Current Ideas of Causes and Management
A.M. Merritt, DVM, MS
Professor Emeritus, University of Florida

Some Essentials of Equine Gastric Anatomy
and Function Relative to EGUS

In contrast to humans, where the whole stomach is lined by a glandular mucosa (lining) that secretes many things, including acid, the top half of the equine stomach is lined with a non-glandular (often called “squamous”) mucosa, which is similar in structure to that which lines the esophagus in all species (Fig. 1). The demarcation line between the glandular and non-glandular mucosa is referred to as the margo plicatus. Normally, this line is very sharp, but it can become quite deformed by ulceration of the non-glandular mucosa in that region.


A. Gastric acid (HCl) is secreted by the “fundic” region of the glandular mucosa. As with other species, the glandular mucosa of the horse has intrinsic complex mechanisms in play to protect it from the acid produced there, whereas the non-glandular (squamous) mucosa is devoid of such mechanisms and is, therefore, much more susceptible to damage from acid exposure.

B. Intra-gastric digestion by bacteria occurs to some degree in the horse. In all monogastric (simple-stomached) species, the stomach serves as a sort of initial holding tank for ingested food. In some, such as the pig and the horse, moreover, considerable bacterial fermentation takes place within the stomach which is probably not the case in other, non-herbivorous monogastrics such as humans, dogs, and cats. So, what=s the trick with respect to support of intra-gastric fermentation within the equine stomach? It probably works like this. The coarser ingesta tends to collect in top part of the gastric contents mass. These contents are the first to be bathed by swallowed saliva (10-12 liters/day in the adult) and, since they are within the non-glandular part of the stomach, they have not been exposed to much acid (in the sedentary horse) and, thus, have a relatively high mean pH (>6.0). The contents then become more liquid, and the particulate component finer, as they settle into the lower part of the stomach, with a concordant drop in pH, such that the mean pH of the contents in the most bottom (ventral) part of the stomach is 4.5) that colonize the contents within the mid-portion of the ingesta mass. The byproduct of such fermentation is lactic acid, and plenty of that can be generated within a horse’s stomach if the meal contains a large proportion of soluble carbohydrates. The regional pH variation was elegantly demonstrated by Baker and Gerring who recorded a progressive drop in value as a nasogastrically introduced weighted pH probe dropped through the gastric contents to the bottom of the stomach where the most acidic components collect.
Peptic Ulcer Disease - General Concepts
Gastric mucosal damage can manifest as inflammation with no break in the integrity of the surface, erosion where just the superficial layer is disrupted or ulcer where the lesion penetrates deep into the stomach wall - sometimes causing bleeding if a vessel is invaded, sometimes penetrating all the way through to cause serious or fatal peritonitis. Erosion or ulcer formation essentially represents the development of an imbalance between corrosive substances, such as acid, or perhaps volatile fatty acids (VFA) within the stomach contents and the mucosal protective mechanisms, with the balance tipping towards the corrosive agents. Mucosal protection mechanisms within the glandular mucosa, dependent upon local prostaglandin E2 expression, are reasonably well understood. Protective mechanisms within the squamous mucosa – esophagus and/or proximal stomach in relevant species – are not as well understood. In humans, infection of the pyloric mucosa with Helicobacter pylori challenges glandular mucosal integrity through its colonization and elaboration of urease to protect itself from gastric acid. Gastric acid itself may be the major instigator of squamous mucosal damage.


EGUS is NOT just one disease. This term was coined by a group of academic clinicians and practitioners that met yearly for a number of years under the aegis of Dr. Frank Pipers of Merial Inc. The acronym was designed to refer to a group of problems with differing causes that result in ulceration of either (or both) the non-glandular (squamous) or glandular mucosa. However, “EGUS” is now often used to refer to the most common form of equine gastric ulcer disease, namely the primary squamous disease (see below), which is unfortunate because it results in people thinking there is only one from of gastric ulcer disease in horses.


Currently Recognized Syndromes In Adults >1 Year of Age
– In Order of Decreasing Frequency
A. Primary Erosion and/or Ulceration of the Squamous Mucosa (Fig. 2). The most common manifestation of this syndrome is in adult horses under intensive training programs, irrespective of breed or program. It can also be found as an incidental finding in younger sedentary horses if they are subjected to gastric endoscopy for some specific reason. The most common place for the damage to occur is on the lesser curvature near the margo plicatus (the junction between squamous and glandular mucosa), but sometimes it can be quite widespread. The lesions can be in the form of discrete ulcers of various sizes and depths, or be strictly erosive. It is tempting to think of this problem as the equine version of “gastro-esophageal reflux disease” (GERD) in humans, where it has been shown that running can increase the incidence of symptoms of “heartburn”. Some studies currently being done in our lab in horses on a treadmill indicate that the intra-gastric pressure sharply increases as the horse moves from walk to trot, probably as a result of increased intra-abdominal pressure related to the exercise. We have further shown that this pressure pushes acidic contents up into the squamous-lined fundic region of the equine stomach, exposing this area, which is normally either devoid of food or exposed to contents of low acidity, to contents of high acidity that are found in the lower part of the stomach. Furthermore, there is experimental evidence from the lab of Dr. Frank Andrews at the University of Tennessee to suggest that volatile fatty acids produced by the intra-gastric fermentation of feedstuffs may exacerbate lesions of the non-glandular mucosa that have been initiated by exposure to the gastric acid. This has some important implications, therefore, with respect to how we feed horses.

B. NSAID Induced Glandular Ulcer Disease (Fig. 4). As is well-known, the non-steroidal anti-inflammatory drugs (NSAID’s), a class of drugs used commonly in horses can, if given in excess, cause severe ulceration of the glandular mucosa, especially in the pyloric region. They are considered to be ulcerogenic by reducing prostaglandin E2 production within the glandular mucosa. Major recognized mucosal protective effects of prostaglandin E2 include suppressing HCl, and inducing mucosal bicarbonate and mucus secretion. If the recommended dosages for the NSAID’s are followed, however, it is highly unlikely this problem will occur, although we do recognize that certain horses appear to be overly sensitive to the damaging effects of NSAIDs and will develop lesions when given recommended doses. MacAllister has shown that the order of gastric ulcerogenic potential in horses is as follows: phenylbutazone>flunixin>ketoprofen.

C. Pyloric Mucosal Ulcer Disease (Fig. 4). With the availability of longer endoscopes, combined with extra effort to remove all contents from the stomach during endoscopy, a form a PUD in the horse that manifests as a primary ulceration of the pyloric glandular mucosa has been appreciated in adult horses. The squamous mucosa is usually free of lesions. Clinical signs of the acute form of this problem can be as varied as those seen with primary squamous disease, however. Furthermore, if untreated in their early stages, lesions near or around the pyloric outflow can induce sufficient scarring to interfere with gastric emptying, which can end up causing severe post-prandial distress to afflicted animals. Of all the variations of equine PUD discussed above, this form would qualify as that most likely to be caused by a Helicobacter-like organism, but, at present, finding of such an organism in the equine stomach in association with this lesion remains to be demonstrated.

D. Secondary Squamous Ulceration (Fig. 5). This problem, where the primary lesion commonly occurs in the duodenum (see GDUD in the EGUS in foals handout), is virtually never seen in horses >1 year of age. What is seen from time to time is the rather acute onset of gastric outflow obstruction due to the formation of proximal duodenal stricture that has progressed to a critical point. Examining the medical history of these cases indicates that some of them may have shown classical signs of GDUD when they were sucklings or weanlings. At this point, this is a problem that requires surgical intervention for possible amelioration. The prognosis for a successful outcome is very guarded. Secondary sequamous disease may also be seen in adults due to any other condition that might disrupt gastric motility, such as extensive pyloric mucosal ulceration.

Anti-Ulcer Therapy
Strategies of anti-ulcer therapy currently in use for horses are those that have been developed for humans. Currently, there are 3 basic approaches: 1) maintain an intragastric pH >4; 2) coat the ulcer with an acid-resisting agent; 3) provide prostaglandin or stimulate its production by the gastric mucosa.

A. Controlling Intragastric pH. The time-honored method of buffering gastric HCl with Al/Mg hydroxide preparations, though potentially the least expensive approach, does work in horses but requires considerable effort. Studies recently completed in our laboratory show that 240 ml of an extra strength oral antacid product (eg: “Maalox Therapeutic Strength”®) will keep the intragastric pH of an average-sized horse above 4.0 for at least 2 hours. Clinical experience has indicated that administration of this dose QID has been effective in treating squamous ulcer disease in some patients. Clearly, however, this is a time consuming process that some animals tolerate better than others. A few horses will actually eat a flavored product mixed in with a little grain.

Acid secretory control can presently be accomplished most effectively in the horse by treating with an histamine-2 receptor antagonist; compounds that primarily have been used to date include cimetidine (“Tagamet”®) and ranitidine (“Zantac”®), although any of the compounds on the market should work - it is a question of effective dose. While ranitidine is effective in therapy of equine gastric ulcers, much larger doses than recommended for humans are needed to affect any reasonable response in the horse. The recommended dose of ranitidine is 6-7 mg/kg orally, or 2 mg/kg systemically, at least 3 times per day, which represents a significant expense in a 500 kg animal. The oral form is much less expensive than it used to be since it can now be purchased over the counter as the generic compound. A recent study from UC Davis indicates that cimetidine at 20 mg/kg TID p/o is not effective in controlling squmaous ulcer disease in horses in training. Another study from Pennsylvania also showed that the recommended dose of ranitidine was also not as effective as a commercially available proton pump inhibitor (see below).

The more effective approach to chemical suppression of gastric acid secretion in the horse is through use of a proton pump blocking agent, such as omeprazole. This class of drugs works, as indicated, at the final step of elaboration of HCl secretion by the parietal cell by blocking a K+/H+-ATPase “pump” that involves an exchange at the secretory membrane. At least 4 mg/kg orally QD is needed to effectively keep the intragastric pH >4.0 for up to 20 hours in adult Thoroughbred horses. There is now a paste formulation of omeprazole for horses that is commercially available and FDA approved called “GastroGard”® (Merial, Inc). However, there is strong clinical evidence that primary squamous disease can be effectively controlled by the giving 1 mg/kg of omeprazole per day, as the “GastroGard”® formulation, once the initial problem has been brought under control using the 4 mg/kg dose (usually about 3 weeks). Merial now also markets a delivery system for their GastroGard product (“UlcerGard”®) that now makes it easier to administer the 1 mg/kg dose. Numerous small pharmacies within the USA also formulate their own generic omeprazole compounds; in a recent study done in our laboratory and at UC Davis have found that, in general, compounded preparations were distinctly inferior to “GastroGard”® with regard to efficacy.

B. Coating the Ulcer. The compound available as an ulcer-coating agent is a polysulfated sugar, sucralfate (“Carafate”®). In humans, it is recommended that this be given on an empty stomach which is a pretty difficult recommendation for application to horses. Nevertheless, this compound is used quite freely in equine patients and many feel it is certainly helpful in controlling the severity of the various ulcer diseases. An additional rationale for its use is its putative ability to induced mucosal protection by activating PGE2 synthesis, but this has not been definitively proven. I, and others, remain to be convinced of its efficacy in equidae. In addition, animal experiments indicate that sucralfate binds to lesions best within an acid medium, so that, ideally, it should not be given concomitantly with, or soon after, an H2 antagonist.

C. Exogenous or Endogenous Prostaglandin. The prostaglandin approach would be most indicated where there is some concern about the effects of NSAID’s, or where there is a recognized stress, as discussed above. Synthetic PGE2 is available and not excessively expensive at the suggested equine dose, but it does not really provide a practical approach to the management of NSAID-induced gastric disease in horses. On a more practical level, some studies done in our laboratory found that feeding corn oil, which contains a large amount of the arachidonic acid precursor, linoleic acid, to ponies at a dose of 20 ml per 100 kilograms body weight significantly increased the amount of prostaglandin E in the gastric contents, similar to what had been found earlier in rats and humans. The true anti-ulcer potential of this approach still needs evaluation, but it would do no harm to supplement the diet of horses being treated with an NSAID with corn oil, and might reduce the risk of NSAID-induced gastritis. It goes without saying that the continued administration of NSAIDs is contra-indicated for a patient in which glandular ulcer disease is diagnosed or suspected. Do not expect corn oil treatment to be effective in controlling non-glandular (squamous) ulcer disease, however.

In summary, there is no question that H2-antagonist treatment in particular has been effective in reducing the severity of signs of, and promoted lesion healing in, some equine peptic ulcer cases. But the proton pump blockers are proving to be more effective and practical, especially for control of development of squamous ulcer disease in horses in training. Prophylactically, future the emphasis may, perhaps, shift away from the acid suppressors and to the fundamental aspects of mucosal protection, such as agents that promote mucosal protection directly, although this may be more difficult to accomplish with respect to the squamous, as opposed to the glandular, mucosa. Furthermore, we should not overlook the idea that another very important component of prophylaxis, particularly with respect to training procedures, may lie as much in preventive management techniques, involving feeding and housing programs, as any chemical means available.


Currently Recognized Syndromes In Foals <1 Year of Age – In Order of Decreasing Frequency
A. Gastroduodenal Ulcer Disease (GDUD). This problem is confined almost exclusively to the sucklings and early weanlings. The most severe, and probably primary, lesion is in the upper duodenum. The impression is that the development and extent of attendant erosions and ulcers of the squamous gastric and esophageal mucosas are dependent upon the degree and duration of gastric outflow obstruction and upper duodenal contents reflux (Fig. 3).

It seems that the GDUD syndrome reached its peak incidence in the mid-1980’s, but it is still a serious problem in regions where intensive mare/foal operations exist. It can manifest as a herd outbreak. Often the first, and sometimes the outstanding, clinical sign is a watery diarrhea. Some foals refuse to suckle and show mild signs of colic and/or teeth grinding. A few may be found dead without forewarning due to perforation of the duodenum. A definitive diagnosis can usually be made by endoscopy of the duodenum where, early in the course, a diffuse duodentitis can be seen, characterized by a yellowish plaque of exudates overlying the mucosa.

Most afflicted animals survive and are well within a week following some supportive or specific anti-ulcer therapy (how many may be asymptomatic and survive with no therapy is unknown). A few become progressively more ill in spite of treatment and develop the “classic” signs of this disease that include drooling, teeth grinding, periodic bouts of colic, especially after suckling, and marked weight loss. If these signs persist for more than a week, it is a strong indication that the duodenum has become severely constricted by inflammation-induced fibrous tissue and is mechanically obstructing gastric emptying. Abdominal radiography will reveal a markedly enlarged gastric gas cap and prolonged retention of a standard barium meal, which should completely leave the stomach within 1 hour. Occasionally, dilated bile ducts can also be seen radiographically. If this occurs, the only relief is a gastrojejunostomy, which is an expensive procedure with a guarded prognosis. When this is done, the squamous lesions quickly resolve.

The cause of GDUD in young horses is unknown. It may be due to a unique combination of factors. There has been considerable interest in its apparent relationship with outbreaks of rotaviral diarrhea, but there is no precedent for this agent causing duodenal ulcer disease in other species in which its pathology is better understood. Also, it does occur in foals in which no rotavirus can be found. The possible interaction of a Helicobacter type agent cannot be discounted at this time.

B. Primary Erosion and/or Ulceration of the Squamous Mucosa. Sometimes these lesions occur in association with some other more apparent disease problem, sometimes they are found when there is a complaint of unthriftiness, vague mild colic, or sometimes they are found in asymptomatic young animals that are being endoscoped routinely to check for the possible presence of ulcers or some other problem. In contrast to indications that prolonged periods of exercise and attendant increase in intra-abdominal pressure may be the underlying cause of this problem in adult horses (See handout on EGUS in adults), the basis for the pathogenesis of this lesion in younger horses is not known. Since, again, it is akin to gastro-esophageal ulcer disease (GERD) in humans, the etiology is more likely to be mechanical and/or nutritional than infectious.

C. Stress-Related Disease. Classically, “stress-related” ulcer disease is attributed to a disruption of the circulation of the gastric mucosa. It may involve reduced mucosal prostaglandin E2 production, which implies reduction in normal mucosal circulation, and bicarbonate and mucus secretion, among other things, but it is no doubt more multifactorial than this. Occasionally this occurs in foals that are suffering from a severe illness or trauma. Recent studies in septic rats indicate that an upregulation of inducible nitric oxide synthase (iNOS) could be a factor. The lesions are usually confined to the glandular mucosa, just adjacent to the margo plicatus in the cardiac gland region, and they can be severe enough to cause a perforation. Unfortunately, the afflicted animal usually shows no prodromal signs that this lesion is present unless perforation does occur, when it is usually too late to do much about it.

D. NSAID Induced Glandular Ulcer Disease. See the discussion in the EGUS- Adults handout.

Anti-Ulcer Therapy – Foals
With regard to ranitidine, Sanchez et al, at the University of Florida, showed that it is effective in suppressing gastric acid secretion in normal neonatal foals, with 6.6 mg/kg given orally maintaining the mean intra-gastric pH >4.0 for 6-8 hours, whereas 2.0 mg/kg IV only maintained a pH >4.0 for only 4 hours. In critically ill neonatal foals, however, the response to IV ranitidine was highly variable, with some responding as expected, but a significant group of others that did not respond at all. Also, it was discovered in this critically ill group that in those foals that were recumbent the intra-gastric pH was often near neutral, suggesting that they either could not produce gastric acid or that there was a profuse and constant duodenal reflux that neutralized any acid that was present. From these findings, we raise the question of whether it is necessary to prophylactically treat sick foals with H-2 antagonists, which has become rather common practice in equine neonatal intensive care protocols.

Alternatively, we have shown that the proton pump inhibitor (PPI), omeprazole, given as the “GastroGard”® product at 4 mg/kg p.o. QD, will inhibit gastric acid secretion for up to 24 hours in neonatal foals (vs. 14-15 hrs in adults). Clearly this is a preferable choice for anti-ulcer therapy in foals. In those foals where such treatment is warranted but their disease appears to be primarily or secondarily disrupting gastric emptying, IV pantoprazole, another PPI product being used in humans, is very effective in foals, given at 1.5 mg,kg QD (studies done at UF by Drs. Ryan et al.).

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