Hello, my name's Nadine, and I'm here to talk to you today about rabbit megacolon syndrome. As rabbit practitioners, we're all too familiar with gut stasis. It's a common symptom of illness, pain, or stress in rabbits, and it's not a diagnosis.

Its underlying causes are many and varied, and it's characterised by periods of inappetence or sometimes complete anorexia in our patients. They also have reduced production or complete cessation of faecal material. They can show signs of pain, including hiding, not wanting to move around, squinting, and cases vary from mild to severe.

In the hospital where I work, we actually record the amount of poo that the rabbits produce every day by collecting them all into these bags so that we can actually see the improvements with our treatments. On presentation, a megacolon rabbit may look exactly the same as any other gut stasis rabbit, but they differ in that they'll often have recurrent bouts of gut stasis, which get progressively more frequent throughout life. They will often be ravenously hungry, and this is something that owners of these rabbits will report, as a major feature of their behaviour.

They're often described as quite greedy. And initially, in mild cases of gut stasis, they differ from a standard rabbit in that they do continue to eat quite avidly at first, particularly if you're controlling their pain. Throughout life, they may get progressive weight loss or loss of body condition.

And they may have a quite a profoundly bloated abdomen as in this case here, but it's not with gas, it's literally with ingestor. They can be subdued at times due to bouts of intermittent pain, and owners will often describe very, very loud gut noises, often audible from across the room. Their faecal production may be abnormal, and that may be another reason why owners present these rabbits to you, with descriptions of abnormal faeces ranging from just very large sized droppings to diarrhoea.

They may also present as a fly strike case due to liquid faeces that can dribble from the rectum and accumulate around the perineum, or they may present just for a routine neuter, but on abdominal palpation, they have a an obviously huge secum, or they may just have a very unstable anaesthetic. If you do investigate these cases, often there's nothing diagnostically abnormal found. No major changes on blood test results.

The X-rays are often just characteristic of a routine gut stasis case, perhaps with a little bit more gas throughout the gastrointestinal tract. They will have a lot of ingestor in the gastrointestinal tract on palpation. They don't really feel empty like other anorexic rabbits do.

But the signs are all really non-specific. CT scans may not pick up any changes at all, and there may not be an obvious cause for these recurrent bouts of stasis. So often we focus on things like dietary modification, reducing stress, to try and stop these rabbits presenting with recurrent bouts of stasis.

Some owners will present these rabbits to you due to faecal abnormalities, which range from incredibly large size faecal pallets that are abnormal in shape when compared to a regular poo palette from a normal rabbit, or they may present with very muoid faeces, often with very hard faecal palates in amongst the mucus, or what owners will describe describe as a cow pat diarrhoea. Some mega colon rabbits will present in the latter stages or more severe stages of the condition, where they're obstipated or they have faecal impaction. This represents a crisis.

These animals are very stressed, very dehydrated. They'll be completely anorexic and showing signs of extreme pain, such as not wanting to move, they'll be completely anorexic. Owners might notice teeth grinding, belly pressing, some of these rabbits are in such pain, they'll actually vocalise, and they may also head turn.

So, what actually causes megacolon syndrome in rabbits? It's actually a genetic condition of English breed rabbits. It's sometimes referred to as congenital egg gangliosis or cowpile syndrome, and it affects English breed rabbits.

You can identify affected rabbits from their coat colour markings. So white markings, which are mediated by the EN gene, are dominant over this recessive EN gene which causes solid or self markings. Homozygous, dominant EN gene rabbits are affected with megacolon syndrome.

So, let's look at some of the traits of your standard English breed rabbit, and how they compared to a megacolon rabbit. English rabbits come in various colours, black, grey, tan, or tricolour. They have pigmented eye patches and a very, very dark muzzle and dark ears.

They have a prominent dorsal stripe, which is evident in these two rabbits here, and a large number of spots on the flank. Compared to a mega colon rabbit, which lacks a lot of the facial markings, the dorsal stripe will be thin or incomplete, and the spots on the flank are thin to absent. So, megacolon rabbits have a predominance of white colour and have reduced markings.

They can come in lop-eared, long-haired, short-haired, and direct-eared varieties. All of these rabbits here are showing signs characteristic of megacolon. So they all have reduced muzzle markings, often, described as Charlies due to the fact that this looks like a moustache or Charlie Chaplin.

They'll have little to no spots on their flanks and a reduced dorsal line. And they can be very easily identified at birth. So, affected rabbits may actually not make it to weaning age.

They'll be the runts of the litter, and they'll be noticeably smaller than their litter mates. It's hard to see within this litter, but we have some normal English rabbits with the characteristic spots and stripes. We've got this rabbit here, which would be described as a solid marking or a self, or sometimes referred to as a harlequin.

And then we have a little mega colon rabbit here who has no spots on his flanks and has a very reduced dorsal line. And there's another one here as well. So this is the same litter of rabbits that we've just seen, a little bit older now, and this is the ENEN homozygous recessive rabbit, which is the solid or self colour.

This is the EEN heterozygous, as is this one here. These are normal English breed rabbits, sometimes referred to in other parts of the world as chequered rabbits. And this would be our EN homozygous dominant megacolon rabbit with the reduced spots and the Charlie Chaplin muzzle.

The underlying genetics behind megacolon syndrome in rabbits is quite complex, as there's more than one gene involved, and mutations of other genes can influence the severity of disease. One such gene is the kit gene, and mutations of this gene are linked to white coat colour phenotypes in English breed rabbits. This gene has a direct influence on the innovation of cells that line the gastrointestinal tract called the institial cells of caja or ICC cells, which are responsible for normal peristaltic movement in the gastrointestinal tract of rabbits.

Mutations of this gene lead to reduced peristaltic function due to abnormalities of innervation to the cells, and that influences the severity of megacolon symptoms. So if we take these two rabbits here, phenotypically, they both have the genetic markings associated with megacolon syndrome. This black and white rabbit here is actually showing much more severe clinical signs.

Of the two rabbits, he was much, much more, aggressively hungry and would never stop eating. He has a very large pendulous abdomen, and abnormal faecal production compared to his litter mate, who actually showed very, very few signs or symptoms of megacolon disease. So what do we expect to see in rabbits with megacolon syndrome?

These rabbits tend to have much shorter small intestines with a lower pH in the proximal small intestine. They will often have enlarged adrenal glands, reduced thyroid function, cardiomegaly. They have decreased sodium absorption, leading to an accumulation of more fluid in the gut, and that can have a direct influence on their diarrhoea that they produce.

They have reduced neurological tissue in the gastrointestinal tract, especially in an area called the myoteric plexus, which is often described as the pacemaker of the gut. And this area is normally richly innervated in rabbits, but that, reduced, ganglia or innovation to this section of the gut is what gives it the name congenital a gangliosis and can contribute to the signs of gastrointestinal stasis. Consequently, they accumulate a lot more ingestor within the lumen of the gut, and that increases their gut weight and makes them appear quite bloated.

And they can have decreased body condition, but their weight may appear normal due to the retention of fluid and food in the gut, but malasorptive issues leading to problems with digestion. Megacolon syndrome in rabbits is actually very similar to a condition in humans called Hirschbrung's disease. It's a genetic condition of human babies, due to lack of innovation to a section of the colon, which results in constipation, anorexia, and vomiting.

These accumulations of material within the gastrointestinal tract lead to abdominal distention, failure to gain weight, and they're usually picked up very, very early in human babies due to a lack of normal faecal production. This condition in humans is treated surgically with removal of the affected section of uninnervated bowel. However, unfortunately, surgery is not an option in rabbits because they're high up fermenters and that would make up the bulk of their digestive tract.

Disease progression is really unpredictable from case to case, because it depends on the severity of several factors, including multiple gene mutations, the influences of other factors such as the diet that the rabbits are fed on, hydration status, etc. The age of onset can be as late as 3 or more years, and some rabbits that I've met have made it to 7 years showing very few clinical signs at all. Those that do present usually have periodic episodes of stasis, with a lot of food accumulating in the gastrointestinal tract, and then longer periods of improvement.

But the condition seems to be progressive and it often gets worse with age. So they develop more complex conditions such as faecal impaction and the frequency of bouts shortens as they get older. Malabsorption leading to vitamin and mineral deficiencies has not been very well studied in these cases, but is thought to also contribute to overall health.

So, how do we manage carriers of megacolon syndrome genes? Well, for me, that very much depends on how they present. If it's a young rabbit presenting for a routine vaccination, and I've identified them phenotypically as a megacolon rabbit, it's all about client education and how we manage them at home.

But for those rabbits that present in a crisis, then I'll also talk to you about how we manage them within the hospital setting. So management within the home setting of a mega colon rabbit, I think the most important thing to make owners aware of is that it's a genetic condition, because, many owners will have read online that perhaps restricting certain dietary items in these rabbits may be beneficial, that there may be a dietary link to the gastrointestinal signs that they're showing, and that's definitely not the case. So making sure that owners are aware it's genetic and not dietary related is important.

These rabbits need to be on a high plane of nutrition, otherwise they get sustained weight loss. So they're one of the few rabbits where ad-lib feeding of pallets is recommended. And in fact, I have had some mega colon rabbits where pellets were restricted by owners, and when they were represented again, they ate them so frantically, they nearly choked.

But you do have to be aware that many of these rabbits may actually have a genetically normal companion, and so we're trying to manage to reduce the risk of obesity in a normal companion. So separating the mega colon rabbit off for pellet feeding, whilst also managing the risk of obesity in a normal companion is important. High fibre foods are needed to promote normal gut peristaltic function, and so it's really important that these rabbits get a really good quality hay.

And I have in the past, recommended vitamin supplementation. Passive transfer of calcium across the gut wall in rabbits, is likely to be affected, but we don't have any proof of this. Anecdotally, I have definitely seen osteoporosis develop in these rabbits, which tends to lead to quite severe dental disease, and I suspect it's just due to, transport of vitamins across the gut wall.

Fly strike prevention is also really important, particularly for those rabbits that are producing horrible diarrhoea or leaking fluid from the rectum. I also recommend that grass be the main source of fibre in the diet where possible, although my practise is in central London, and grass is not always easy to come by. But I suspect that the increased moisture provided by grass compared to hay, helps maintain sort of fluid content within the gut and may reduce the risk of the gut contents drying out, which could then lead to problems such as, obstipation or cecal impaction.

Fresh herbs can also be a really great source of food for these guys. So, the properties of plants like celery, coriander, raspberry leaves, thyme, lemon balm, and fen fennel all have mild anti-spasmodic abilities, and they can promote normal gut function. And we would definitely encourage exercise to help with gastrointestinal motility as well.

Owners should be instructed to intervene really early in these rabbits, if there are any signs of pain. So they're not the kind of case where you can sort of manage them at home or sit and wait and see how they go. So, any signs of hiding, reduced or absent appetite, belly pressing, anything like that, they need to be brought to the veterinary clinic straight away.

In an acute episode, these rabbits will often present in extreme pain, and they may be slightly hypothermic as well. So, the focus there is on pain relief, very similar to how I would manage a gut stasis case. So, we tend to use meloxicam at 0.6 milligrammes per kilogramme orally every 12 hours.

We give buprenorphine 0.05 milligramme per kilogramme subcutaneously. But they can also be given intravenously or intramuscularly, anywhere from every 6 to 12 hourly.

We put these rabbits on a lidocaine constant rate infusion. The recipe for that is here. And I found that that's a real game changer for pretty much any rabbit in gut stasis, but particularly for these megacolon cases.

It tends to manage their pain and help with their peristalsis a little bit better than, just when we were using standard analgesic agents. So, these patients, as I said, often present hypothermic, so warming them up is really important, and monitoring their temperature whilst in hospital is also essential. A lot of the management strategies that we utilise in these rabbits are direct extrapolations from the way that Hirschsprung's disease is managed, prior to surgery.

So, in humans, they usually use olive oil, which has actually been shown it can stimulate bowel movement and can help with the passage of. I obviously I am using this completely anecdotally, but I don't believe it's likely to cause any harm at all, and often in these cases, because there's no cure, we do get a little bit desperate to try and alleviate some of their discomfort. So, I will certainly recommend that.

Lactulose can also rehydrate the gut contents, and keeping the gut contents hydrated is essential in these rabbits, because, if the material is sitting in the gut for a long period of time and gets all the water reabsorbed from it, that predisposes these rabbits to a prolonged hospital stay, much more discomfort, and certainly, unfortunately, obstipation or scal impaction. So, although we do tend to provide fluids intravenously, we always do give oral fluids to keep the GI contents hydrated. And then, if the hydration of the gut contents, is good, we will actually start them on prokinetic drugs such as ranitidine, cisapride, and metoclopramide, used simultaneously.

If you have dry gut contents, then hold off on using prokinetics until you rehydrate them, as that would cause pain. Nutritional support is absolutely essential in these rabbits, and depending on what phase they're at in terms of severity, they'll often have really good appetites. So this little megacolon rabbit was avidly taking syringe feeding formula, which is not always the case with our inpatients.

Some of them will present anorexic, but often once you control their pain, they'll avidly eat anything you put in front of them. So, we use a range of high fibre feeding formulas with them, and we'll often pop them in a bowl for the rabbits to help themselves as well. And if you make up those feeding formulas a little bit more liquidy at first, that's one of the best ways to rehydrate gut contents, too.

Will usually soak their pallets, just to help hydrate the gastrointestinal tract as well. Providing fresh water in bowls and bottles is important to, accommodate their preference. And if you've got a rabbit that is a bit of a sweet tooth, then providing them with an additional water source with a little bit of fruit juice, added to encourage intake can be helpful as well.

Finding out what their favourite foods are, and offering those things like grass, fresh aromatic herbs such as lavender, nettle, mint, marjoram, oregano, those sorts of things can be really good at encouraging these rabbits to eat. And then, of course, providing ad-lib hay as well. So, managing these rabbits in an acute crisis can be really challenging.

If there's been a delay in them being presented to the hospital, due to the owners not being aware that they even had the underlying problem, which is often the case, sometimes they'll have progressed all the way to, seagull impaction before you get to see them. For me, seagull impaction is the major thing to try and avoid. It's usually palpable as rock heart faeces within the secum.

You can also take X-rays. This particular rabbit had obviously quite severe thy tympani throughout the entire gastrointestinal tract, and the food sitting inside his secum was very, very firm indeed. I think for many of these cases, once they've progressed to this level of severity, because it's not a curable condition, and they have such a poor prognosis at this stage, euthanasia really should be considered.

If the owners, would like to attempt to trial treatment, I think you need to put a time limit on that just for the welfare of the animal to make sure that they're not suffering. So, that's a conversation that needs to be had, through before the initiation of any treatment for these rabbits. If you're not seeing adequate improvement, then it is also time to have another conversation about euthanasia.

Pain relief is a really challenging thing to address in a patient like this, because they've got quite severe stasis of gastrointestinal movement, and we know that any opioids are going to further reduce peristaltic function. But you should never withhold strong opioid analgesia in any rabbit, just because you're worried about causing gut stasis. Pain is just as potent a cause of stasis in a rabbit as opioids would be.

So, we do give them stronger opioids such as methadone. We continue with meloxicam and place them on the lidocaine CRI usually at the twice maintenance rate. And then they also get additional fluid therapy through a separate line, as well as aggressive oral fluids too.

Faecal softeners such as lactulose are often used at substantially higher doses, because at this stage we're just desperate to try and rehydrate that faecal impaction, to the point where we can actually get things moving along. Again, I also rely upon larger doses of olive oil at this stage, in truth, mostly in desperation. It's really important not to give prokinetics until the faecal softeners and the fluids have taken effect, because you can imagine, trying to cause peristaltic movement, in a gut that's full of dry food, it's gonna be a major source of pain and discomfort.

So, I thought it could be useful to go through a recent case of megacolon syndrome that I saw. So, this is Kelly. She presented, actually, for a broken nail at 11 months of age.

She was unneutered and unvaccinated. On physical exam, her heart rate was 160 beats per minute, which seemed a little bit low. They're normally up around about 260 beats per minute when they first get removed from the carrier.

She had dental disease diagnosed on a physical exam, which at 11 months of age seemed to be quite early. And her diet was pretty standard. She was on a small number of, pellets, and, nothing horrific, no muesli mixes or anything in her history at all.

She was getting access to ad-lib, hay, which she ate avidly. So it just didn't seem to quite fit with her age. The vet that saw her recommended a spa and also to do a dental at the same time.

So, Kelly presented for her spay the following week, and during that time, she'd managed to change colour. I'm actually really sorry. I have very, very few photos of Kelly, which is always the way.

I was seeing her on a weekly basis, almost, for her entire life, and yet managed to not take a single photo of her, which is always how it goes. So obviously, this is not a megacolon pigmented rabbit, but, there's a rabbit coming in for a spade. Her physical exam preoperatively was fine, but again, her heart rate was a little bit lower than expected.

The vet used our regular anaesthetic protocol, which we deemed to be pretty safe, and she went into cardiac arrest. She was then resuscitated. Bloods were drawn.

Her econicular serology was negative, and there were no changes at all on her blood tests. X-rays were unremarkable apart from the dental disease which she had. ECG was normal, she was given a couple of weeks to recover, and the owner was advised that we would try again once she was a little bit more stable.

So, 3 weeks later, Kelly represented for her spay. The owners reported no problems at all at home. In fact, they reported that she ate very well.

She ate substantially more than her companion rabbit. Her preoperative check again, was normal, apart from bradycardia, her heart rate of 160. Bradycardia in rabbits is a little bit hard to quantify.

Sometimes the cut-off limit that I might use will be a little bit different to other vets, but certainly in a conscious rabbit, 160 seems a little bit low. We changed the anaesthetic protocol, not because we were worried about the protocol that we had used before, but it seemed sensible to try something else in case it was an individual drug reaction. She had a really unstable anaesthetic, but she was spayed successfully, and her cheek teeth were bared short at the time.

Dental disease at this age, again, just did not seem right. Her diet seemed fine. She wasn't a Netherland dwarf.

There was no evidence of renal disease or anything that would might, alter her calcium metabolism at all, evident on bloods or on physical exam. So we were just a little bit confused. So, the first time that I met Kelly was about 2 months later.

She actually presented for a skin checkup. And on physical exam, I diagnosed her with kylatella fermide, as well as seroptes caniculi, which, again, didn't really seem to fit for a supposedly young, healthy rabbit, but the owner assured me that her age was correct. But when I examined her, I realised that she had markings consistent with megacolon genetics.

We asked the owners to, send us a photograph of the poo that she produced, as well as the poo that her companion produced, because she had mentioned in the consult on questioning that was a little bit abnormal. And this is actually the photo that the, the owner sent through. So you can see, Kelly's faeces is substantially larger than her companion rabbit.

When we did a physical exam at that stage, it was obviously obvious that her dental disease has actually reoccurred. She had severe step mouth, and she actually had the beginnings of incisor malocclusion as well. And I wondered whether this might be due to problems with the passive transport of calcium across the gut, but, this is not something that I can prove.

I also hypothesised that this persistent bradycardia that she had might be due to increased vagal tone due to her very, very full gastrointestinal tract. So, at that stage, I had a long conversation with the owner regarding her genetic condition. The companion was unrelated and unaffected.

The owner was advised to consistently monitor, Kelly's body weight, and also, we taught her how to do body condition scoring, comparing Kelly to her companion. The difficulty that we had was that the diet that is good for her dental health, so promoting her eating more grass and hay was actually causing weight loss. And the diet that was good for her body condition and weight, tended to predispose her to further development of dental disease.

So, over the course of several months, we just tried to monitor her weight and get that balance, as good as we possibly could. If we were concerned about gastrointestinal upsets or pain episodes, she was managed with meloxicam and gabapentin. And it's difficult to explain why prokinetics would work in an animal like this, if we know that some of the genetic abnormalities are related to a lack of innovation to the gut.

But anecdotally, owners have reported to me over and over again that they do work, and so we do use them. She was also treated with topical ivermectin for the kylitiella and seroptes ear mites, and throughout her life, she seemed prone to both of those conditions flaring up again, despite what would be considered adequate treatment for another rabbit. Due to a lot of the underlying physiological effects of the megacolon syndrome, these rabbits tend to be poor candidates for anaesthesia.

And so, we had very frank conversations with the owner about the potential risk, knowing that we would have to get Kelly in regularly for management of her developing dental disease throughout her life. We managed her bradycardia with, preoperative glycopyrolate. You could also use atropine, but atropine is plant-derived, and, rabbits have evolved atropinase enzymes, or at least many of them have, meaning that atropine is not a bad choice.

It may not work in some of them, and it may not last for as long as it, as it should, but it's certainly not gonna do any harm. So, we happen to have glycopylate in the practise, and we use that instead. She had repeated X-rays several months after the first set of X-rays were taken, and it was very obvious at that stage that her dental condition was progressing quite rapidly.

We thought, probably due to osteoporosis of the bone, but the teeth staying very firm and hard. And so managing client expectations about what progression of dental disease might cause, for example, things like retrobulbar abscesses, worsening maoclusion of her incisors that may necessitate removal, and potentially mandibular abscesses. And you can see on this X-ray here that we've got rapid growth of her tooth roots and loss of cortical bone of the, the ventral mandibles.

So, we could actually palpate changes to the mandibular bone due to the tooth roots abnormalities that she had, and that progressed at a much more advanced rate than a normal rabbit would. So, throughout Kelly's life, we basically spent the entire time just firefighting all of her different problems, monitoring her incisor maleclusion as it developed, doing things like reverse bevels to try and, prevent the maleclusion getting to a point where, we might have to do extractions of her incisor teeth because she wasn't the most stable candidate for anaesthesia. And we really had no way of predicting how long she was gonna live for, and we weren't sure whether the removal of her incisors would be in her best interest if she was going to have a very short life expectancy.

But one of the challenges, the challenges of these cases is their unpredictability. Every case seems to be a little bit different. And so in the end, as, the, the sort of preventative strategies that we employed became less effective, we ended up having to remove her inside the teeth.

So, sadly, most of Kelly's clinical signs seem to be related to, the, the rapidly progressing dental disease, rather than what would normally be expected in a case like this, which is frequent bouts of gastrointestinal stasis. So she was quite unusual in that regard. And just about everything that we had predicted as a worst case scenario, regarding potential eventualities happened.

So, Kelly, unfortunately, went on to develop quite a severe retrobar abscess, which you can see outlined here on the CT scan. So, these are her eyes on each side here, and you can see that this progresses from the mandibular bone abnormalities, all the way up behind the eye. We were able to successfully manage this palliatively with pain relief and debacilin injections for a course of about 3 to 4 months, and she had an excellent quality of life during that stage.

But sadly, it progressed to the point where we thought her quality of life was affected, and she was eventually put to sleep. So, this is actually a 3D rendering of her CT scan, just to demonstrate the bony abnormalities that were seen. So, this is her normal side here, and you can see the destruction of the bone of the mandible, as those tooth roots become elongated and infection occurs, obviously tracking up into that retrobulbous space.

So, Kelly, unfortunately, only lived to about 1 year, 8 months of age. But many of these rabbits with mega colon syndrome will have much, much longer life expectancies. And the cases are really variable in severity.

Many have no problems with dental disease at all. Some will show only really mild intermittent gut stasis signs throughout life. Some may make it throughout their entire lives with the owners completely unaware that they even have a problem.

So, prevention, I think that the key point here is client education. I think because mega colon syndrome in general is not a very widely recognised condition. It's not unusual for owners to get a little bit desperate as well, would I, that their rabbit keeps on having these recurrent bouts of stasis.

It's had multiple investigations and no significant underlying cause has ever been identified, because, maybe the genetic markings have not been recognised as megacolon markings. And so, desperate owners go on searches online to try and find out what the underlying cause might be. And so often by the time they present to me, they'll have been on all sorts of wonderful and wacky dietary restrictions.

And any dietary restriction in an animal with a malabsorbed genetic condition is going to potentially exacerbate the problems. So, the most important thing is just making owners aware that it's not due to gassy vegetables or any particular thing in the diet. And also just making them aware that it's absolutely nothing they've done.

A lot of these owners feel extreme frustration and guilt and worry. That they're causing the problem, and so just making sure that owners are aware that that's not the case is really important. We try and encourage water intake in these rabbits as best we can.

So, rabbits tend to have a preference for drinking from bowls rather than from water drippers. And at the very least, providing them the opportunity to choose is important. I have no problems at all with people adding a little bit of fruit or vegetable juice, so long as they also have a fresh water source as well.

As I said before, grass, I believe is probably more likely to keep the gut contents better hydrated than dried grasses such as hay, but, in truth, so long as they're getting a high fibre food source, it probably has very little impact. And then the most important thing is to actually be prescriptive in our, recommendations of breeding practises. So trying to, prevent breeding of these megacolon rabbits in the first place.

So crossing, chequered or English marked rabbits with self rabbits, rather than chequered rabbits with chequered rabbits, or, as they referred to here, English versus English rabbits, is going to dramatically reduce the incidence of this condition within the population. Thank you very much for listening to my presentation today on megacolon syndrome, how it occurs, how to identify it, and how it differs from regular gut stasis cases. I hope it's been useful.