Equine Gastric Ulcer Syndrome (EGUS)
Due to it’s multiple causes and complex nature, the term Equine Gastric Ulcer Syndrome (EGUS) has been used to describe gastric ulcer disease in horses. Current studies suggest that EGUS is fairly common, with a prevalence ranging from 25% to 50% in foals and 60% to 90% in adult horses.
Gastric ulcers have been identified in multiple regions of the equine stomach including the non-glandular stratified squamous mucosa, margo plicatus, glandular mucosa, and pylorus.
Two age-related syndromes have been described. One is in foals less than 9 months of age and the other is in yearlings and adult horses greater than 9 months of age. Although ulcers appear to be physiologically similar between foals and adult horses, the syndromes often have different inciting causes and clinical presentations. Diagnosis of EGUS generally relies on recognition of clinical signs, results of gastroduodenoscopic examination, and/or empirical response to anti-ulcerative therapy(ies).
STOMACH ANATOMY & PHYSIOLOGY
The horse stomach is divided into two distinct regions: the esophageal or non-glandular region and the glandular region.
The esophageal region is covered by squamous mucosa and covers approximately one-third of the entire stomach. The glandular region covers the remaining two-thirds of the stomach and contains glands that secrete hydrochloric acid, pepsin, bicarbonate, and mucus. The esophageal and glandular regions are separated by a distinct demarcation called the margo plicatus or cuticular ridge.
The horse stomach secretes hydrochloric acid (HCl) continuously, regardless of the presence or absence of feed material. Foals tend to maintain a particularly high level of acidity (low pH) within their gastric fluid; this environment has been implicated as a predisposing factor in the development of EGUS.
The adult equine stomach secretes about 1.5 liters of gastric juice hourly; acid output ranges from 4 to 60 mmoles HCl per hour. The pH of gastric contents ranges from 1.5 to 7.0 depending on region analyzed. A neutral pH can usually be found in the dorsal portion of the esophageal region near the esophageal sphincter, whereas lower pH can be found near the margo plicatus (3.0-6.0) and in the glandular region near the pylorus (1.5-4.0).
Gastric emptying of a liquid meal generally occurs within 30 minutes, whereas complete gastric emptying of a roughage (hay) meal requires about 24 hours.
Equine Gastric Ulcer Syndrome occurs as a result of disequilibrium between mucosal aggressive factors (HCl, pepsin, bile acids, organic acids) and mucosal protective factors (mucus, bicarbonate).
Esophageal Region. As you might guess, ulcers in the esophageal region typically occur as a result of prolonged exposure to aggressive factors. The severity of squamous ulceration is directly related to duration of exposure.
For example, gastric ulcers are often most severe in the squamous mucosa near the margo plicatus where there is near-constant exposure to aggressive factors. Since fasting and irregular feeding can increase exposure of the stomach to acid, these regimens have been implicated as potential causes of ulceration. Recumbency, which overexposes certain portions of the stomach to acid, has also been implicated.
Glandular Region. Since a higher percentage of protective factors are present in the glandular portion of the stomach, different causative mechanisms tend to lead to ulceration in this region as compared to the esophageal region.
Ulceration of the glandular mucosa is usually due to disruption of blood flow and a secondary decrease in the secretion of mucus and bicarbonate (which are mucosal protective factors).
Of course, overexposure to aggressive factors (as a result of decreased gastric/ esophageal motility, delayed gastric emptying, recumbency, etc.) can also result in glandular ulceration.
Inhibition of prostaglandins (PGs) may also play a role in the pathogenesis of glandular ulceration. PGs help maintain the integrity of squamous and glandular mucosa by activating production of surface-active phospholipid which stimulates mucosal repair and prevents mucosal damage.
Suppression of prostaglandin synthesis results in decreased mucosal blood flow, increased gastric acid secretion, and reduced bicarbonate secretion by the glandular mucosa. This in turn leads to breakdown of mucosal protective factors and increased predisposition towards glandular ulceration.
Non-steroidal antiinflammatory drugs (NSAIDs) block prostaglandin synthesis (primarily PGE2, I and A) and have been associated with glandular ulceration, especially in foals.
Stress has also been associated with the development of glandular ulcers, presumably via the excessive release of endogenous corticosteroid, which also inhibits prostaglandin synthesis.
Volatile fatty acids (VFAs) have been associated with acid injury to gastroesophageal (squamous) mucosa in horses. VFAs are generated by resident bacteria during the fermentation of carbohydrates. VFAs penetrate squamous mucosa more easily when acid concentrations are high. Since many performance horses are fed diets high in fermentable carbohydrates (e.g. grain), they are more at risk for gastric ulceration.
Desquamation or “shedding” of the squamous epithelium in foals has been linked to the development of gastric ulcers. Desquamation occurs in 80% of foals up to 35 days of age.
In a study using rats, loss of epithelial cells along the margo plicatus resulted in increased susceptibility of this region to acid injury. Acid injury, in turn, resulted in delayed healing (reepithelialization) of the affected area(s). Eventually, ulcers developed as a result of persistent HCl injury to the deeper mucosal layers.
The diagnosis of EGUS is based on the presence of clinical signs, videoendoscopic findings, and/or response to empirical treatment.
Abnormal history and clinical presentation are the first clues to the potential existence of gastric ulcers.
Clinical signs in FOALS include:
Intermittent colic (usually manifesting following suckling or eating)
Frequent laying in dorsal recumbency (on the back)
Intermittent nursing (i.e. interrupted nursing due to gastric discomfort)
Inappetance (poor appetite)
Bruxism* (grinding of teeth)
Ptyalism* (excess salivation)
*Bruxism and Ptyalism are often suggestive of compromised outflow of gastric acid, such as occurs with pyloric obstruction.
Clinical signs in OLDER HORSES include:
Although suspicion of EGUS is often derived from the presence of typical symptoms, a definitive diagnosis is rarely made based on clinical signs alone. A definitive diagnosis of EGUS can only be made using video- or fiberoptic endoscopy. In fact, it was the development of this technology that dramatically increased veterinary awareness of gastric ulcers in horses (especially adults).
An endoscope must be at least 2 meters long to reach the equine stomach. A longer endoscope (~2.8 meters in length) is necessary to observe the duodenum (i.e. the first part of the small intestine below the stomach) in adult horses. A shorter scope may be sufficient to see the stomach of foals.
Foals up to 20 days of age are allowed to nurse but should not consume solid feed for 8 to 10 hours prior to endoscopic examination. Older foals and mature horses are also fasted for 10 hours preexamination. This time period is required to ensure adequate emptying of gastric contents and enhanced videoendoscopic visability.
Healthy squamous or non-glandular mucosa at the top of the stomach appears as a pale to white tissue. In very young foals (neonates), the squamous mucosa is very thin and displays a pale pink to pale white color.
By contrast, the glandular mucosa at the bottom of the stomach is normally dark pink to red with a smooth, glistening texture. The duodenal mucosa should have a uniform pink, velvety appearance.
RESPONSE TO EMPIRICAL TREATMENT
It should be noted that lack of definitive endoscopic abnormalities does not confirm the absence of gastric ulceration. In fact, a false negative endoscopic evaluation is not uncommon. Since only relative large (macroscopic) lesions will be observed endoscopically, smaller (microscopic) lesions may escape visual detection.
In these cases, a positive response to empirical therapy is often considered diagnostic, especially if the change in clinical presentation is dramatic. In many cases of equine gastric ulceration, abolishment of overt clinical signs has occurred pursuant to treatment of endoscopically-normal individuals.
A number of strategies have been used for treatment and prevention of gastric ulcers in horses and foals.
Successful therapy is directed towards:
MINIMIZING RISK FACTORS (such as medication or stress). Eliminating risk factors is fairly obvious, although this stategy is often overlooked.
Horses with ulcers should be stressed as little as possible.
Medications that have been shown to promote ulcer formation should be used with caution. Non-steroidal antiinflammatory drugs (NSAIDs) such as Bute, Banamine, Ketofen, etc.) are frequently used to alleviate the clinical signs (namely inflammation and pain) associated with arthritis in horses. However, consistent use can result in gastric ulceration as well as kidney and liver dysfunction. Therefore, we recommend this form of therapy only for horses that perform very infrequently, such as once or twice weekly (or less).
There is a relatively new product called EQUIOXX (firocoxib) that was developed by Merial. Equioxx has been shown to reduce inflammation and pain associated with osteoarthritis in horses. At the same time, it offers a much better safety profile when compared to other (more traditional) NSAIDs. Equioxx is the first coxib class nonsteroidal antiinflammatory drug that is highly selective against Cyclooxygenase-2 (Cox-2) prostaglandins which are responsible for inflammation. Unlike other NSAIDs, however, Equioxx spares the beneficial Cox-1 prostaglandins required for normal gastric, renal (kidney), and hepatic (liver) function. A single dose lasts for 24 hours and can be administered for up to 14 days in a row. Equioxx comes in an oral paste form; each tube contains 1500 pounds of medication. Each marking on the syringe treats 250 pounds of body weight, and each notch corresponds to a 50-lb weight increment. Equioxx can be administered with or without food. Equioxx can be ordered through our Pharmacy by calling 678-867-2577 or by contacting firstname.lastname@example.org
For more information, contact our office or visit http://www.equioxx.com/
At The Atlanta Equine Clinic, we have observed a comparable effect of a much lower (and less-expensive) dose of the small animal preparation of firocoxib, known as PREVICOX, to that of its large-animal counterpart (Equoxx). In our experience, a 57-mg dose of Previcox (which costs less than 67 cents) produces similar clinical results to that of an extire tube of Equioxx (which costs $9.75). This product can also be ordered through our pharmacy.
PROTECTING THE STOMACH LINING. This strategy involves the use of mucosal-protective feeds and/or medications, which are designed to “coat” the stomach lining.
Alfalfa hay, which is high in protein and calcium, appears to have an extra-potent buffering effect in the stomach. Horses fed alfalfa hay have less acidity and lower gastric ulcer scores than horses fed other types of hay. The buffering effect of Alfalfa hay can last up to 5 hours post-feeding.
Moreover, horses fed hay continuously have less gastric acidity (i.e. a higher pH) in comparison to those that are fed intermittently or fasted for a period of time. For this reason, we typically recommend the use of slow hay feeders for horses with gastric ulceration. Small mesh hay nets (such as the Freedom Feeder) provide continuous access to hay but effectively regulate the horse's rate of ingestion.
The most common drug currently used to coat the stomach lining is Sucralfate (Carafate®), which is only effective for the glandular lining of the stomach and the duodenum, where ulcers are less likely to occur. Although this treatment strategy has proved to be helpful in many cases of EGUS, it is not considered adequate when used as the sole treatment.
INHIBITING ACID SECRETION IN THE STOMACH. Inhibiting gastric acid secretion is the mainstay of gastric ulcer treatment in horses.
There are 3 categories of acid suppressants:
ANTACIDS simply absorb whatever acid is in the stomach. They are the least-expensive form of acid suppressant. On the other hand, they are also the least-effective. Antacids must be administered in large doses and with frequency to provide any benefit. This approach, for example, would necessitate the administration of 8-10 ounces of Maalox to an adult horse a minimum of every two hours around the clock. Even at that dose, the therapeutic effect is questionable. Therefore, antacids are also not considered adequate therapy when used alone.
Cimetidine (Tagamet®) and Ranitidine (Zantac®) have historically been the most frequently used, and both effectively inhibit gastric acid secretion in horses. A 3-week treatment period is usually required to ensure complete healing.
Two other H2 antagonists on the market for use in humans are Famotidine (Pepsid®) and Nizatidine (Axid®). Effective dosages for horses have not yet been established.
Omeprazole is a proton-pump inhibitor that is labeled both for treatment of EGUS (GastroGard) as well as prevention of recurrence (UlcerGard). Omeprazole is the only FDA approved medication for use in horses. In addition to being the most effective drug, it is also the most expensive.
Compare the effect, dosage and cost of commonly-used ulcer medications HERE.
Therapeutic treatment with omeprazole involves oral administration of paste (in the form of GastroGard) once daily for 28 days. Preventative therapy requires only one-quarter of the treatment dose (in the form of UlcerGard). The medication contained in these products is the same ingredient found in the “purple pill” known as Prilosec that is currently sold to humans for gastric ulcer treatment. We currently sell GastroGard for $32-$39/ tube (depending on the quantity ordered).
Recent research suggests that Aloe Vera Juice may also have potent anti-ulcerative effects, possibly comparable to those of omeprazole. Although nothing has yet been published, initial results are promising. Aloe Vera Juice is much less expensive and can be readily purchased at Wal-mart (in the Pharmacy section).
At this point in time, most veterinarians don't carry the same degree of confidence in Aloe Vera Juice as with Omeprazole with regard to gastric ulcer treatment. However, daily Aloe Vera Juice administration is a potential option if omeprazole is cost-prohibitive.
We recommend administering 1/4 cup of Aloe Vera Juice (along with feed) twice daily as needed.