The podcast that makes veterinary medicine simple.
In each episode, Dr. Lottie breaks down clinical conditions, cases, and concepts across species, focusing on pathophysiology, decision-making, diagnostics, and what actually matters in practice. It’s the kind of context that makes your knowledge finally click.
Every month, we’ll also have honest conversations with guests about the incredible variety of veterinary medicine, what you can do with a vet degree and how to think bigger about your career.
Whether you’re cramming for exams or looking for a soundtrack for your dog walk, Current Vet will make veterinary medicine simple
Intro
Hello, hello, and welcome back to Current Vet, the podcast that makes veterinary medicine simple. If you're new here, I'm your host, Dr. Lotti, and today we're talking about a condition that is very common in equine practice, and that is equine gastric ulcer syndrome, or EGUs, I'm gonna call it. Most people have heard of gastric ulcers and horses, but.
What can be missed is that EGUs isn't one single disease. It's actually includes two different conditions with different causes, different mechanisms. So this is gonna be really key in understanding these different approaches to treatment and prevention. So let's start with our case.
Case
You've been asked to visit a racing yard to see Ace, a 4-year-old thoroughbred gelding who's currently in full training.
The trainer isn't panicked. There's no acute problem, but over the past couple of weeks, something just hasn't felt quite [00:01:00] right. He's not finishing his feed consistently. He's become a bit moody during exercise. He's a bit less willing to go forward and occasionally resentful when being girthed. His race times are slipping a little bit, but nothing too crazy.
But it's enough for the trainer to notice a change. On exam, ACE looks well, he's bright, he's alert. His temperature and heart rate are all normal. Gut sounds are present and there's nothing overtly strange, so you have a racehorse with some subtle behavioral changes, slightly declining performance, and no clear abnormalities on exam.
Aetiology & Pathogenesis
To understand what might be happening with ace, we do need to kind of go over a little bit of anatomy and physiology for the equine stomach. So a horse's stomach is divided into two different regions. The upper third is the [00:02:00] non glandular part and it's lined with squamous epithelium, and the lower two thirds or the glandular stomach are gonna be lined with glandular mucosa.
These two regions meet with the Margo in the middle, which is essentially just line that divides the two regions other than its normal epithelial surface. The squamous mucosa has no protection against gastric acid. In contrast to this, the glandular mucosa produces acid, but it's protected by the mucus and bicarbonate, barrier prostaglandins, and the fact that it has a really good blood supply that encourages rapid mucosal healing.
The other key factor, remember, is that horses produce gastric acid continuously, whether they're eating or not, obviously. Historically, horses are like continuous grazers, the herd animals. So in [00:03:00] a grazing horse, that's really not a problem. Constant forage intake means that saliva production is gonna be constant, and saliva contains bicarbonate that's gonna buffer that constant secretion of gastric acid. But. Modern management of horses, especially race horses like Ace. This is gonna be very different. Race horses are generally fed at distinct mealtimes. Often feed that is high concentrates.
They have periods of fasting in between meals. They're exercise really, really intensely, sometimes on an empty stomach. And all of these factors increase. Acid exposure to the mucosa of the stomach. So this is where we now are gonna differentiate between the two forms of AGAs. So we have the equine squamous gastric disease form, which is gonna affect the squamous upper region.
And then we have equine glandular gastric [00:04:00] disease, which affects the lower glandular region. So for ESGD, the squamous form, the problem is generally acid exposure. So during exercise, the intraabdominal pressure increases, the stomach is compressed, acidic gastric contents are forced upwards, and that is gonna splash the squamous mucosa with acid.
This is called acid splash. The effect is gonna be worsened, obviously, if the horse hasn't got forage in the stomach, if the stomach fill is really low, and that's gonna expose more of the mucosal surface to the stomach acid because the squamous mucosa has very minimal protection. Repeated exposure to acid causes epithelial damage, inflammation, erosions, and eventually ulceration.
These lesions are especially common around the area of the Margo.
So [00:05:00] essentially, squamous gastric disease is best thought of as acid injury driven by modern management practices. So. Those changes to feeding the feeder concentrates, feeding specific mealtimes, fasting periods, intense exercise, and just basically all those different management changes. It is actually much more common than the glandular gastric disease with about 80% of the lesions diagnosed are found in the squamous mucosa.
So in contrast, the equine glandular gastric disease has a different mechanism.
It's not fully understood, but it's thought that the issue is not due to excessive acid exposure because that glandular stomach actually. is constantly producing acid itself anyway, but it also has those protective mechanisms. So it's thought that this disease is caused by a failure of the glandular [00:06:00] mosis protective mechanisms.
So normally we have mucus, we have bicarbonate, we have prostaglandins, and we have that good blood flow protecting the glandular stomach. When those defenses are impaired, so potentially something like chronic stress or NSAID use or systemic illness, the acid and digestive enzymes can then damage the epithelium.
So in a nutshell, the squamous gastric disease is essentially an acid exposure problem.
And the glandular gastric disease is a mucosal defense problem, but both of them result in ulceration of the stomach.
Clinical Signs
So now we understand those mechanisms. Let's talk about clinical signs. The hallmark of EGUs, whether squamous or glandular.
Is that clinical signs are vague. [00:07:00] They're non-specific and they're often intermittent. So things like irritable and resentful behavior, intermittent, incompetent, inconsistent, or worsening performance and mild colic, or maybe a little bit of weight loss. And in Ace's case, this is exactly what we're seeing.
We're seeing That slightly decreased performance, a bit of irritability, resentment of girth thing, and inconsistent appetite. We are not gonna see fever, dramatic colic or any really obvious sickness in general.
It is worth noting though that squamous disease is more commonly associated with discomfort around feeding and exercise, where glandular disease often presents with more persistent behavioral changes.
Diagnosis
Okay, let's talk about diagnosis. So, because the clinical presentation is so vague, it is [00:08:00] really not very helpful for diagnosis. So definitive diagnosis of EGUs requires direct visualization of ulcers in the stomach, which obviously is gonna require gastroscopy. You need to fast the horse for about 1216 hours to make sure the stomach is nice and empty, and the mucosa is actually gonna be visible when you pass the scope.
, And in Ace's case, you see multiple erosions and ulcerated areas. We see them around the squamous mucosa, especially around the Margot PLAs.
With squamous lesions, we grade these on a scale from zero to four, and the higher the grade, the more extensive and deeper and coalescing those ulcers are. Glandular lesions, if they're present, are actually. Qualitative, can't ever say this word qualitatively described rather than graded in a [00:09:00] quantitative way.
So you would comment on things like the location of the lesions, their appearance. Are they hyperemic? Are they bleeding? Are they multifocal? are they single, are they coalescing? Basically anything that is gonna help you to paint a really. A beautiful picture of these ulcers for the person who isn't looking at the scope.
But in Ace's case, the glandular mucosa looks normal and those squamous lesions are about a grade two. It's also worth saying that blood tests are really not useful for diagnosis. There are no reliable biochemical markers. So hematology and biochemistry are pretty unremarkable.
Treatment
So now we have seen those lesions in a stomach. How are we going to treat it? Okay. Treatment of [00:10:00] EGUs always involves a combination of medical management and supportive care and management changes. So the mainstay of medical treatment is omeprazole. It is a proton pump inhibitor that irreversibly blocks the hydrogen potassium APAs pump in the gastric parietal cells.
Basically, this is gonna prevent. Hydrochloric acid secretion. So less acid produced is less acid exposure is less mucosal damage. So for squamous disease like ACEs, omeprazole is very effective, but it's also very, very expensive and is may not be accessible for everyone. It can also be combined with other medications.
So gastro protectants, like sucralfate, , histamine antagonists, so cimetidine, and that is gonna prevent histamine from [00:11:00] stimulating gastric acid secretion. We also need to remember that NSAIDs are contraindicated for these patients because they block Cox enzymes, which reduces prostaglandin synthesis.
Prostaglandins are one of those defense mechanisms that are key for maintaining the mucosal defense barrier. So a lack of prostaglandins is then disrupting the protective barrier and increases the risk of epithelial damage and ulceration. So we really don't wanna be using these unless they are. absolutely necessary. And if it is necessary, then using the minimum effective dose and the shortest duration possible is gonna be the aim.
In these cases, medication alone is not gonna be enough. So if ACE goes back to the same feeding schedule, those long fasted periods, high concentrate diet, intense exercise, blah, blah, blah, all on an [00:12:00] empty stomach, the ulcers are very likely to recur. So all of our omeprazole, all of our money, all of our efforts has gone for nothing.
So this means that. What we should be doing are some key management changes. We need to maximize forage intake, making sure that the stomach is nice and full and there's less exposure of the mucosa. To stomach acid, we need to avoid prolonged fasting periods. Feed forage, feed something before exercise to protect the mucosal surface, reduce that acid splash effect, reducing concentrate feeds where possible. We wanna minimize stress and we want to avoid unnecessary NSAID use.
Prevention
Prevention of EGUs is. Uh, again, closely tied to those management changes. To a large extent, it's a disease of modern horse management. So true prevention in performance horses [00:13:00] can be really difficult because of this intense lifestyle. But we can reduce the risk by using some of those same management changes that we mentioned before.
So that high forage intake, maximizing turnout, reducing periods of fasting, not exercising after fasting, and moderating the intensity and the duration of exercise. And also a couple of things like increasing positive social interactions between horses because this can help reduce stress.
One other thing we can do for prevention is a short term prophylactic use of omeprazole. If we're anticipating a really high risk period, so, and maybe an intense training period or a stressful environment, but it should never replace good management. And we also have to be very careful about using these PPIs around competitions as they're used is often banned.
So check your competition rules very carefully [00:14:00] before recommending use.
Key Points
So what are the key points that you should know about equine gastric ulcer syndrome? Equine Gastric ulcer syndrome describes the formation of ulcers in the gastric mucosa of horses. There are two forms of the condition based on the location of the lesions, so we have the squamous gastric disease and the glandular gastric disease, which both have different underlying mechanisms.
Squamous disease is most common and is driven by acid exposure to the unprotected squamous mucosa. And glandular ulcers are more likely to be caused by a failure in the glandular mucosa protective mechanisms. Clinical signs are typically quite vague and subtle. We may only see some mild behavioral changes, A little bit of irritability [00:15:00] and gastroscopy is gonna be the best way of definitively diagnosing and grading the condition.
Omeprazole is key for medical management, but medication should also be combined with good management changes. So looking at that forage intake and regulating our exercise routine in order to prevent recurrence,
Outro
and that is equine gastric ulcer syndrome.
Thank you so much for listening to this episode. If you found it helpful, please follow or subscribe wherever you get your podcasts, and feel free to share it with a colleague or a friend who needs to hear about this topic as well. You'll find all the resources used for the episode linked in the show notes.
And if there's any topics that you'd like to hear next, let us know in the comments or come and find us on Instagram and TikTok at Veterinary Vista. We'll see you next time. [00:16:00]