Hi, my name is Doctor Adele Williams. I am an RCVS and European recognised specialist in equine internal medicine, and I did my PhD on equine asthma. I'm head of equine at VETAI and I'm a specialist consultant for virtual veterinary specialists.

I've worked throughout my career in equine academia and equine first opinion practise, all over the world. And I'm gonna do this presentation today on management of equine asthma. So the synopsis for today's webinar is that we will review the evidence base for the management of equine asthma, and that will include a basic pathophysiology overview to help you understand the triggers management and treatment choices.

We will review, peer reviewed evidence for environmental triggers. And their management. We'll review the usefulness of diagnostic tests and also peer reviewed evidence of treatment options for equine asthma.

And we just go over some myth busting, of equine owner beliefs for treatment and management of equine asthma. So for the learning objectives, at the end of the webinar, I'd expect you to be able to appraise environmental triggers of equine asthma, recommend improvements for air quality in an asthmatic horse's environment, choose appropriate diagnostic tests and understand how to interpret their results. Debate with clients where some treatment options are not suitable, and design an appropriate treatment plan for asthmatic patients using peer reviewed evidence.

So, starting with an an overview of equine asthma and the pathophysiology, equine asthma syndrome is a term officially adopted to encompass all reversible allergic and inflammatory airway disease in horses, the symptoms of which can be transient or long standing and range from mild to moderate to severe. This includes the diseases previously referred to as inflammatory airway disease or IAD and heaves or recurrent airway obstruction RAO at opposite ends of the spectrum, and they should all be considered a continuum along a spectrum based on the severity of the clinical symptoms. Asthmatic exacerbations or flare-ups represent acute and chronic worsening of airflow obstruction.

In asthmatic horses. Exposure To inhaled environmental triggers leads to an inflammatory response in the airways. This includes inflammatory cell infiltration, which is usually neutrophilic of the airways, airway smooth muscle contraction causing bronchoconstriction, and mucus secretion into the lumen.

These factors act synergistically to reduce the effective available airway lumen diameter available for airflow to and from the alveoli. This can impact on alveolar gas exchange, and the resultant increased blood carbon dioxide concentration drives hyperventilation. The muscular effort required to expel air from the lungs is increased due to the reduced functional luminal diameter, and the abdominal muscle muscles are recruited along with the intercostal muscles and diaphragm.

The resultant clinical signs of exercise intolerance, increased effort and rate of breathing, cough, nasal muccoid discharge, and a heave line are attributed to the reduced airway lumen, increased mucus in the airways, inflamed irritated mucosa, and increased effort of respiration with continued exposure. Airway mucosal remodelling occurs, inducing airway smooth muscle hyperplasia, increased numbers of mucus producing goblet cells within the epithelial lining and deeper submucosal secretory cells. And increased vascular permeability.

This makes airways hyperreactive, rendering chronically exposed asthmatic horses vulnerable to exaggerated airway responses to any inhaled environmental trigger, including allergens, viruses, and pollutants. If you look at the sort of schematic graph figure that I've created here, on the left there's a healthy non-asthmatic horse's airways, which will only be pushed over their threshold into an inflammatory airway response by an abnormally high load of inhaled environmental triggers. Of course there's no allergens for for a healthy horse because they're they're not allergic to, to things that they're breathing in.

In a on the right hand side of the graph, there's a chronically exposed asthmatic horse will have a hyperreactive airway so that any inhaled environmental trigger, be it something the horse is specifically allergic to, or any inhaled irritant, will push the horse over its lowered threshold into an inflammatory airway response. So chronic exposure without appropriate treatment and relief over time leads to fibrosis within the lung parenchyma from prolonged increased matrix metalloprotein activity on the lung extracellular matrix fueled by the continued inflammatory insults. Environmental triggers and management.

Triggers in the environment can generally be attributed to exposure to organic dust debris in the air, of which there is usually a strong association with airborne mould in severe equine asthma sufferers. Endotoxin indust has an additive effect to allergens in equine asthma, sometimes being more important in the end in the disease process than the allergens themselves. Equine asthma sufferers have a more profound inflammatory response in their airways to inhale dust and mould than healthy control horses.

There are also a subset of equine asthmama horses that have exacerbations during pasture turnout in summer months. Presumably the triggers in these cases are inhaled environmental particles such as pollens, dust in dry fields and pasture moulds. In human asthma, upper respiratory tract viruses are the most common causes of acute disease exacerbations in adults and children.

In horses, however, the contribution of infectious agents to asthma development and exacerbation remains uncertain. It is highly likely that in some instances, the clinical signs of equine asthma are attributable to generalised hyperreactive airway that overreacts to any non-specific irritant, be that inhaled viruses, bacteria, funguses, endotoxin or other dust particles. No matter what the etiological trigger is that instigates clinical symptoms of asthma, it is clear that maximising the air quality in the individual horse's environment to reduce inhalation of all potential triggers is the primary goal to address the propagation of inflammatory response in the airways.

The practical consideration of this is second nature to us as vets, but it might not be so obvious to clients. Time should be taken to examine the horse's environment and take stock of potential irritants that will be exacerbating the condition. These should be pointed out to the owner and clearly explained as environmental management is the singularly most important part of therapy because it is the one thing, if well controlled, that can prevent initiation of the inflammatory action in the airways.

This should be discussed in depth with the owner and not just brushed over and assumed that they know what they're doing. It should be stressed that if environmental triggers can be kept to a minimum, there will be an improvement in clinical disease. Client compliance with recommendations for environmental management is typically very poor, meaning that clinical signs of equine asthma continue and pharmacological management is needed for longer.

Furthermore, continued exposure to poor air quality and environmental triggers in time leads to airway smooth muscle remodelling, whilst conversely, environmental management to control air quality and allergen exposure will improve lung function. There are some references for this in the PDF to accompany this webinar. So the importance of the air quality of the entire stable yard and barn, not just the horse's own stable or loose box, in having an effect on a horse's asthma symptoms, should be stressed to clients.

It is well recognised that bedding on straw and feeding dry hay will exacerbate clinical symptoms. But what owners fail to appreciate is that if another horse in the facility is bedded on straw or fed dry hay, this will have a negative effect on their asthmatic horse's airways. This can be explained by the fact that most asthmatic horses are particularly sensitive to mould spores, which are in abundance in moist baled hay and straw.

It is important to consider the potential inhalational irritants around the horse's breathing zone, i.e. The nose, which is perhaps why changing forage from dry hay to a low dust alternative such as haulage, pellets, or steamed or soaked hay usually results in better improvements in clinical signs.

Than changing the bedding from straw to a lower dust alternative, this makes sense when one considers that horses spend an average of 10 to 17 hours of their days grazing with their noses in their feed. However, I would still emphasise the importance in changing both forage and bedding. Feeding from the ground rather than feeding from elevated hay nets or mangers aids the natural drainage of mucus from the horse's mucociliary escalator, and this has been shown to help improve clinical signs of equine asthma.

I usually explain to owners that horses would naturally spend most of their day with their heads down on the ground grazing, so it is a very natural way to help them clear their mucus. Consideration should also be given to timings and management practises at the yard that may influence dust and airborne particle movement in particular areas of the yard and at specific times of the day. This is something often overlooked by many owners but can be highly significant in helping to control asthma symptoms.

Suggest to owners that their horse should be placed outside at a significant distance away from stables during and for enough time to allow dust to settle after mucking out, sweeping, and feeding times since human and horse traffic along with manual debris moving practises will all temporarily increase the airborne particle concentration and movement in the air. Secondly, a stable door next to the barn doors may seem like a good option for asthmatic horse, as it's closest to the open doors and fresh air, but it's not so great if this is the main entry and exit point for all human and animal traffic that will inevitably create movement of airborne particles as they pass in and out of the stable block. In equine asthma cases exacerbated by summer turnout, although little can be done to control the outside air quality at a premises, the aforementioned management changes should at least still be implemented to do everything possible to improve air quality for that horse.

Some outdoor summer triggers appear to be very local to a particular yard or field, and sometimes moving a horse to a different premises, even if it's only a few miles away, can help relieve their symptoms. Gonna talk about the usefulness of diagnostic tests now. So diagnosis in practical terms is based on clinical signs and evidence of lower airway inflammation, which may be by confirmation of visual of visualisation of excess, airway mucus on respiratory tracts, endoscopy, and cytology of lower airway fluid.

Under research settings, demonstration of abnormal lung function by lung function testing and airway pressure measurement is also used, but these tests are not widely available in the field. For acute bronchoconstriction, the parasimpatholytic drug atropine, at a dose of 0.01 0.02 mg per kg IV, will give instant bronchodilation and is a crude diagnostic test for the presence of bronchoconstriction.

So if breathing doesn't improve after administration, something other than bronchoconstriction is going on, such as fibrosis in long standing cases. This Remember that we, we don't want to give repeated doses of atropine as it will cause gastrointestinal stasis, and we don't want to cause an impaction colic. The effects of atropine last anywhere between 8 hours and 3 to 4 days in a horse.

And if you don't have any atropine, but you have some hyosine or or buscopan, this could be used to relieve bronchoconstriction, but the effects are short-lived in the horse, so it's not really a, a treatment option for, for asthma, but it can be used as a sort of diagnostic option. So on to airway sampling and the good old debates on BAL or or trackwash. So what samples should you be taking for diagnosing and monitoring equine asthma?

It's desirable, where practically possible to endoscope the airways so that the presence and the amount of tracheal mucus can be assessed and to permit sampling. There are differences between clinicians and their preferences and controversy in the literature and between different parts of the world. Some horses tolerate tracheal endoscopy and tracheal wash without sedation and without the need for local anaesthetic, which is an important consideration for competition horses and makes the procedure cheaper and quicker to perform.

However, some severe equine asthma patients need sedation and local anaesthetic, just to permit endoscopy in the trachea as their airways are so hyperreactive. And to perform a BAL all horses need sedating and local anaesthetic must be instilled to be able to advance past the point of the tracheal bifurcation without causing a severe cough reaction. However, a bowel can be performed with a bowel tube or a long 3 metre endoscope.

So if a, a longer endoscope is not available, a bowel can still be performed. And a bowel tube is significantly cheaper than an endoscope. A track wash can be performed without an endoscope, but that involves, putting a skin lab of local anaesthetic over the mid trachea, inserting a short gauge, .

Hard, 1212 gauge short catheter as an entry guide for passage of a, a 6 French dog urinary catheter to perform the sampling. Either technique is of equivocal technical difficulty, and if a clinician is able to do a track wash via endoscopy or . Blindly, then they should also be able to perform a BAL either using a long endoscope or a bowel tube.

Track wash samples fluid originating from the entire lung fields, whilst bowel samples from one section of one lung only. Bowel is considered to be more sensitive for detecting lower airway inflammation and correlates better with histopathology of the lungs and is thought to be superior for collection and is superior for collection and analysis of mast cells which are rare in the trachea. Track wash is therefore useful for investigation of suspected infectious disease whilst bowel is superior for non-infectious diffuse lung disease such as asthma.

As a general rule, neutral percentages over 5% for bowel and over 20% for track wash samples are indicative of airway inflammation. There are differences of opinion in the literature regarding agreement between bowel and trackwash sampling for diagnosis. One recent study found a good correlation of neutral percentage between trackwash and bowel, with an overall impression that trackwash was more sensitive and specific than bowel for detecting respiratory disease in their study population.

However, several other studies have indicated significant differences in clinical interpretation of results between track wash and bowel done in the same patient at the same sampling time point. My gold standard approach to maximise the opportunity for diagnosis and monitoring is to perform both trackwash and BAL performing cytology on both and then submitting track wash fluid for microbiology investigations if I suspect an infection. Bowel fluid neutrophils are not affected by steroids.

The the neutrophil count isn't affected by steroids because, well, for some reason, airway neutrophils are insensitive to corticosteroids, which is some as yet unelucidated thing to do with the local tissue environment in the lung dictating this because horse blood neutrophils are sensitive to corticosteroids. A positive change in environmental management will lead to a reduction in the bowel fluid neutrophil concentration. Therefore, this is actually a good way to monitor owner compliance with environmental management.

What I suggest, what I normally do is I repeat bowel cytology after a certain period of time. Usually I give them 2 to 4 weeks. And the clinical symptoms of coughing and weaving may have been improved with the pharmacological preparations that they've been given.

But only the environmental improvement will improve the bowel neutrophil picture. So if you find that despite an improving clinical picture, repeated bowel neutriil counts are not changing, it's worth revisiting the environmental management with the owner. Because once they start to tailor off the pharmacological treatment, the clinical signs will recur if the environmental triggers persist.

The owner will blame the pharmacological withdrawal and the use of drug therapy will continue for longer when it wouldn't have been necessary, had they fixed the environment. And so, in, in that way, they won't be resolving the inciting cause of inflammation in the lower airways. So that's, that's a really important message, is, is use your bowel samples for monitoring the owner compliance.

Endobronchial biopsy via endoscopy is really valuable for confirmation of diagnosis of active asthma, but unfortunately, there are not significant histo differences between healthy and remission asthma airways, so it's not currently recommended for day to day practise, we'll, we'll keep watching that field for developments there. And for culture, cultures only indicated when infectious disease rather than just inflammation is suspected. So when you see toxic degenerate neutrophils and intracellular bacteria on your cytology samples.

Trackwa samples must be collected aseptically for culture. And any results must be interpreted in line with cytology and and your clinical picture. You know, do you actually suspect infectious disease in in this horse?

Is it acute systemically unwell with pyrexia, etc. And of its food? Particularly if you culture pseudomonas, it's worth investigating the cleaning regime for the scope and swapping the scope channels, particularly if it's becoming a repeat offender, because, you know, they're normally very, very sick if they've got a, a true pseudomonas pneumonia.

So if, if, if you weren't expecting to culture that, then do check that you've not just contaminated your sample with your scope. So, we'll talk about the treatment options for equine asthma. Now, obviously, I'm not recommending asthma cigarettes for, for anybody.

I just found this, this picture, and I, I just thought it was fascinating that, that at one point, cigarettes were marketed for the treatment of asthma. Anyway, so environmental management remains the absolute mainstay for treatment of equine asthma, and this should be strongly emphasised to clients. And I'm just gonna repeat and repeat and repeat that, really.

But there are always instances where pharmacological treatment is needed alongside this. So we'll start with, My favourite corticosteroids. So, corticosteroids, whether systemic or inhaled, are indicated in severe equine asthma episodes alongside management changes to help improve airway obstruction and reduce airway remodelling, as demonstrated by this study here.

They followed two groups of asthmatic horses over a year and looked at airway smooth muscle remodelling. The groups were antigen avoidance only or corticosteroid treatment group. The corticosteroid group had antigen avoidance for the last 6 months of the year, but not the 1st 6 months of the year, in addition to inhaled steroids.

At the 6 month mark, when the steroid group had not had a change in environmental management, there is a significant reduction in airway smooth muscle mass attributable to the continued treatment with inhaled steroids. However, as I said before, corticosteroids improve airway obstruction, but they have no effect on airway neutrophilia if environmental management is not changed. This is exemplified in the same study I just discussed, where bowelf neutrophil count is dramatically reduced in the allergen avoidance group by 6 months.

And Only reduces in the corticosteroid treatment group when they have also been subject to antigen avoidance management changes as you can see with the highlighted figure at the top of this page. Another study by In the box on the bottom right, that treatment with corticosteroids, whether oral or inhaled, does not affect bronchoalva levage fluid neutrophil count. It's also worth noting when we talk about steroids, the intra-articular and I even trimicinolone will improve lung function in asthmatic courses for 28 days.

So it may be worth considering. In the interim, if obtaining or use of an inhaler are an issue for the owner, well, and the horse. It is thought that the risks of adverse effects of steroids are reduced with inhaled compared to systemic steroids, though, the evidence for that is not actually that strong.

And actually, a review highlighted here examining the evidence for laminitis risk associated with the use of systemic versus inhaled corticosteroids for the treatment of equine asthma, found that corticose Steroid-induced laminitis is a relatively rare occurrence and that although caution should be used in overweight and insulin resistant horses, and those that have had a recent bout of laminitis, corticosteroid use, especially inhaled, is an acceptably low risk for laminitis compared to the benefit for their use in asthmatic patients. So this review basically says. Even if you've got a laminitis susceptible animal, if it's got severe asthma and it needs treating, treat it with inhaled steroids.

For inhaled steroids, then, belamethasone, fluticasone, Budezonide and cycloinide have all been shown to improve lung function in asthmatic horses, and there's there's a long list of of papers from the literature in, in the PDF document accompanying this, webinar. Inhaled fluticasone use can suppress serum cortisol levels for 8 to 24 hours. However, this has not been associated with any clinical significant findings, and prolonged inhaled fluticasone use for over 6 months does not result in immunosuppression.

And anti antibody response to vaccines is not affected. Furthermore, fluticasone combined with the long acting bronchodilator salmeterol has been shown to be more effective at improving asthmatic cause lung function and reduced remodelling than either drug on their own. The only side effect currently attributable to inhaled steroid therapy is adrenal suppression.

And only cyclicinide, which has recently been licenced for use in asthmatic horses in the UK via a nasal misdeploying device, is not associated with this adrenal suppression. So, portable nebulizers, they're expensive, they're very popular. The development of them has increased the interest of use for horses of asthma and has increased the interest in using injectable corticosteroids for the treatment of equine asthma.

However, IV dexamethasone, administered using the nebulizer, so from the bottle into the nebulizer and inhaled rather than given IV, was proven, on this study to be less effective than the same dose given orally, also off licence, which really puts into question the use of this therapeutic approach for severe equine asthma. And I would not be recommending to clients that they do this. We'll move on to bronchodilators now.

If a horse has respiratory distress, they are probably going to need therapeutic, at least in the short term, bronchodilator to improve airway function by reducing inflammation and bronchoconstriction. The best way to achieve this is directly into the lungs we've inhaled bronchodilator and steroids, allowing drug deposition directly where it's needed and minimising the side effects. So, clambuterol, which is a sympathhomimetic beta 2 agonist, has been available for a long time, as oral granules and liquids, for treating horses, .

It also is said to increase mucociliary clearance and has anti-inflammatory properties. However, it should be borne in mind that only 24% of horses respond well at the recommended dose of 0.8 mcg per kilogramme peros twice a day.

More horses respond to higher doses, but they also get more side effects such as sweating and tachycardia. And probably, and this is more important, I would say, and what most people are unaware of, is that persistent use of, clambuterol, as is shown in the graph in this study here, so used for over sort of more than 14 days, leads to down regulation of the beta receptors. Just as a reminder, the beta 2 receptors function to relax airway smooth muscle, dilating and opening the airways.

So that is not a desirable long term goal. We do not want to. Not be able to relax airways, move muscle, and not be able to dilate the airways.

So really, this should be used as a rescue drug only and not as a long term option as a bronchodilator. So oral clambuterol is thus inferior to an inhaled bronchodilator for opening airways in equine asthma. Inhaled bronchodilators include salbutamol, which is, got a very short duration of action.

You'd need to give it every 3 hours, and salmeterol, which is longer lasting, sort of every 6 to 8 hours, so you could perhaps give it 2 to 3 times a day. And it's anti-inflammatory as well, but it is more expensive. I'm just gonna talk about metre dose inhalers and delivery devices for inhaled therapies.

There are some important notes to to think of regarding the metre dose inhaler and the spacer use and training the horse, which should be reiterated to the owner. So, a build up of drug, will happen on the chamber if you're using a chamber over time due to static. To prevent this, every few days, the spaces should be disassembled and washed in detergent, so washing up liquid, and then allowed to drip dry overnight, not towel dry before being reassembled.

And that will stop the static buildup and that will stop the drug sticking to the inside of the chamber and get it into the patient where you need it to be. With the use of the metre dose inhaler, note that each canister contains a limited number of actuations that contain the active ingredient. Some of the newer metre dose inhalers have a counter device, so you can keep track of when they're running low, and that's highlighted by the red circle on on this device here.

In the pictures, otherwise advise the owner to keep a record of the number of puffs used so they know when the drug is depleted. It's worth noting that the MDI will continue to spray even when the drug runs out, as there will be propellant remaining after the last dose is gone. So it's really important to pay attention to the number of puffs used.

When medicating the horse, the inhaler canister needs to be warmed to body temperature and shaken for 30 seconds before use. The first puff should be discarded, and this will contain no drug, just propellant. You attach the MDI to the spacer, keep the keeping the inhaler vertical.

Then ensure the spacer has an airtight seal over the nostril. There's no need to cover the other nostril. Watch the horse's breathing pattern.

Then actuate the inhaler once just before or at the start of inspiration. And then you need to shake the inhaler again before the next actuation. There are various equine spacer and inhaled drug delivery devices on the market, including a new novel equine-specific misproducing device for loceide.

But a human paediatric spacer placed over one nostril works just as well and can be readily and affordably obtained from a human pharmacy and is sometimes better tolerated by some animals than the intranasal mist device. One has to take into account, of course, the prescribing cascade and licenced treatments in any clinical decision making. Products licenced for horses for treatment of equine asthma should be used unless there is reason to not use the product as set out in the cascade.

It is beyond the scope of this webinar to go into detail on the cascade, and you should familiarise yourself with the latest government guidance on the prescribing cascade, which does not take into account individual animal and animal owner considerations. Some horses don't mind the spacer and inhaler, but most do need little training, and there is a really useful video on YouTube on clicker training the horse, which I normally direct owners to for help. Just thinking of some other sort of different types of treatment that are that are coming out and just reviewing some other things now.

Inhaled . CPG immunotherapy. So there's there's a handful of of relatively small studies have shown promise for the use of nanoparticle bound cytosine phosphate, guanine or or CPG therapy, independent of specific allergens for use in the treatment of equine asthma.

These studies. Have demonstrated an improvement in clinical signs in asthmatic horses treated with this. However, each of those studies, which are all written by the same authors has its limitations in terms of sample size, uncontrolled environmental management for patients, and blinded assessors, .

And, and so on. And so although this therapy as promised, the evidence for its use at this stage is not strong compared, example for the evidence for steroid use, which there's lots and lots of publications, on. And so further well-controlled studies are needed to better inform clinicians about their suitability for use in practise.

It is a promising, therapy for the future, but still, environmental management is always the mainstay of treatment. Though longer term respiratory health feeding a supplement which is rich in omega 3 will be beneficial to help reduce inflammation, and most owners after all relish the opportunity to add a supplement to the diet. One word of caution though is that it needs to be.

DHA type of omega 3 fatty acid, and that is not made by plants that that live on the ground, it is, is only available in marine sources, so it's it's made by algae. And so. You need to make sure that you're advising clients to to buy the right stuff.

So if they're buying flax seed source omega 3, it, it won't be beneficial and it won't show the, the improvements that are seen here. So in this study here, these are horses at the controls have just had airway management improvements and the the other horses have, have had the supplementation with this, DHA omega 3 fatty acid, and you can see that the, Owner responses on the cough scoring and and an increase in cough score is an improvement in, in the cough, so less coughing. It increases, more with, with the addition of omega 3 to the diet.

And the owner, perception of respiratory effort is that it's improved, . In, in time, with, with this addition. So, so that's a nice bit of of science to, to let owners know about and permit them, to, to give, to spend their money wisely on on this particular supplement.

So, I'm gonna talk a little bit, about mucus and mucins. You, you won't get away from that with me having done my, my PhD on it. Mucus is made of a, a complex massive cross-linked glycoprotein matrix noses, which are called sort of mucins of the of the molecules, basically, they make this massive matrix.

A basic mucin molecule is a protein core with many complex sugar side chains. So you've got the very basic structure of a mucin molecule in A and then B is what one of these, the side chains looked like. So there's several different sugars added on the side chains.

That's one unit and then this is all folded up together. To, to make this massive mucin molecule. There are strong disulfide bonds within mucins, as well as weaker ionic bond cross links between mucin glycoproteins holding the mucin matrix together.

So within the secretary, mucous cells, and the, Highlighted in this histoic by the circle in the deeper mucous cells and on by the arrow, the epithelial goblet cell, there you can see some nice mm mucus staining inside those, . That the mucins are packed extremely tightly within those secretory cells. And then on secretion, the mutins expand immediately, forming this complex matrix.

I'm just gonna So. So this is a really interesting video of, of a hagfish. And they just take a little bit of, mucus from this hagfish and add it to a, a beaker of water.

And then you can see what the, the addition of water does to the, the small amount of, of mucin. So it's a really good way to visualise what occurs on mucus secretion and what the addition of Salt water essentially or saline does to to the the volume of a mucin, it massively increases the volume. So why am I talking about, about mucus and mucins?

Well, mucus is a large part of the physical blockage of the airways in asthma. So it's attractive to look for ways to break up the mucus and remove the mucus that's adding to the blockage of the airways. So, what about mucolytic agents?

So there are various muolytic agents in widespread use in asthmatic causes, but should they be, do they do any good? So, oral drexene, which you might know as stulosin, is a phenolic benzyl amine, and it's theorised to change the glycosylation of the sugar side chains of mucin glycoproteins and thus, in theory, alter the mucous viscosity. Unfortunately, the one paper by Matthews, Hackett and in 1988, examining its use in horses is methodologically flawed, and subsequently no further scientific evidence has been published to support its use in asthmatic horses, so that's.

Not one that I that I recommend at all, to owners because it's not proven to do anything, to help with the mucus. Another thing that people are interested in is inhalation of an acetylcysteine. So an acetylcysteine acts via its free sulphur hydro group to break the disulfide bonds in the mucins.

Thus, this action on mucins partially breaks up the mucin matrix. And unfortunately, although this works in vivo. There's yet to be any good quality controlled research demonstrating the effectiveness of inhaled acetylcysteine in asthmatic horses.

The next thing I want to talk about is inhaled saline, which is extremely popular in the, asthmatic horse owning population of clients. But, so going back to the hagfish video, when mucins mix with water or saline, some cross links within and between the mucin molecules are altered, which leads to expansion in terms of size and volume of the glycoproteins. Now this mucin expansion is theorised to reduce the mucus mucous viscosity, and thus the theory that inhalation of saline will reduce the viscosity and aid the expulsion of mucus from the airways.

However, if the mucus volume is being expanded, what if it's expulsion by the mucociary escalator doesn't become easier, then in effect inhaled saline is causing mucus to expand within the airways with the danger of worsening the blockage of the airways. There is no scientific research to support the use of inhaled saline in asthmatic horses. There is nothing published which tells me that probably it doesn't do any good.

And furthermore, a paper from the human literature, it's quite an old paper, but it highlights the dangers of nebulized inhaled saline causing bronchitis in healthy people. If you look at those two images there, that's from that paper. So that's quite scary and a reason to encourage your clients to not do that.

So how do we get rid of the mucus? Well, the, the best thing to do is to feed from the floor, to encourage the mucus drainage, via the mucocillary escalator. It's what's natural, naturally, the, the horse has done for millennia.

And, measures to reduce airway inflammation and thereby curb the mucus oversecion in the first place are probably the best ways to tackle the excess airway mucus at present. So, no hay nets, no mangers, for, for these horses is absolute no no. So, if we just go over myth busting of the equine owner beliefs for treatment and management of equine asthma, I think we can summarise what what I've said in that laminitis and steroids, the risk outweigh is outweighed by the benefits in most cases of equine asthma.

For nebulized dexamethasone, it's less effective than oral dexamethasone, so no reason to give it. Nebulli saline, no evidence to support its use, and potentially it could cause bronchitis. Nebulized Nnacetylcysteine, there's currently no evidence to support its use, but the theory is lovely, and oral drexene, there is no real evidence to support its use.

In terms of supplements, the omega 3 is beneficial, but it needs to be a marine source because that's the only type of omega 3 that contains DHA. So the conclusions then from my talk that environmental management is always vital and forage is probably the most important thing to change, but they should endeavour to change everything that they possibly can. If atropine doesn't improve clinical signs, then you might be looking at fibrosis.

I would recommend that you do both BAL and track wash wash cytology, and you can do also culture if indicated on the track wash fluid, which needs to be collected sterilely. You can monitor client compliance with environmental change by monitoring the bowf neutral count. Steroids are really useful, particularly in severe exacerbations of equine asthma.

And they, they help, reduce airway, remodelling, and inhaled is preferable to systemic. Nebulized decks is not useful, and bronchodilators should be used for rescue, in severe cases, but they should not be used long term. Again, inhaled bronchodilators are preferable to systemic, bronchodilators.

Eucalytics are not useful, and inhaled saline is not useful. So thank you very much for listening. There's an extensive references list accompanying the, the PDF written documents to, to accompany this webinar.

I'm Adele, you can get me on these email addresses, and if you need any help with any equine internal medicine consultations in your own practise, please give us a shout at virtual veterinary Specialists. We are. Very happy to help you in that with your cases and help you do referral work in your own practise.

Thank you very much.