with chronic nasal discharge, Chronic sneezing, chronic rubbing at their face with their paws. There are a number of things, of course, that can cause this, and this slide demonstrates most of the things that potentially can cause symptoms of chronic nasal disease.
And of course, in that includes masses that are commonly cancerous, infection for chronic disease that would be fungal or viral, calicivirus, herpes in a cat, for example. Dogs can inhale foreign bodies, twigs of grass, etc. Can have chronic nasal discharge, toothro abscesses can cause it, parasites can cause it.
And the disease we'll mention briefly now, lymphocytic plasmocytic inflammation. I make the point in this slide that the primary cause of chronic nasal disease in the dog is actually never bacteria. Now let me say that again.
The primary cause of chronic signs in the dog of nasal disease is actually never bacterial, and if that strikes is a little peculiar, think for a second. In your life or the life of anyone you've ever known, has anyone in your life ever had a chronic, primarily bacterial, nasal infection? And my experience, because I'm lucky enough to travel in many different places, when I travel to other places and I ask this question, it's always the same answer.
We don't know anybody who's ever had a chronic, primarily bacterial infection in their nose. And the thing is, that's true for dogs too. That doesn't mean that as a result of inflammation, they don't get secondary infection by bacteria.
But if you clear that up, it doesn't clear the chronic disease, which is really the point that it's never the primary problem, it's always secondary to underlying inflammation. So I guess the point of this slide is, if you have a dog with chronic signs of nasal disease, if you are able to rule out cancer or a foreign body or tooth good abscess, your primary differential is a non-infectious disease called lymphocytic plasmacytic rhinitis. I show you for purposes of illustration, a sagittal section of a canine skull, and I think you can appreciate as I bring the mouse around, the very delicate fine scoli turbinate bone that's there to try to trap particulate matter, bacteria and viruses in the nasal cavity, and of course, it's all lined by epithelium.
This is a CT of the same sort of cross section now where you can see the symmetric fine scroly bone in the nasal cavity, specifically the turinates of the dog, to appreciate the fact that this tissue, these turbinates that are fine and scrolling and rolling and cause turbulent airflow on purpose are all lined by mucosa, and the mucosa is one that gets affected by the inflammatory process. So consider this. In a dog that has chronic nasal disease.
What's the real problem? If you rule out infection and you realise that an inflammatory disease in the nose isn't really a life-threatening disorder, what's the real problem? Well, consider that you may have a cold or an allergy.
And imagine if someone tied your hands behind your back, so that you couldn't blow your nose. What would you do? And that's fundamentally the problem with our patients with chronic non-infectious nasal disease.
It's not life-threatening, and in the dog, they'll eat even if they can't smell the food as well. But the real problem is, as you can imagine, when you and I have a cold or an allergy, we blow our nose when we need to to clear our nasal cavities. And our patients can't.
So fundamentally, it's a mechanical problem of clearance that they don't have the ability to clear, but of course we do. So on a clinical level, that's really the issue they face. Now, when you ask the question, what is this lymphocytic plasmocytic rhinitis?
What does that actually mean? I'm showing you one paper from the Journal of Small Animal practise a few years ago, asking the question is, can some fungal organisms somehow cause or trigger an inflammatory response in the nasal cavity to try to explain these chronic symptoms. In this particular paper, as in every paper that's ever been written to try to explain this syndrome of lymphocytic plasmacytic rhinitis.
The answer is we don't know. We don't know why dogs or cats develop lymphocytic plasmocytic rhinitis, but I think it's fair to say you can consider almost You go back for a second, you can consider it almost as inflammatory bowel disease of the nose. If you consider an inflammatory bowel disease in the patients that we see that cause some degree of anorexia or weight loss or vomiting or diarrhoea, fundamentally is an inflammatory disorder of the mucosa of the GI tract.
Mostly lymphocytes and plasma cells. We understand that the antigen in those cases are often food and if we substitute for some non-allergenic food, they get a little bit better. We can't identify the allergen or the offending organism in the environment of our canine patients, but you can appreciate that because most of the inf infiltrates or lymphocytes and plasma cells, this is basically inflammatory nose disease, for lack of a better expression.
So what do we do with chronic nasal disease? Well, the first thing is to recognise that, in fact, while bacteria are not the primary problem, they absolutely play a role secondarily because the inflammatory process caused little microfractures in the nasal mucosa and disturbance of IGA, etc. So the normal bacteria in the nose become infections, even though they were initially commensal, now they're actually infectious agents.
Now the good news is that because they're conmensal organisms, Almost any antibiotic you would tend to use the first time around will clear the bacterial part of the chronic nasal infection. So that's easy enough. If you've been using antibiotics for a long time, because we haven't recognised the inflammatory component of the disorder, recognise that you can use tetracycline, Zithromax, redofloxacin, because in some of these cases, there is an anaerobic bacterial component.
That we don't test for, but you have to make sure that the antibiotics you're using have some effectiveness against anaerobes. And one of the most common, easy ways to do this nowadays is by using cratofloxacin because it covers anaerobes and anaerobes. But that's just to get the secondary bacterial component.
What do we do with the rest of the disorder? Well, once we get rid of the bacteria and a lot of the mucus is gone, We still have the edoema and the nasal obstruction that you and I experienced just like dogs. And for that, if there is the desire on the owner and you're comfortable doing this, if you do briefly anaesthetize them and do a nasal flush, you really have the best chance to get to the mucosa, which is really where you want to get the drugs to.
Independent of that, it always helps to use a local decongestant, just like you or I would. Now, there are trade names for that, and I'm using one little noses in the states this is sold for children, but it's quarters strength phenylephrine, and it's just the local vasoacting agent. If you don't have anything commercially, you can take 1 CC of epinephrine, which is a 1 to 1000 formulation.
And you can add 9 ccs of saline, which makes it a 1 to 10,000. Preparation of epinephrine. And if you place 1 or 2 drops of that solution on a dog's nose as you face their head up, and as it goes into the nasal cavity, they'll snort it in and that acts as a very powerful vasoconstrictor to open up the nasal cavity for just a couple of days.
So if you do this once or twice a day for 2 or 3 days, you really have pretty good opening of the nasal cavity and exposure of the mucosa. Because the third thing you want to do after you've dealt with the bacteria and the edoema is dealing with the underlying inflammation that we've discussed, and that turns out to be lymphocytes and plasma cells. And we don't know what the cause of it is, but we do know it a very effective treatment of corticosteroids, and what better way to deliver the steroid into a dog with lymphocytic plasma cytic rhinitis than by inhalation.
It's a very common method of treating people, and this is the perfect scenario to be using inhaled steroids into the nasal cavity of these dogs. So the combination of antibiotics for short term to get rid of the secondary bacteria using vasoconstricting agents for just a few days to get ridding the edoema. And then using inhaled steroids to get into the nasal cavity of the dog.
I will tell you in practising respiratory medicine for 30 years, this is the single most effective approach I've found to be able to deal with these symptoms long term. We move down the respiratory tract to the pharynx, there's a really interesting disorder that we all see that we call reverse sneeze. Now, because we don't have a movie, allow me to try to imitate this noise.
Here we go. So I apologise if that was a little strange. But I think you can recognise it.
This is when you see these, especially, short breed dogs or richocephalic dogs that have what looks like to the owner to be having a very serious life-threatening attack. And when we see dogs with adversities in the emergency room, I think we can agree, owners really believe that the dog is dying. It's really quite frightening to them.
When you actually examine these dogs endoscopically, what you realise is that inflammation is what's causing that gagging, choking sensation, and it's occurring above and behind the soft palate. Now, the tissue that's actually affected, I'll show you in a second, is tonsillar tissue. It's not the tonsils and the crypts.
There's another form of tonsil called adenoids, which are very commonly recognised as adenoids in people. We just don't use that term in veterinary medicine, and I'll show you what I mean. This is from a new slide.
I'll show you some dogs and cats in a moment, but it's an interesting phenomenon that we've never used the term anoid in our patients, but they're found in the caudal pharyngeal wall of dogs and cats as well as people, and it's really just a tonsilar tissue. It's just not in a crypt. Now the symptoms for people are exactly the same as for dogs.
When people get adenoiditis, which actually is what most dogs with reverse sneeze have, they have symptoms of sneezing, reverse sneezing, gagging, and choking. And that's really what we see in our patients as well, isn't it? Now, the history of this is kind of interesting.
Removal of these tissues were probably performed in, Copenhagen a couple of 100 years ago, Wilhelm Meyer, the act of tonsillectomy to remove the tonsils from the cryps has been performed for 2000 years, and it was described as early as 50. When I was a kid, I had what was called a tonsillectomy, an adenoidectomy. These operations were performed in children in the early part of the 1900s through the 1950s and 1960s because they were considered reservoirs of infection and they're responsible for all kinds of problems that we realised down the road, they really weren't and the reason why I had my tonsils and adenoids out probably weren't valid for today.
Having said that, I wanna show you what these look like in people, and then in a dog and a cat, especially the dog for today's purpose is to talk about reverse sneeze. If you look at the top picture going from left to right, 1 to 6, on one, you see this red dot. Now, what we're seeing is a rhinoscope placed into the patient's mouth and flipped 180 degrees over the soft palate.
So now we're looking at the posterior pharynx above the soft palate. And you can actually see here, this is what a large adenoid looks like. If you biopsy this tissue, it's a raft of lymphocytes.
And plastic cells. Now, in people, they do this sort of ablation, and as you can see in three different steps, they do it by electrocautery for 56, they've ablated the tissue. If you go down in the slide on our left, this is a dog with adverse sneeze and that's that same adenoid.
If you biopsy that tissue with lymphocytes and plasma cells. It happens, it actually happens in cats too. So on the right, you can see the se adenoid in the back of the throat of a cat.
But the take home message is, when we see patients with reverse sneeze, the great majority of them have an allergic adenoiditis. It's just a term we've never used in our profession, but it's very easy to document endoscopically and histologically. And because these are lymphocytes and plasma cells, it's the respiratory mucosa doing what it's supposed to, responding to inflammation by the response to allergens in the environment.
This is just an overreaction. And the good news is, again, because it's respiratory mucosa and because this is inflammatory cell problems, the adenoids, the reverse sneeze is actually pretty responsive to corticosteroids. The thing is, reverse sneeze is really not a threatening problem to the dog, and if the owner can tolerate it, it really is something the dog can deal with for its entire life.
But having said that, lots of times the dogs seem bothered by it, and certainly owners are bothered by it. And if we're gonna choose to treat it in my own mind, in my own practise, using systemic corticosteroids seems like a little bit of an overreach. So, here again, by using anti-inflammatory steroids, by inhalation, you avoid the problem of systemic side effects and yet the inflammatory.
Treatment is really very effective. The inhaled steroid goes directly to the posterior pharynx, to the surface of the adenoid, to reduce the inflammation and reduce the side effects. Earlier on my career, I thought, well, maybe we could just use the antihistamines for this.
And it seems on the surface that you should be able to cause it's an allergic response to the environment and the respiratory tract. In my experience, I just haven't found antihistamine at the right dose and frequency to control these symptoms, so I've given up that attempt. But certainly, if we first need the disease you want to treat, using the inhaled steroids is a very effective mechanism for treating them.
So let's go to the larynx. Again, the larynx is covered by epithelia and mucosa. Now, when we think of laryngeal disease, of course, we see paralysis, paresis, secondary edoema, sometimes we can have masses on the laryngeal folds or the area, retinoid cartilage, but for purposes of the conversation, what we see most commonly, of course, is some degree of paresis of paralysis.
When we see laryngeoporesis of paralysis, while trauma can cause it and neoplasia can cause it, typically, historically in the literature, we've said it's idiopathic, we didn't understand the mechanism. We now know by doing nerve conduction velocity studies and muscle and nerve biopsies that many of these dogs have an underlying systemic polymyositis or polyneuritis. Now, it's been characterised most carefully in the Bouvier, but it happens in most larger breed working breed dogs when they get a little later in life.
If you actually did try to diagnose polymyositis or polyneuritis, you'd find it to be true. It turns out that's one of the reasons about 40% of dogs with laryngeal paralysis have coexisting esophageal motility disorders, because it's actually a systemic disease. But for purposes of today's talk, We can't, it turns out, effectively treat the polymyositis or the polyneuritis.
So we are left with treating the laryngeal paralysis itself, and that's what we'll talk about. This is a picture of what would have been a movie showing, in fact, This laryngeal area is moving. This one is straight up and down, so you have unilateral laryngeal paralysis.
In the next picture, picture shows that it's bilateral. Here are the religion of folds. Cartilage, cartilage, and you have a glottic opening, which is really quite small.
Now, the treatment of this at some point will involve surgery, but when you examine the effect of a narrowed glottic opening on the respiratory mucosa, it turns out that while you get harsh breathing and a voice change, and the dog who becomes exercise limited, what you actually see. When you look into laryngeal opening, even grossly, is enormous erythema and swelling. And I think you can appreciate that on this view, but I'll show you another one.
If you take a look at this laryngeal vault, you can see the enormous areas of inflammation in the respiratory mucosa. Now that's not because of infection, but what happens is when you have a narrow glottic opening, airflow instead of being normal, smooth and laminar, becomes turbulent. And t with airflow causes edoema.
And then what happens is with a small hole, the speed of air actually goes up. And when the speed of air goes up, pressure drops, which means that the laryngeal opening will get more narrow, turbulent airflow will get more turbulent, and edoema will get worse, and that further narrows the airway. So the value of using Anti-inflammatory drugs is not, of course, a long-term solution.
But as a short-term solution, Until and unless the dog is treated with surgery, using an inhaled steroid significantly decreases that inflammation that you're seeing and the subsequent edoema of the tissue, which causes small but significant openings in the glottic airway, and that makes it easier for them to breathe. Now just parenthetically, when we treat dogs with paralysis with anti-anxiety drugs, It's really the only disease I can think of, for which the body is responding to a problem in the respiratory system by increasing air flow, and by doing that, they're increasing the respiratory rate and effort. This is the only condition where you don't want that to happen.
So, if a dog has pulmonary edoema, they're breathing harder and faster, that's appropriate. If a dog has heart lung infection and they're breathing harder and faster, that's appropriate. But in the case of laryngeal paralysis, If they breathe harder and faster, they force the airways to get more narrow, and the harder they breathe, the more narrow the hole gets, the less air they're getting, and the more the tendency to breathe harder and harder.
So, it's just ironically, in this particular disease, using anti-anxiety drugs to decrease their anxiety so that they breathe less forcefully. It's the one situation that's actually in their best interest to do so. So, the point of treating sial paralysis, of course, is to fix the glottic opening, and that requires surgery.
But until that occurs, it's surprising that a very small change in the size of the glotticc opening by reducing the mucosal edoema has a very significant effect on how much air is getting through the glotticc opening. If we move now down to the trachea, we're facing the same exact thing. What I mean by that is it's a mechanical problem, isn't it?
When we talk about tracheal collapse, we're talking about a structural deformity in the tracheal cartilage. So that the rigid cartilage, which should be a rigid tube, now becomes rubbery, and now rather than the tube staying open during inspiration and expiration at sleep and during exercise, now that deformed cartilage, which is rubbery, now can collapse on inspiration. So if that's a mechanical problem, what would be the role of anti-inflammatory drugs?
This is a classic description of the four grades of tracheal collapse, and as you see grade 123, and 4, you go from very mild narrowing of the trachea because the tissue above it is starting to get pull out and start to collapse. As that falls into the tracheal opening, you see in the last stage of trachea collapse, basically, the top and the bottom walls of the trachea can actually touch, and I'll show you a better picture of that now. A, B, C, and D are different stages of tracheal narrowing as a result of this disease, and A is the least affected area where if you follow the mouse, you can see the dorsal tracheal membrane is flattened because it's being pulled.
As you go to the bottom of the cartilage, you can see that the dorsal and tracheal walls actually can touch. That's the part of this disease for which you can make some difference by anti-inflammatory medication, because as the top and bottom walls of the trachea touch, it creates tremendous inflammation. This is the picture endoscopically as you get to the carina of a trachea, and on our left is the dog's right main stem bronchus.
On our right is the dog's left main stem bronchus, but from the top down, I'm showing you with the arrow, the dorsal tracheal membrane splitting into the dog's right and left side. But really what I wanted to emphasise is the redness of the tracheal mucosa. It typically is not like that.
And so the redness is the result of certainly when you get down into the lower airways of the complete collapse of the airways so that the dorsal and ventral membranes are touching, that causes tremendous inflammation which stimulates cough receptors to cause more coughing. So while it's true that the treatment for tracheal collapse isn't really just steroids, let me go through what it really is for. First, I'll just argue that, and this is controversial, but I'm pretty comfortable with this, bronchodilators aren't really indicated in this disease because it's not a disease of bronchoconstriction.
This is a structural problem with the cartilage weakens and it pulls the dorsal tracheal membrane out and eventually the dorsal tracheal membrane loses rigidity and just falls passively into the lumen of the trachea. But that's not a disease that bronchocon, that's caused by bronchoconstriction, and bronchodilation is really not something that's gonna help these patients. Really, what the dogs need are cough suppressants so that they can let the mucosa heal and become less susceptible to inflammation.
If that doesn't work, at some point, if you give up with mechanical with, medical attempts to treat mechanically, we always can go to stenting and that's certainly the topic of a different evening. But for purposes of this conversation, the reason why inhaled steroids are helpful even in this case is because again, you're avoiding the complications of systemic use of steroids, but you're directly dealing with the inflammation within the tracheal mucosa, which is stimulating cough receptors to cause more cough. So the combination of the inhaled steroids to reduce the inflammation in the tracheal mucosa and cough suppression can often be the medical management that you're really looking for if you're trying to avoid having to have a dog go through stenting.
And finally, of the diseases that we talk about that I guess we're most commonly interested in using steroids, it would be chronic bronchitis in the dog. When we talk about bronchitis, people often use the word COPD, chronic obstructive pulmonary disease, and that's a term that really is much more appropriate for human medicine. While the COPD syndrome involves asthma, bronchitis, bronchiectasis, and emphysema.
Because people smoke cigarettes, the typical COPD patient in people is a person who has chronic bronchitis and emphysema. But it turns out that emphysema, which is a disease typically caused by cigarette smoke, is rarely, rarely a clinical problem in our canine population, and dogs don't get asthma. So when we use the word COPD, actually, what we're talking about is chronic bronchitis.
Now, when we talk about chronic bronchitis, think about for a second what's happening. The lung is the vital organ. The lung is pal.
The lung is where gas exchange occurs. So nature has provided mammals, the patients that we take care of as well as us, with a couple of protective mechanisms to protect the lung. And the way they protect the lung is by putting reflexes into the airways, which is what the bronchi are.
Bronchi are tubes. They don't do anything else except allow air to go from outside the organism into the lung. So it's really just plumbing.
And what nature has provided these tubes reflexes are, is number one, if something enters the bronchi that could be harmful to the lung, mucus is immediately secreted to trap that harmful substance. The second thing that happens is a cough expels the bad material. In some species, cats and people more specifically, the third reflex is bronchoconstriction to narrow the hole that the bad thing could get through to get to the lung.
But that third part doesn't happen typically in dogs as a species. So what we're looking at is increased mucus production and cough. Which is exactly what we see in chronic bronchitis.
Now, the tricky thing about chronic chronic bronchitis to recognise is that it's not chronically due to infection. And I wanna say that again, in people who get chronic bronchitis, the smoking has caused tremendous damage to cilia and to the ability to secrete secretory IgA. That's not the problem in the dog.
So we don't know what the cause of chronic bronchitis is in the dog. We do know that they don't get chronic bacterial infections as they do in people, which is why antibiotics are really not the primary treatment for chronic bronchitis. Bronchodilators I mentioned earlier, also not indicated because as a species, dogs don't really bronchoconstrict all that much.
So, because this is an inflammatory disease, here we are talking about anti-inflammatory drugs. This is a disease for which the primary treatment is not surgery, the primary treatment is corticosteroids, and if you give them by the inhalation route, they are as effective as systemic steroids without causing any of the side effects. And of all the disorders that I've mentioned so far, this one is most satisfying to treat with anti-inflammatory steroids, cause it can be a single treatment to cure the symptoms.
Once the inflammation is controlled, then it makes sense if you need to, to use cough suppression. But if the inflammation is not controlled, it's not in our patient's best interest to stop the cough. Because the cough is the protective mechanism that's allowing mucus to be expelled.
And if we only treat the cough, but we don't treat the inflammation, mucus is still being made, it's just not being expelled, and it winds up building up more and more into the tracheal tree and the bronchial tree. So if we highlighted a whole number of chronic respiratory diseases for which steroids make sense, the use of inhaled steroids for me has been something I've been excited to use for about 20 years or so because of the one difference. It is equally effective to systemic steroids, but it doesn't cause the side effects, the polyuria, the polydipsia, the increased hunger.
The behavioural changes, the tendency to urinary tract infections and skin infections, and it has no effect on insulin sensitivity. That's the advantage. So let's talk about that for a little bit.
Why do we use a drug called fluticasone? Well, there are any number of inhaled corticosteroids available on the market, but it turns out of all the inhaled steroids, fluticasone is the most potent steroid of all that they're available. And there's a test that in In these kinds of studies, one of the very basic tests is called the McKenzie skin blanching test.
That's not important. It's just to say that these kinds of things are studied pretty intensely, and it's pretty clear that fluticasone is the most potent corticosteroid by inhalation that's available. So, that would be the first reason to use fluticasone.
And the second reason is when they look at the half-lifes of these drugs, it turns out that Flovent has the longest half-life, which means it lasts longest. And clinically, what it's important to us, of course, is that because you need to use less of it. Typically, when we talk about dosing in a minute, we need to use it twice a day rather than 3 or 4 times a day.
And after a while, many of our patients can do very, very well with once a day inhaled administration of Clovi, which makes it even more convenient. But there are 3 reasons why we use fluticasone. The first is because it's the most potent.
The second is because it lasts the longest, and the third is because it doesn't get absorbed. Now, what does that mean? Well, I've been making the point that the value of inhaled corticosteroids is that they don't get absorbed, so you don't get side effects.
But in fact, when you or I or a dog or cat inhales fluticasone. About 70% of it impacts on the back of the throat where it condenses and winds up getting swallowed. So this material winds up in the gastric glucosa, which is a good absorptive surface, and it turns out of all the inhaled corticosteroids, Flovent is the largest molecule with not very lipid, it's lipid soluble, but it has a strange pH and all that means is that it doesn't go through the gastric mucosa.
So of all the inhaled corticosteroids, the one that's least likely to be systemically absorbed at all is fluticasone. So, it's the most potent, it lasts the longest, and it's the least likely to be absorbed, and that's really why we chose that for all the studies that we did. So that's what it looks like and it comes in what's called a metered dose inhaler.
And I think you can see on the right of the screen, that's what these things look like. Now, the history of these drugs is that the metre dose inhalers have been used to treat respiratory conditions since the 60s. So it's not new information, it's been going on for almost 60 years.
It's only in the last 15 or 20 that we've started applying the same technology to our patients. And the reason we use it just to summarise it is it's the most effective long-term treatment of persistent canine non-infectious airway disorders. It reduces chronic inflammation without causing those side effects, and you may read it in the literature as referred to as a preventer or a controller medication.
Now of course, the problem with mutter dose inhalers is that we're talking about dogs and cats, so we don't have any compliance. Now this is a picture of a young girl when I was at the University of Chicago, who was being treated for asthma. And when you consider the fact that infants and small children don't comply any more than dogs and cats for purposes of this particular medication, they had to come up with a way of getting these drugs into infants and children, and they did what's called a spacer.
And as you can see in her hand, she's holding the end of the spacer where the metre dose inhaler is. This plastic tube is the spacer, and this mask over her nose and mouth simply allows the little girl or her mom to press down on the metre dose inhaler, so that the drug goes into the spacer, and whenever she breathes, it'll go into her respiratory tract. More recently, for those of you who have conditions for which you need inhaled medications or your family, you know they use dry powder inhalers rather than the metre dose inhalers, but it turns out this mechanism of giving inhaled medications really is not amenable to our patients, and you just know the picture of a disc inhaler, but in any case, the dry powder inhaled drugs are not something we can get into our patients, which is why we continue to use the immediate dose inhaler.
That don't give up on me now because at the end in a couple of slides, I'm gonna show you what this cost and if you had the sense that it was a very expensive treatment, it turns out it isn't anymore. Now, why do we use a specific Device for this purpose. It turns out I do use the Aero Academy Aerodog made by Breathe Easy and Trudell for a very specific reason.
It's a chamber that is more effective at getting drugs into our patients because it was made for our patients than other spaces made for people. And the reason that's important is singular. If there's a more effective way to get drug into our patient, it means we need less drug.
If we need less drugs, it means it costs less, and that's really overwhelming concern when we're trying to use this therapy. Because frankly, getting inhaled drugs into a dog is very simple. If you've tried it in cats, it's a little more challenging for a lot of reasons, but dogs adapt to this very, very easily.
So, to get to the end of the conversation and then we'll open it up for questions. What's so interesting about inhaled steroids is this, in terms of dosing. We know that when we take pills, for example, to know how much of a drug we should take and how often they've done any number of pharmacokinetic studies.
And if they haven't done it in dogs and cats, we extrapolate what we know in people to our patients, and that's the system that we use. But inhaled steroids aren't really studied in terms of pharmacodynamics in the sense that the amount of drug if you inhale 220 mcg, what percentage gets into the mucosa, it really isn't studied with any sort of rigour compared to Where pharmacokinetic studies of pills are done and all that is to say, whether you're a 5 year old child who weighs 60 pounds or a man like me who weighs 220 pounds, if you have asthma, they put you on about the same dose of Ventolin or Proventil. If you have asthma, for the steroid, they'll put you on some combination, maybe 125, up to 250 mcg, 1 to 3 times a day, and it's all actually completely arbitrary.
And one of the reasons they can do that is because it doesn't matter how much is given, you really can't overdose a patient with inhaled steroids, and there are really no side effects to it. So it really comes down to what's practical and what's cost-effective. And that is just to introduce the idea that for all the diseases that I mentioned, going from the nose down to the bronchi, whether it's a 30 pound dog or a 150 pound dog.
It's kind of arbitrary on one level to say how much we should give, as it is if you're treating a 5 year old child or a 40-year-old adult. And what it turns out that we do know is true is that if it's a dog, 10 kilogrammes or less, the aerocat device that's made for cats is a very effective delivery system for the dog. Dogs that are more than 10 kilogrammes benefit by using the aerodog spacer because aerodynamically, it allows more drug to be distributed to the airway of the dog.
We do know that's true, but in terms of the dose, whether it's lymphocytic plasma cytic rhinitis or reverse sneeze or laryngeal edoema or tracheal edoema or the bronchial inflammation, the dose is about the same. Fluticasone comes as 110 mcg per puff in the United States. It may be 125 in England.
And so that's a reasonable starting dose. One puff into a spacer allowed the dog to breathe 7 to 10 times and you do that twice a day. Now, it takes about 7 to 10 days to reach its full effect.
So if you find after 7 to 10 days, you're not getting the effect you expected, it is likely a dose phenomenon, which means you can go to 2 puffs of the 110 or 125 mcg dose twice a day, or you can order the bigger size. It also comes as 220 or 250 mcg depending on the country, and you can use that once a day, I'm sorry, one puff twice a day. Depending on how the responses, but really, to try to be more clear, the dose is not as dependent on the size of the patient as it is on the response to therapy.
So to be conservative, you start at the lower dose, one puff twice a day, you can go to larger dose one puff twice a day, and the only difference really is that it costs more, which is why we tend to be more conservative to start with. We remind ourselves also that it's easier to prevent symptoms from occurring and reverse them once they appear. What that means is if the patient is doing well on inhaled steroids and you lower the dose and the symptoms come back, it takes a while to get them back to where their symptoms are doing much better.
So typically, when I have patients on inhaled steroids that are doing well, if the owners are OK with the dose and frequency and cost, I keep them on that for long periods of time. Now, in terms of cost, it turns out in the UK 125 mcg canister is about €45. And the canister has 120 puffs.
So if you're using one puff twice a day, That turns out to be 60 puffs a month. So a metre dose inhaler will last 2 months. So that means if it's €45 and you divide it into months, it's about 22 or €23 per month, which isn't inexpensive, but it tends to be something most owners are able to afford nowadays, at least I'm very lucky in the world that I live in, that cost is something most of our clients can tolerate.
So it turns out it's a very effective delivery system in the dog. It's easy to administer cause dogs don't fight the mask nearly so much as cats. It tends to be very effective without causing any of the side effects.
It's available for a whole host of inflammatory conditions and the respiratory mucosa, and it turns out it's not as expensive as it used to be in the past. So with that, I'm gonna stop. I'm gonna open the conversation up for whatever questions you have, and I, in advance, genuinely thank you for your time.
I thank Breathe Easy for their sponsorship at Trudell, and I want to remind everybody that this mechanism of delivery works very effectively and it's Most effectively delivered through the Aeroca and the aerodog because Breathe Easy and Trudell spent many years examining what the most effective delivery system would be for dogs and cats, and for that I'm very happy to be part of their. Network. All right, thank you.
And let's open this up for questions now. Thanks, Phil. That was absolutely fascinating.
Folks, I promised you a great presentation and Phil hasn't let us down. So thank you so much. Before we go to questions, I just want to remind everybody, when we are finished here tonight and we close off the presentation, your browser that you logged in with will have a survey monkey on it.
Do us a favour. Give us some feedback both on the, the topic tonight as well as other topics that you would like to hear. Remember that the webinar vet is your channel and the more feedback you give us, the easier it is for us to know what it is that you are, are wanting us to present.
Phil, I can tell you that we have loads and loads of comments coming through and a lot of them are saying thank you and fascinating. And really people are appreciative of your time tonight. So thank you very much.
There are some interesting questions and I'm going to ad-lib some of them because some of them are very similar. What would be the role of NSAIDs in chronic respiratory disease rather than steroids? Well, I think we're pretty familiar with the fact that the role of the NSAIDs typically is to block the prostaglandin pathway.
And if you start with the racodonic acid, the two pathways that are typical goes down into the prostaglandin pathway and the leukotrian pathway, neither the prostaglandins nor the leukotrians appear to be particularly important in the generation of inflammation in the canine respiratory tract. In people who look a train pathway, at least for asthma, turns out to be very significant. And in fact, people that have what's called exercise-induced asthma, including Olympic athletes who sprint, they typically during exercise can have an An episode of bronchoconstrictions.
So those people typically will pre-treat with the bronchodilator because they get that form of asthma, and that's because of leukotrians. So the long-term treatment for these people are drugs that block leukotrians or the receptors. But in the dog as a species, that mechanism doesn't seem to play as much of a role.
And we're pretty clear that the prostag glandin pathway doesn't play a role either. So the long answer to that question is, NSAIDs in these conditions in the dog probably not a very effective form of therapy. Following on that, the question has been asked, what about Apaquil if we're dealing with allergic conditions?
Well, you know, Abacol has been studied. It's not been studied as an inflam anti-inflammatory in the respiratory system so much as in the skin, but The only reason I'm not wholeheartedly advocating is because I just don't have the experience with it. And there aren't many people who've actually published, well, say it more than that.
I don't think there are any publications, maybe one or two, that talks about the role of Apaquil in treating inflammatory disorders in the dog, so I'm just a little hesitant to say anything about it. OK. Interesting phenomena again is obviously the Boers syndrome, syndrome that we see.
Questions varying about the use of inhaled steroids for controlling the symptoms of boas and also as a, your opinion on using it as a pre-operative treatment. Well, let me get the second answer first. Inhaled steroids are not a drug to use in the acute setting because they take about 7 to 10 days to reach full effect.
Now, the fact that they don't get absorbed is the reason why they take so long to work because they're giant molecules, and that's why they don't get into the bloodstream. It's also why it takes 7 to 10 days to get enough of a concentration mucos to be effective. So, as an acute scenario, I probably wouldn't advocate inhaled steroids.
But brachobolic airway syndrome, remember, it's some combination of elongated palate and glottic edoema, and maybe some of the The folds, come out of their crypts and, and block the area a little more. So there is inflammation involved in that. Now, because the brachi area syndrome is such a dramatic, disease when I see it, I really am an advocate for surgery to open up the nasal cavity and to shorten up the soft palate, and in that setting, I don't typically use inhaled steroids very much.
But having said that, If you have a brachocephalic patient, that is snoring at night and is making all kinds of noise and during exercise and maybe the exercise limited, you can assume that the soft palate and the glottic opening is einous. There's no question to that. And by using inhaled steroids, if you decrease the inflammatory component and the mucosal edoema by even 1 millimetre.
It's surprising how very small changes in the size of a hole produce big changes in how much air flow can go through. So I certainly wouldn't recommend inhale steroids as a primary treatment for BOA, but until and unless they're gonna go through surgery, that is one effective form of decreasing at least the edoema associated with the disease. Excellent, thank you.
Rebecca has an incredibly good question. And she says, as the absorption rates of inhaled steroids are so low, are they safe to use with oral NSAIDs in patients? Oh, what a great question.
So, absolutely, now, when I say that, I don't know absolutely that's true in dogs. I know that's been studied in people for at least 30 years. And then on my own experience when I've had dogs with arthritis on Corofin will also have had bronchitis and I've treated with the inhaled steroids because I had a respiratory only practise and because I was able to see all these patients on return visits, I'm very comfortable that I never saw a complication associated with gastric erosion, ulceration, etc.
I'll also say to segue on to that. Even in cats, just to say we have to cats for a second, in the face of an active herpes infection, you can use inhaled steroids, and one of the examples that's used is in people where you can have bronchiolitis obliterate in infants. Which is a viral disease which causes secondary severe bronchoconstriction, bronchial narrowing in those children with active viral infection, they use inhale steroids.
So it's an excellent question, and because it isn't systemically absorbed, it really doesn't affect the body's ability to. By primary infection, which makes it a beautiful treatment as well for patients with diabetes. What better way to use steroids in the diabetic patient as in inhaled steroids where it's not absorbed, it doesn't cause insulin resistance, and it doesn't change the response to insulin.
Fantastic. Lauren's got a good question. She says, do you ever recommend nebulizing with water to keep nasal mucosa moist in chronic rhinitis cases?
Oh, absolutely. When I was a child, if I had a cold, my mother would boil up some water and put my head over the boiling water and cover my head with a towel so I can inhale the fumes on me and the, the secretions coming up. And we've taught people for many, many years to take their cat or the dog into a bathroom, if it's small, run the shower very hot and let that act as a sort of a, a nebulizer.
Now, in truth, it's unless you actually Buy a nebulizer where you're decreasing the particle size to 5 microns or less, it's really a humidifier, but having said that, that's very helpful. One of the reasons it's helpful is because not necessarily that it liquefies the secretions so much as it liquefies the area around the secretions and stimulates sneezing, which makes it easier to get rid of the mucus and the nasal cavity. But that's one of the most time-honored and least expensive ways to try to make our patients more comfortable.
That's, that's a great question. Mark has asked a question and I think you've covered half of it already, but I'm gonna give you the whole question. He says, typically how long do you sustain first line antimicrobial therapy to ensure primary bacterial components can be excluded before initiating steroid therapy?
So that's a great question, and I guess the, the real question is, when I see a patient with chronic nasal discharge. And it's not been going on for 2 years, it's just been going on for a week or two, and you don't think it's a tumour because it's a young dog, and you don't think it's a 2 or abscess because the dentition spine, etc. And you're just wondering, is this some sort of short term or to tell a response or an allergy or something?
That's all very reasonable. I don't have a precise answer in the sense that there's never been a study to show what the answer is. I can only give you my experience.
If a dog has had a nasal discharge more than about 3 or 4 weeks, I've never seen a patient like that, that has been the result of a bacterial infection. Dogs don't really get upper respiratory viral infections that last for a month, and allergies, typically, the one time you can look at mucus and try to determine it. When the discharge from the nose is absolutely clear, it is much more likely to be an allergic phenomenon, and that's only because with infection from virus or bacteria, the dead neutrophils are what gives it its green or yellow or grey colour.
So green or yellow doesn't tell you it's a bacterial infection or a viral infection, but very clear discharge does suggest it's gonna be allergic. So if it goes past a month, and I'm not getting response certainly with antibiotics, I stopped thinking that there's a bacterial component to this. It's not a perfectly satisfying answer because it's really just based on my experience, but it's the best I have to offer.
Is another couple of questions that I'm gonna paraphrase because they all relate more or less around the same way. Would you ever consider initiating inhaled steroid therapy without a workup just to monitor response? So again, it, these are, these are the best questions.
I appreciate this. In our profession, it is not uncommon for us to make a diagnosis as by the response to treatment. And when we do that, we just have to be pretty clear that we're not doing harm.
So, well, I wouldn't typically use high doses of oral steroids to try to confirm a presumptive diagnosis. One of the interesting things about being on steroids again, one of the primary values is they don't get systemically absorbed and I've said that many times so that you can believe me, people have actually studied the HPA axis before and after inhaled steroids, and there's really no effect on the HPA axis, which is really the most important question when you're trying to figure out if there's going to be immunosuppression. So we're pretty clear that whatever absorption occurs with luticasone.
It is not likely to cause any sort of immunosuppressive effects. And that's why in this particular case, If you think you have chronic bronchitis in the dog, and use inhaled steroids and they get better, well, they got better because they had chronic bronchitis with an inflammatory component, and I don't say that facetiously. Having been in a pulmonary department of the medical school for 11 years, I can tell you it's extremely common if a physician thinks the patient has asthma, to start them on inhaled steroids and the bronchodilator for 10 days, and if they Get better, the presumptive diagnosis is asthma.
If they don't get better, then they work them up further. But that's not an unusual way to try to determine the inflammatory component of airway disease as long as you're not really concerned that they're very, very sick or they're getting worse, or they're systemically ill, but they're just presenting with signs that are referable to airway inflammation. That's one of the few times when it's not an unreasonable thing to try.
Excellent. Alistair's got a question. It's not really about inhaled steroids, but it does fit in with our respiratory theme tonight.
And he says, I have been told that furosemide stops small breed dogs from coughing because it has bronchodilatory effects, giving widespread false impression that we have been successfully treating congestive heart failure for years. A similar question arises really anti-cough effects of xanthines. Could you please comment?
Sure, let me use the Xanthes first in people. So we'll go there first cause there is a very big difference in the human airway's ability to constrict versus the dog. People and cats get naturally occurring asthma.
Dogs don't. If you try to cause bronchoconstriction in the dog, it's not easy to do. And when you measure by pulmonary function test, bronchoconstriction in the dog with bronchitis or congestive heart failure, it's really minimum, and they really don't, when you actually study this, they don't really respond to bronchodilators.
So, When you use Xanines, if you had asthma, one of the reasons why you're coughing is because if the airway contracts, it stimulates cough receptors. If you use methylzamines to relax the air was of muscle, you reduce the stimuli on the cough receptors and you decrease the cough. So that's one of the mechanisms in people with asthma.
But in dogs, because they don't bronchoconstrict, I don't use bronchodilators primarily, and I don't have experience of using methylxamines will reduce the cough in the dog with chronic bronchitis. So that's the second end of the question. The first thing the question has to do with furosemide, and I certainly wouldn't represent myself as an expert in furosemide pharmacodynamics or and I'm certainly not a cardiologist, but I will tell you what is true, and I learned this when I worked in a cardiac care unit in human medicine, many, many years ago.
Intravenous Lasix drops pulmonary artery press. And that may not have an all a real big deal effect on dogs walking around with chronic bronchitis unless they have secondary pulmonary hypertension. And again, the furosemide effect on the pulmonary artery was not when it was given orally, only when it was given intravenously.
So that I'm pretty comfortable with, but whether or not furosemide has a primary effect on cough. I just don't think that's true. I don't think there's little to support that, and I'd be very interested in learning more about that if there is good data to support that idea.
Thanks, Phil. A lot of questions coming through about the steaming and nebulizing with water and everything else. Loads of different questions about do you put anything in the water, ranging right through the whole spectrum of oils and and various products.
Sure. When we were dealing with, quote unquote Kenov 40 years ago. And there were not good oral antibiotics to treat these diseases, we had gentamicin and Amicain.
People were using aerosolized gentamicin a long time ago to treat these patients because by aerosolization, it didn't cause the systemic side effects that gentamicin causes on the kidney, etc. So we learned to use nebulized drugs many, many years ago to treat quote unquote kennel cough. Since then, because we have so many good oral antibiotics, we've pretty much stopped nebulizing or humidifying gentamicin.
But to get more specifically to this question, when you use a humidifier, you have humidification and it only affects the upper airways. If you had a nebulizer and you attach it to an endotracheal tube, it wouldn't be much condensation and you could get nebulized drugs into the lung. But that's not what we're doing.
We're talking about awake patients, not intubated patients, and oftentimes you're not even using a nebulizer. So recognise that what we're aerosolizing, mostly get condensed in the back of the throat and you're affecting mostly the nasal cavity. If you wanted to use bronchodilators, for example, you can get away with those if you knew what dose to put into the water that you're humidifying.
But when you're talking about antibiotics, it's just not an effective delivery system compared to oral antibiotics, and we have enough familiarity with oral antibiotics to be reasonably comfortable with their use. When you talk about other substances, I am truly ignorant. I'm not, excuse me, an expert on the subject, and they may be very effective.
I just don't have any experience to comment on. Excellent, and that's fair enough. Folks, I'm afraid we have run out of time.
I'm sure we could carry on and on and on tonight with all the various questions and I have absolutely no doubt that Phil would have all the answers for us. But as I say, we have sadly run out of time. So Phil, it is my absolute pleasure to thank you for your time tonight.
And the comments have been coming through about how amazing it was and how much people have learned. So thank you once again for giving us your time tonight. You're also very, very welcome and I appreciate your attendance and your attention.
Folks, that's it for tonight. And once again, thank you so much to Breathe Easy for their sponsorship of tonight's webinar. And don't forget to fill in that survey monkey for us.
Give us some feedback and give us some ideas about other topics. To my controllers, Rich and Paul in the background. Thank you for all your help tonight.
And from myself, Bruce Stevenson, it's goodnight to everybody.
