Hello and welcome for this new lecture. Today, we are going to discuss about the asthmatic cat. I think it's a fairly common disease, something that most of you will see either as a regular consultation or through your ER, service and your ER, presentation, as these cats can present in very stable or unstable states.
First, we will review some pathophysiology around feline asthma and discuss about the definition of, that disease. Asthma is a syndrome, that covers for, different type of lower inflammatory diseases in the respiratory tract of cats. It's a fairly common lower airway inflammation, and it's thought to be mostly of allergic origin.
And therefore we suspect that they are aeroallergen that will induce a stimulation, leading to activation of lymphocyte T, specifically T helper two, and that will lead to cytokine release, and that therefore will promote further inflammation and changes through the airways of these cats. The three major hallmarks of asthma include airway inflammation, airway, hyper responsiveness and airflow limitation. And obviously, the last one is the life threatening, aspect of the disease, but also the part that we can act on the most with the medications that are available for us long term.
These chronic inflammation these chronic changes will lead to airway remodelling, and, may contribute to a fixed obstruction, which will be more difficult to treat and address. There is kind of a lack of consensus in terms of what the actual definition of asthma is, and, between human equine pine medicine. There are slight variation in the definition of that disease, and so I think it's it's more likely to be considered as a syndrome.
The airway inflammation is usually characterised by infiltration of the airways by eosinophils, and there will also be an excessive, abundant mucus production in the airways of these cats, leading to the formation of plugs. The airway. Hyper responsiveness is characterised by that bronchoconstriction that we have all heard about, and that is one of the main risks when you are doing any form of intervention in feline airways.
And for those of you who perform endoscopies, we know that this is a major risk at the time of endoscopy or at the time of, Broncho al Avage. Because that bronchoconstriction might be life threatening. Finally, the airway.
The airflow limitation is kind of a resultant of, the two prior issues associated with edoema. So, contrary to the inflammation and the accumulation of mucus in airways leading to mucus plug, these plugs can obstruct sometimes a full lung globe and obviously the bronchoconstriction due the due to the airway. Hyper responsiveness is also a concern for these cats in terms of clinical presentation.
There are several clinical signs that we will discuss throughout the presentation. And they can vary very widely between the most stable kind of chronic ones. That will come for a regular appointment versus the one that are in the stress.
And we have, a much more acute, life threatening presentation. Roughly, it's estimated that felon asthma is affecting about 1 to 5% of the feline population, and the median age is usually across the publications around 4 to 5 years. However, chronic signs can be seen for weeks.
There is a recent publication that showed that the average number of weeks, of clinical signs is around 12 weeks before that presentation to, to a veterinarian. Mm. These clinical signs, associated with F and asthma include cough, which is the most common one and the most commonly reported one by the owners but also tachypnea open mouth breathing respiratory distress with usually a very prolonged expiratory phase.
So they have an expiratory, component to their respiratory distress and sometimes an abdominal component as well. With an abdominal push associated with the respiratory distress, patients may have one or several of these clinical signs. There is no rules there.
And the acute respiratory distress might be, kind of, pushed by any form of stress like being boarding in a cattery, a new person moving into the household, a new cat, or, just without any evidence of a specific trigger, leading to these acute pieces of respiratory distress, they can be self resolving, or they may require emergency attention and hospitalisation and specific treatment. The severity is not necessarily associated with the chronicity. Some cats will present right away in respiratory distress.
Some of the cats will have a chronic history of cough and then progress more towards, respiratory distress forms of their, asthma cats that have very acute life threatening episode of dyspnea are considered to be in status asthmaticus, and this is something that we will discuss a little bit later in the management of these patients. Sometimes cough is difficult to identify for the owners and might be confused with vomiting or vomiting herbal without any production of any material. So it's very important when you are taking the history, of these patients to quee the owners and query, if it's really vomiting that they are describing versus cough.
There are a lot of videos on YouTube about cat coping that can be used as, a help for you to, clarify the history from the owners when you are, going through, with them at the time of presentation on physical examination, you might have a relatively normal cat in terms of hair, coat, body condition, even auscultation. You might have tachypnea, which might be mild. You might have an inducible cough on tracheal palpation, but not always.
You might have some increased bronchial vesicular sounds, but not always or some expiratory wheezes. But again, this is not necessarily present in every cat at every time, so nothing is very specific for asthma. But it's something that you have to consider in your differential diagnosis when you have cats with respiratory signs and specifically lower respiratory signs, considering now the differential diagnosis if we think about cats in respiratory distress or dysnea.
The two big categories that we have to consider are pulmonary disease versus cardiac disease. And the definitive diagnosis of fear and asthma can be very challenging because they are overlap between several pathologies, either from the pulmonary sphere or from the cardiac sphere. And it sometimes takes time to be able to, differentiate between them because these patients are so unstable and you can run all of the tests that you would like right away.
And therefore some treatment might have to be implemented a little bit blindly. And response to therapy can be a way to refine your, differentials and achieve your definitive diagnosis in terms of cardiopulmonary condition that have to be considered as a differential in cats with respiratory distress or dyspnea, you will have inflammatory diseases and lower respiratory tract inflammatory diseases like chronic bronchitis and asthma. Parasitic diseases with lung worms such as IRS.
If you are in an endemic area or, erratic migration of toxic which could colonise the lungs and then all forms of cardiac disease, leading to congestive heart failure and respiratory distress and dyspnea. The first step would be to perform thoracic radiographs. Common radiographic findings in asthmatic cats include usually a bronchial or bronchial interstitial lung pattern throughout all lung lobes and the entire lung field.
Sometimes lung lobes can be collapsed, and that's most often the right middle lung lobe. We suspect that mucus strapping will lead to Actis of these lung lobes, and so therefore they can look very collapsed, very attic on radiographs. And it's very important to differentiate that from, other patterns that could suggest, aspersion pneumonia, For example, air trapping can result in a hyperlucent lung field and the impression that the lungs are over inflated.
This will lead to a cuddle push of the diaphragm more within the abdominal cavity. But it is also possible that your radiographs are going to be normal, and that will not rule out feline asthma. It's been reported that about a quarter of the cats have normal radiographs.
Yet once the BAL is performed. There is evidence of inflammatory cells in the BAL in an abnormal number. In in these cats.
So 23 25% of cats will have no radiographs. And that is not ruling out the disease at all. Other lower respiratory diseases have to be considered again.
Depending where you practise infectious diseases have to be considered, and less likely some neoplastic changes. If we look at the radiographs that we have presented to us, we can see that kind of hazy, opacity throughout the the lung field. And then we can discern, some dots as well, which, highlight the, the bronchi and will be like the hallmark for a bronchial pattern in this cat.
This is a nice example that we have seen recently, with, our hospital and you can see that. Sorry. My pointer is being a little bit finicky.
You can see that there is a collapse L lobe here, and you have a diffuse generalised bronchial pattern with this, highlighting of the thickened bronchial wall in this cat CT or computer tomography can be used in the evaluation of asthmatic patients. This is something that is very common in, in a human. For example, in cats, these thoracic CT can identify abnormalities.
They can identify bronchial wall thickening. As we've discussed for the radiographs, they can, like, identify these like patchy, diffuse alveolar patterns. They can confirm the presence of bronchiectasis maybe better than radiographs.
But again, none of these findings are very specific to asthmatic cats and can be seen with other lower airway pathology. Thoracic CT has not been shown to be superior to radiograph to identify bronchial wall thickening. So the specificity and sensitivity are not necessarily better.
But they might highlight changes that couldn't be seen on the radio gras, for example, these Patiala patterns in some of these cats So thoracic city can be of help if you have more subtle lesions. Which were not appreciated initially on your survey radiographs. You can perform CT as well in, unsedated animals that would be respiratory compromised.
And that might be one of the advantages compared to Ridge Gras, where movement is obviously a big, big problem. CT the acquisition is very quick. And so, there will be some movement artefact, but overall will be much more useful of an image acquisition from an image acquisition point of view.
Then your survey gras. So this cat could be placed in a trap, which is basically a plexiglass box in which you can deliver oxygen. They will necessity just a very slight chemical restraint.
But as we will discuss in the emergencies stabilisation of your patient Toan is a very good first line drug that we will use in this patient and therefore a cat on Beto and only dyslexic class chamber might be thin enough to perform AC T in a quick few seconds, and you can deliver obviously oxygen through that plex cage. And therefore you can acquire images, send them for review, without having to take the risk to sedate your patient heavily so that they remain, immobile during the acquisition of the images, which would be the case for the radiographs bronchoscopy and Broncho Avage are also useful and indicated when you are investigated investigating lower airway disease. Unfortunately, the patients have to be stable enough to be able to undergo an anaesthesia general anaesthesia, and you need equipment that is small enough to be able to go down feline airways and reach the Corina and then the mens bronchi and then the different L lobes.
But it's a very useful test for visualisation and inspection, as well as collection of samples in patients with lower airway disease. The lesions that we often identify are, the accumulation of mucus. As you can see on this image here, with a lot of mucus coming out of that bronchi, you can also see Hyperemia.
And you can see that, for example, here there is a very, very red appearance to the mucosa. You can also see mucosal, and epithelial irregularities like the aspect of the bronchi is not smooth. And, just, like, very homogeneous.
You can see sickening and sickening, leading to a partial obstruction of the airway or even a full collapse of these airways. And all of these are, suggestive of airway inflammation. They are not discriminative towards asthma and a very specific type of inflammation that can be associated with any type of inflammation.
Infectious agents as well. And that is why collecting sample is also quite, important and indicated so if you see that accumulation of mucus hyperemia epithelial irregularities. Then you want to, perform, collection of samples.
For comparisons. Here you have, cat with, asthma versus cat with a strong and you can see that mucus is present. Irregularities are present.
And, therefore, visualisation, does not differentiate between these two ethologist your BAL your bronchial V Avage will be the way to differentiate that bronchial VA needs to be performed. Safely. I usually perform it under, well through the, bronchoscope itself by advancing a catheter, a sterile catheter in the bronchoscope and then infusing a lung lobe with, predetermined volume of water.
I usually use between 0.5 and one ML per kilo per ali and I do two alls per site, and I usually sample two sites. The fluid that is retrieved is then split between cytology culture and some leftover might be kept for PC R, as some infectious agents are a bit more difficult to identify on culture or cytology for your parasitic infection.
You also want to consider collecting faeces to perform a burin, and that will help you identify larvae for aoss. If you live in an area that is endemic for Aeros strongylosis again. Nothing really specific for asthma, as I've said before, And then once you have collected your, bronchial lavage and you send it for, cytology, that's when things start to become a little bit more specific.
So historically, asthma based on the human on the, equine definition was an eosinophilic airway inflammation, and we wanted to identify more than 17% of eosinophils in, the leukocyte differentials of BAL fluid. However, more and more research I've shown that probably eosinophils over 5% should be considered abnormal in feline BL fluid. Therefore, the cut off being lower, we will increase, our sensitivity for the detection of the disease.
It means also that we allow the disease to be, neutrophilic, and therefore, these BL fluid might be predominantly neutrophilic yet have an increased proportion of E ail if we use that cut off of 5%. So each clinician should request an evaluation of leukocyte differential on their BL fluid. And, that, in light of the clinical signs, will help you determine if you suspect asthma or lower inflammatory disease in these cats or not.
But again, neutrophils can be the Prem the prevalent population in these, in these samples, As I said, BEL can be collected via bronchoscopy. And this is my preferred method because then you can really target the lung lobe with the most lesions. Or that looks the most abnormal on your, visual inspection.
But you could also perform a blind BAL if you are not equipped with the bronchoscope. The same risks of bronchial bronchial construction and complication exist. As for BAL that are performed through the bronchoscope, form a blind BL, you will insert a feeding tube, usually a smooth, flexible feeding tube, for which you did cut the end to have an open ended, feeding tube, and another side ended one.
And you will pass that feeding tube down the ET tube, as far as you can, And infuse once or twice an ad of 0.5 to one ML per kilo of sterile saline, and then retrieve it with a syringe and perform the same, split between your cytology culture and eventually left over for PC R. So as we said further testing can be, initiated.
And on your BL fluid, you want to perform a bacterial culture. It's very important to rule out any concomitant inflammation and infection. Sorry.
That infection could be opportunistic. For example, mycoplasma might probably be an opportunistic infection. We suspect that cats with asthma have a decreased kind of immunologic response, at least in the local area.
So the airway is probably more prone to get infected. You can culture for mycoplasma, although it's a bit of a difficult one. So depending on the lab you're working with, you might prefer to do a PC R for mycoplasma in endemic region, you will test for heartworm and you can test on the BL fluid as well.
Similarly, for a strongylosis, you can test on the BL fluid if you needed to. As mentioned as well, we would perform a faecal flotation and the burin to rule out parasitic diseases of the lungs, and eventually perform an empirical treatment. Moreover, if we have a very abundant population of eosinophils, which can suggest a para disease, to rule out any form of parasitic disease before we end up treating for asthma with some more specific treatment but also some immunosuppressive treatment.
Therefore, it's very important to have ruled out any form of infectious agent before that. In terms of treatment, there are a few situations to consider, and one of them is, the status asthmaticus and the other would be your chronic asthma patient, which will be much more stable. And, obviously the the the management will differ fairly.
Strongly. Cats that present in status asthmaticus require an acute management, and that will consist of your stabilisation with supplemental oxygen, reduction of stress, minimal ending and bronchodilation, with, inhaled agents such as albuterol or in the very unstable one injectable bronchodilators. If they are available in the country you're working in, such as terbutaline, some authors would prefer tra butty line.
I have mostly worked in places where it was not necessarily available, and I've used inhale albuterol and sedation and minimal handling, and I will say that we do have good results. Even with that, this is the situation where your best friend is your pinol and, your albuterol or your salbutamol, to stabilise this patient. This is a patient where you want to do the least, at least to start and maybe administer some intramuscular sedation, place in an oxygen cage and wait for the patient to calm down for the breathing to calm down for you to be able to safely handle that patient.
If you try to restrain the cat to perform a blood draw or place an intravenous cat, you might lead to even more severe respiratory distress and death. Once the patient is a little bit more stable, you want to perform a more thorough physical examination. It is very impossible to have a very good heart auscultation in a patient in respiratory distress because a you're not focused on your auscultation and B.
There are a lot of, noises that are going to be parasitic to your heart. Osculation. So once the cat is calm, oxygenated and sedated with the Beto and all, that's when you can perform a tea fast.
Either presence of a pro fusion. Yes, no. Is there the presence of beeline lung lobe consolidation?
Do I have a murmur? Do I have a gallop? Rhythm?
This is very important to kind of finalise your physical examination and rank your differentials in terms of priority. At this point in your investigations, you can't be sure that what you are dealing with is asthma, yet, HM, once you have finished your physical examination and your patient is very, very stable, that's when you can finally perform thoracic imaging in the form of photographs to start with, and then eventually consider general anaesthesia for bronchoscopy and airway assembling. If you deem the patient to be stable enough, in some cases they will need to have a day or two days of medication and oxygen supplementation before they are deemed stable enough to do that.
In some patients, it's very difficult to determine if the cat is affected by a lower airway disease or by a card disease, and therefore, echocardiogram might be considered as part of your work up. And furosemide might be also initiated in the early stages of the treatment. For example, if you are only able to do a T fast and you have a lot of beelines, you might want to do a furosemide trial to see if there is any response to it to try to determine if you need a furosemide trial versus, more of bronchodilation.
Well, a You could start both drugs and see how the patient evolve. We also know when we will see it a little bit later. That patient with profusion are more likely to not have lower airway inflammatory disease.
And so maybe that's where you consider cardiac disease to be one of your main differentials, then similarly patient with an expiratory respiratory pattern and an expiratory push, may be more patient with bronchial constriction, and that might make you want to prescribe your, bronchodilator, first, rather than your first semi trial. Now, if we consider the patient with chronic asthma either the one that came through your ER was stabilised and did well and then it comes back for a recheck or the ones that are coming for investigations and treatment of a chronic cause, what is very important is then to perform your investigations, confirm the lower inflammatory disease, as we said with imaging, endoscopy, bronchial vav, ruling out infections, et cetera, et cetera, And then, in terms of long term management, we are looking at trying to prevent, airway inflammation and you can, use, rules with the owners to try to limit the exposure of the cat to environmental allergen. Any form of smoke candles sent, in the house.
Any, like, aerosol sprays for cleaning? That might be airborne. Inflammatory molecules.
There are some panels that are available through, commercial labs to try to determine if there are specific allergens that are, more, important for one cat compared to the other, so that might be available, depending which external laboratory you're working with. And the main stray of the therapy is going to be the administration of glucocorticoid To decrease the airway inflammation and try to prevent, the airflow limitation and the bronchoconstriction these glucocorticoids can be, administered orally initially. And then the animals can be transitioned toward, inhaled glucocorticosteroids to try to limit the side effects and the systemic side effects of these drugs.
Once the inflammation is controlled, that will control the bronchial construction and overall improve the airflow in the patient. We are obviously not curing this cat. We are just managing the condition and trying to prevent further progression of the inflammation leading to more remodelling and leading to maybe a more irreversible changes in Broncho bronchoconstriction and obstructed ways.
In terms of glucocorticosteroids, The recommendations are to initially start at two milligrammes per kilogramme once a day, and that is an immunosuppressive drug. We need to stop the signalling and chemotaxis of inflammatory cells to the bronchi and the infiltration of these bronchial walls, creating edoema, et cetera, et cetera, and self sustaining further inflammation. This dose is then tapered by 25% every 2 to 4 weeks, based on clinical response and clinical stability of the patient.
And that's usually based on tachypnea present at home and at rest yes or no. Effort is difficult to assess in cats, but something to discuss with the owners that the cat's life and quality of life seems completely normal. And then the question is, do we maintain the lowest efficient dose?
Are we trying to win them off? I would probably try to wean off these glucocorticosteroids at least initially and see how the cat does if we perceive that when we reach lower dosage. When we stop, the, tachypnea comes back or any form of clinical relapse is present, then that's when we want to discuss the switch to inhaling therapy.
The issues that we have with these glucocorticosteroids, as you can see here, are weight gain, di Milius in cats when it's been administered chronically for a long time. And also the fact that there is no guidelines and no specific protocol that is available for these cats in terms of regimen of administration when to decrease, when to switch to inhalant Could we start with inhaled therapy in health therapy is very appealing because there is no systemic administration of corticosteroids. There is no side effect, associated with that because the absorption is very limited through the, the respiratory tract.
As you can see, you have, an inhalant and, aerosolized form of, drugs. That is then delivered through a spacer and a little mask. And you can see here there is a little valve that the owners or yourself can look at to count the number of breath and ensure that the cat or the dog, if you were to use it in a dog, are inhaling properly.
And enough of the drug. So it is important to use this chamber because obviously you can't like, for a child or an adult Be, ordering to your cat to inhale when you press the, the button on the fluticasone bottle. So you deliver the drug in the annihilation chamber, and then you give time to the patient to inhale the drug, and that's the best way to optimise that delivery.
And you also ensure that the mouth of the patient is closed, And so most of the drug goes through the nose and will go directly to the respiratory tract, limiting the amount of drug that will be, swallowed or deposited through the mouse and oesophagus in this patient. And therefore, there is a better deeper delivery in the lungs in, in general, we we recommend to have about 10 inhalation, for each, puff of the flutic zone that is, delivered. This might be very challenging with a cat, because to apply a face mask on a cat is not necessarily very easy.
There is a bit of a noise, a bit of a taste to it. So there are a lot of recommendation in this review paper, about how to get cat to use the inhaler and how to, accustom them, to the inhaler, using food tricks, using the inhaler without the drug first and then bringing in the drug. As we go.
And that leads to, obviously an overlap between the oral therapy And when you start using your inhaler, to be able to accustom the cat to that, you can use these inhalant drugs as well in an emergency setting, or in an anaesthetic setting. So, for example, when I perform a BAL, I will use the, bronchodilators, the albuterol, or salbutamol inhaler, and I will deliver it through the ET tube, to try to prevent bronchoconstriction at the time of the endoscopy and the BAL. As we, discuss the administration of a bronchodilator in chronic patient is not recommended because it will promote more inflammation, so they should be only limited to acute respiratory distress.
R to finish with the inha and therapy devices. There are nebulizers that do exist. But they also require face masks.
So, there is maybe a better, deeper penetration of these particles because they are, they are. They can be kind of inhaled much more easily and will deposit much lower in the airways. However, the same Well, they are limited in availability.
And there is the same restrictions in terms of, getting a cat to accept a face mask on on them. So these are all of the factors that have to be taken into consideration when you are planning to switch your patient to an in nailed therapy patient factors. Some cats will never be compliant with the device and their ability to In N the drug is NN.
So you really can't use that strategy. Some owners, some owners, are more, able than others to handle their pets or more comfortable than others, to use the masks and the chambers and all of that, and and that will impact the, the delivery of the drug, and the compliance of the owners. With the administration of the treatment properly, there is a device factor.
Some cats are too big or too small for the masks. And, it's a lot of things to carry around for the owners when that, administration is daily, and then finally, the drug factors. But the drugs have been made to match the delivery systems that we have to control further the bronchial constriction.
We could use bronchodilators. So we hope that by reducing the inflammation, we will have a control of the bronchoconstriction. But the use of bronchodilators would help us to control the bronchoconstriction as well.
And, if, we use fluticasone, which is a steroid, we have been able to prove that in, research CAT, it decreases the inflammation, and that will lead to, control of clinical signs. But would the addition of Bronchodilator help with that? These bronchodilator are going to target the smooth muscle of the airways to relax them, and prevent, acute construction and obstruction Sometimes of the airways when they are exposed to sensitising agent but it's also been shown that the chronic use of this bronchodilator A is not very strong and B, have no anti inflammatory effect or sometimes promote further inflammation.
So they have not been shown to be clinically beneficial. And they are therefore only recommended for use during the acute crisis. This is from the same review paper, and they give you the current recommendations, for inhalant medications to use, in asthmatic cats.
So fluticasone is the, glucocorticosteroids. And that's the mainstream of the treatment for these cats. Albuterol or salbutamol is a bronchodilator, and then you have other bronchodilators that can be eventually used.
But as you can see, they are rescue treatment. And they are to be used in acute crisis or at the very beginning of the treatment when the patients are being stabilised in terms of prognosis. There are a fairly good prognosis that has been shown in this patient with up to 94% of cats surviving hospitalisation and having a good, long term quality of life.
There is a survey in the GF MS about quality of life perception by the owners as well. Which shows very encouraging, numbers. Finally, I wanted to discuss through a case to show you that this theory that seems very straightforward, you know, clinical presentation, investigation, inflammation treatment might be sometimes a little bit more challenging.
So I want to talk about Apollo, an eight year old and, well 8.5 year old male neutered cat who was presenting initially to a New York clinic for breathing fast. The owner were back from holidays.
The cat was in a cattery, and, when they took him home, they felt like he was a bit restless. And they could visualise and perceive, even as non medically trained people that the cat was breathing very fast compared to what they were used to. They went to an ER clinic, which confirmed tachypnea and suspected that the cat was painful.
Therefore, they prescribed, non steroidal anti inflammatory drugs, and gave him an injection of meloxicam. The cat went home, but the owners perceived that there was no improvement on the breathing. Continued to be very, very rapid, but progressed towards abdominal breathing as well.
So they were concerned and went to their vet on presentation to their vets. The cat was open mouth breathing, with abdominal efforts and tachy nick. And therefore it was referred to us for an emergency, consult and stabilisation on presentation.
The cat was in very good condition. It was very tacky. Neck was open mouth breathing.
Yet still pink. So we were not overly concerned about oxygenation at that point in time, we decided to administer the cat pol. We administered 0.3 milligrammes per kilogramme of Pol Intramuscularly, and we placed the cat in an oxygen cage.
Before doing any further investigations wide in oxygen, we could see that the cat's breathing improved. And it was still take it neck. It still had abdominal, but there was no more open mouth breathing that could be, observed.
And the cat was also much more quiet. Therefore, after a good few times, a good few times in the oxygen cage, the cat was brought out. We osculated him.
There was no murmur, no gallop with him. And we placed an IV in case we need to say anything more. We used that IV to collect bloods.
And we actually did a T fast that revealed some beelines and some, air artefact. And we decided to proceed with radiographs as the cat was appeared to be stable with a good SPO two J if nick, but none more in respiratory distress. These are the two lateral radiographs that we obtained from this cat?
Fortunately, I could not get the, VD because the cat started to, be distressed. And so we brought him back into, his oxygen cage. If we look closely to these radiographs, you might feel like there is maybe an increase opacity here in the caudal aspect of the lung lobe.
But most of all, there is a weird separation between the sternum and the heart. The heart kind of looks squished, and there is, like, very dark air accumulation underneath the heart. That is suggestive of a pneumothorax.
With the accumulation of air in the pro space on the contralateral radiograph, we can see that very dark accumulation of air where you you perceive that there is no PMA because there is no extension of any of the bronchi. There is nothing. The air seems to be just pure air.
Here, underneath the spine, squishing the lungs down. And also the trachea seems to be very, very easily seen quite like if it was enhanced by air on both sides of the tracheal walls, meaning air in the trachea, but also air in the mediastinum, to enhance the tracheal wall. So well, So this cat was diagnosed with a pneumothorax and a pneumomediastinum at this stage because the lung paran chema is squished by the accumulation of air in the pearl space and less, importantly, but still in the, me as well.
You cannot interpret the lung pattern because obviously it is artifactual that opacity that you perceive in the lung field. We did a chest up and we removed 100 and 40 millilitres of air. And you can see that on the photo photographs.
We have a marked improvement, in terms of the lung expansion. Yet we can perceive that there is a bronchial pattern through that, airway on both sides. With these donut shaped opacities, that represent bronchial wall thickening, which we can see in most of the lung lobe.
And there is still some air left in the pro space as well. We couldn't remove it all fully. So this cat was diagnosed with a pneumothorax.
Following that, we were suspecting a lower airway disease and lower airway disease in cats. Lower inflammatory airway disease in cats. So asthma is one of the most common cause for idiopathic pneumothorax in cats.
There was no recollection of the pneumo. That cat went home. And then we pursued further investigations and confirmed that he had a lower inflammatory airway disease.
No infectious agent could be seen. He never recollected from his, pneumo thorax. And he was initiated on his, steroid therapy.
Looking at a very recent survey, with about 500 cats with respiratory disease, that was a very big paper from Japan Looking at upper and lower respiratory system. If we focus on the inflammatory lower airway disease, which is what we have been discussing for, this lecture, we can see that they had a lot of cat, and it was the most common lower airway disease that they could identify. By far with 92 cats versus about like between 10 up to 30 in the other categories, which would be, bronchial pneumonia, interstitial lung disease, aspiration pneumonia and pulmonary tumour versus 92 in the inflammatory lower disease.
If we look at these diseases, we can see that cough is really the top one. Clinical sign. For these lower early disease cats with 85% of them having cough being reported by the owners.
It's not specific to lower, to inflammatory lower airway disease. We can see that it's actually quite high for all of the diseases in the lower respiratory for his system. But it's the highest for the inflammatory lower airway disease.
We can see that respiratory effort and open mouth breathing is not uncommon, but not necessarily specific, or more prevalent in these cats. Compared to other pathologies, we can see the duration of the, clinical signs is actually higher than previously reported, with 20 weeks as the median duration of clinical science and arranged between one week and, like, 320 weeks of, clinical science compatible with, inflammatory lower airway disease. Finally, one that I found interesting was that a quarter of them were sneezing.
And I assume that could be probably from bringing up some mucus on having like some discharge, going up their nasal pharynx and leading to inflammation in the nose. But I, I found this finding interesting. There is a second paper that's quite interesting.
That was published just before in 2023 looking at trying to differentiate cats with inflammatory lower airway disease to other cat with respiratory distress, but that were non inflammatory lower airway disease. So your card neoplastic other cats with lower airway problems but non inflammatory, and they were hoping that they could see a difference on the blood gas based on differences in oxygenation. Unfortunately, they could not achieve that.
But what they were able to show is that this cats had a higher respiratory rate, and for every increase of 10 breaths per minute, the cats were 1.5 more at risk to be diagnosed with inflammatory lower airway disease. These cats were younger, significantly younger compared to cats with non inflammatory lower L, a disease.
Cats with plural effusion where 7.5 times less likely to have an inflammatory lower airway disease compared to the control group. So, basically, if you have profusion, the likelihood of the cat having asthma is very, very low, and you have to prioritise a lot of other differentials such as cardiac disease and neoplastic disease.
Before you think about an inflammatory lower airway disease in these cats, the cough was also very present in that population of cat as we've just seen in the previous table. And here what? I found interesting.
And this paper was specific on respiratory distress. Cat presented to an ER room. The abdominal component to the breathing was also significant, and significantly associated with, the presence of, an inflammatory L with disease.
So cough, increased respiratory rate presence of an abdominal component in respiration. Absence of PE effusion in a younger cat is highly suggestive of an inflammatory lower airway disease. This is what this paper basically said, they had very good survival rate, and much better survival rate in the inflammatory lower airway disease cats than the control group, with 94% survival rate to that emergency presentation.
Emergency, consult versus 61% for the comparative group of non inflammatory or airway disease. So, in conclusion, asthma, inflammatory, lower airway diseases in cats can be a challenging diagnosis. There are several steps that have to be followed between the imaging.
The airway examination, dissembling ruling out of the infectious diseases. The ruling out of a cardiac disease in some cats might be a very challenging thing to do as well, and This is even more challenging that when they present as a respiratory distress case, they are in a state of life threatening emergency. They require appropriate care, and that may delay your investigations.
Yet interventions are needed to stabilise these cats and keep them alive, basically, to be able to achieve the proper diagnosis and initiate the, proper treatment. And it's important to achieve a diagnosis in the sense that the prognosis is very different. We know that cats with inflammatory lower airway disease have a very good long term prognosis.
94% of them will be discharged from their ER consult for respiratory distress, and they will be managed for a couple of years with chronic medications. A cat with a congestive heart failure has a much kind of dear prognosis, and therefore it's a very essential piece of information to give to the owner. So to achieve a diagnosis is important to respect the different steps of investigations and is necessary to be able to be as thorough as possible and, and provide the owners and the patient with the best care and the best informations.
Thank you very much. And if you have any question, please, feel free to contact me