WARNING: This article contains images that some viewers may find disturbing.
EGUS Equine Gastric Ulceration Syndrome
You may have heard that term before. Maybe not, but I am sure you have heard about stomach ulcers in horses. EGUS stands for Equine Gastric Ulceration Syndrome, the term has been widely used since 1999 in order to describe gastric ulceration in horses. Further research has shown that not all ulcers are created equal; it has been suggested by scientist and specialist groups to distinguish between EGGD (Equine Glandular Gastric Disease), and Equine Squamous Gastric Disease. While this might sound confusing, it is important to know and differentiate between these two similar, but so different presentations of EGUS.
Here are a few numbers to think about: Several studies (Eg. Hammond 1986, Murray 1996) have found gastric ulcers in approximately 80% – 90% of show and race horses. In the rest of the equine population, the prevalence of EGUS has been estimated to be around 50% in apparently healthy horses!!
In order to understand equine gastric ulcers, we need to understand some anatomy first, because the equine stomach has some unique differences compared to ours.
The overall volume compared to the size of the horse is small (8-15L). It basically has two compartments. The dorsal part lined with squamous mucosal cells (a flat, smooth layer of cells stacked over each other); this lining is very similar to the lining of the esophagus, which ends actually in that part of the stomach, near the lesser curvature. The lower (ventral) part is separated by a prominent line called the Margo Plicatus. Below that line starts the glandular mucosa in the ventral fundus leading to the area called Antrum, ending at the pylorus, the opening into the duodenum – the first part of the small intestine.
The glandular mucosa is lined with cells that secrete the gastric acid and digestive enzymes, which help to digest food, especially proteins. This part is coated by a layer of mucus that helps to protect the stomach from digesting itself. The top, squamous layer does not have this protective mucus layer.
Ulcers that occur in the lower glandular part are very similar to the human peptic ulcers (causing PUD- Peptic Ulcer Disease) and cause EGGD in horses. ESGD is the proper term of use if ulcers cause disease in the top squamous part.
Researches looked into the nutritional risk factors for the development of ulcers and came to some interesting conclusions.
Risk for EGUS increases when:
- Straw is the only forage
- More than 2g/kg BW starch/day or
- More than 1g/kg BW per meal is fed
- When water is not available in turnout paddocks
- The interval between forage feeding is more than 6 hours
- Horses are stabled and fed more than 1% BW grain
- No turnout
Clinical signs of EGUS include:
- Poor appetite, picky eating
- Weight loss, poor body condition
- Abdominal discomfort
- Poor coat condition
- Teeth grinding
- Behavioral changes – aggression or nervousness
- Recurrent colic
- Poor performance
Photo #1: NO ULCER
Photo #2: ULCERATION
In a consensus statement regarding EGUS by the European College of Equine Medicine published in 2015, the committee concluded that a wide range of clinical signs might be present in individual cases of EGUS with varying degrees of reduced appetite and poor body condition, behavioral changes are not uncommon, and poor performance might be a result. But, they also acknowledged that there might be numerous factors involved in poor performance. They stated that the differences in clinical signs between ESGD and EGGD are unknown and warrant further investigation.
Due to the wide variety of clinical signs and their unspecific nature, their recommendation was to not base the diagnose on “characteristic sign”, but they suggested that EGUS should be confirmed and diagnosed with gastroscopy.
In an ideal world, this would be my preferred way, however due to several limiting factors in the everyday practice, this does not always happen and horses are often put on a trial period of Gastroguard™ or Omeprazole, and monitored for improvement of signs. My deal with clients is, that if there is no significant improvement and we have ruled out other conditions, the horse will have the stomach scoped as the next step.
During gastroscopy the ulcers are graded according to their severity, however lesion grade does not necessarily correlate with clinical signs.
What causes ulcers?
As far as ulcers in the dorsal squamous area of the stomach are concerned, we have quite a good understanding.
A variety of management factors contribute to the development of ulcers, their common denominator is that they expose the squamous (because they are flat) cells of the stomach lining in that area to the hydrochloric acid in the stomach, thereby damaging the cells. This is increased due to byproducts of bacterial fermentation of the sugars in a concentrated diet.
Because there is no protective mucus layer in the top part, the only protection against splashing of gastric acid on the wall above the Margo Plicatus is a layer of fibrous forage on top of the pool of caustic acid. If this layer of fibrous material is disturbed due to exercise or lack of forage, then gastric acid will spill on the unprotected stomach wall, damaging the cells and creating ulceration. This explains the high prevalence of EGUS in performance and race horses.
In contrast the development of EGGD is not well understood, the glandular mucosa is normally exposed to the gastric acid and much better protected. However, if the defense mechanisms of the cells break down, they are exposed to the acid, and the formation of a peptic ulcer starts. Helicobacter pylori, a bacterium well-known in human medicine has been identified in some cases. We know that NSAIDS like bute can also contribute to ulcer formation. However, only after given at much higher than recommended dosages.
What can we do to help and what can we do to prevent EGUS?
In humans, the quote “ no acid – no ulcer “ is used quite frequently – and acid suppression is also considered the essential step in order to fight both ESGD and EGGD, regardless of the underlying cause.
So-called Proton Pump-Inhibitor drugs like Omeprazole, are considered the most important line of defense in the fight against stomach ulcers. The development and availability of the drug Gastroguard™ has been a game changer in our fight against EGUS. Omeprazole is a tricky substance and numerous studies have shown that if the molecule is not protected properly against the gastric acid, it will lose its efficacy and its bioavailability becomes unpredictable.
The other substance group that is still commonly used are so-called H2-receptor antagonists, Ranatidine (Zantac TM) might sound familiar? Cimetidin belongs to the same class of drugs and does not reduce acid production reliably in the horse.
Misoprostol, a synthetic prostaglandin, is the third drug that can be used in order to suppress acid production in the stomach, often in combination with Omeprazole. The same drug can cause abortion in humans. This does not seem to be the case in horses, nevertheless I would be careful.
As an adjacent treatment, Sucralfate can be used. It binds to the ulcers and coats them, therefore protecting the ulcer from acid exposure and also has some neutralizing effect. It is not meant to be a stand-alone treatment in the horse. Calcium Carbonate (TUMS™) has a very short lived neutralizing effect on gastric ph, so while it might seem like a cheap and easy solution, it is not worth the effort. In contrast to humans and dogs, the horses stomach produces gastric acid continuously, and this might explain the short-lived effect of “TUMS™” and other similar products.
How long does it take for ulcers to heal?
We know from recent publications that 21 days might be long enough in many cases, but the usual recommended period is 28-30 days. My personal preference is to use Omeprazole for 25 days at full dose, and then keep them on a lower dose for long term while we sort out the cause and contributing factors. If that is not addressed, the ulcers will re-occur within a few days!!!
That is why certain changes in the feeding and “lifestyle” of the horse should be addressed.
Ideally free choice of hay, with alfalfa being the preferred roughage! Alfalfa helps to buffer the gastric acid. The amount of starch should be reduced and can be replaced with oils.
Supplements and Nutraceuticals
These have their place in the treatment and recovery plan. Pectin-Lecithin supplements have been around for a long time now, and we have enough supporting evidence that there is a beneficial effect, especially in combination with probiotics and antacids (magnesium hydroxide).
Seabuckthorn berries and pulp have shown some promising beneficial effects on the gastric lining as well.
Quality grass pasture, minimum 1.5 kg/hay per 100kg and lots of turnout.
One quite interesting finding was that concentrated electrolyte paste and concentrated electrolyte solutions given orally increase the risk of ulcers. However, this is not the case when it is mixed in feed or given in lower doses into the water.
And as always: Talk to your vet about it!