Clinical TechniquesPrevalence of Gastric Ulcerations in Horses with Colic
Introduction
Gastric ulceration has been documented to occur in both adult horses and foals.1, 2, 3, 4, 5, 6, 7, 8, 9, 10 The prevalence of gastric ulceration ranges from 70% to 90% in actively training racehorses,1, 6, 7, 11, 12, 13, 14, 15 but up to 52% of retired racehorses also have been diagnosed with gastric ulceration.1 Three-day event horses have a 75% prevalence of gastric ulceration, and Western performance horses have similarly reported rates.8, 16 An endoscopic survey of foals without signs of gastric disease found that 43% had ulcers.5 Of 22 foals without a previous disorder, 15 (68%) had evidence of gastric erosion or ulceration.5 Although this syndrome has been recognized with the advent of elongated endoscopes for over 20 years, it continues to remain a clinically important disease entity.
The high prevalence of gastric ulceration in equids is thought to be related, in large part, to the functional anatomy of the equine gastric mucosa.17, 18 The equine mucosal lining of the stomach is histologically divided into four layers.19, 20, 21, 22, 23, 24 The proximal half is stratified mucosa with no glands or mucus-producing cells. The cardiac gland region is adjacent to the margo plicatus and secretes mucus and bicarbonate. The largest portion of the equine stomach is the fundic gland region. This is the site of the gastric glands including parietal cells, which secrete hydrochloric acid (HCl); zymogen (chief) cells, which secrete pepsinogen; and enterochromaffin-like cells (ECL), which secrete both histamine to promote HCl secretion by parietal cells; and serotonin to control gastric blood flow and secretions. The pyloric gland region lines the gastric antrum and comprises three different types of cells; G cells, which are a major source of gastrin; D cells, which secrete somatostatin; and ECL cells, which secrete serotonin.
Equine gastric ulcer syndrome (EGUS) is a term used to describe multifocal or focal ulceration, gastric emptying disorders, and generalized gastritis. According to Murray,25 the pathogenesis is an imbalance between aggressive and protective factors influencing the microenvironment of the gastric and duodenal mucosa.25 Aggressive factors that can damage the mucosa include HC1, pepsin, and bile acids. Factors that are protective to the mucosa include the mucus–bicarbonate layer, prostaglanding E2, mucosal blood flow, cellular restitution, and epidermal growth factor.16, 18, 26
According to Andrews and Nadeau,27 protective factors appear to be better developed in the equine glandular mucosa than in the squamous mucosa.27 Glandular mucosal ulcers typically occur because of inhibition of prostaglandins and decreased secretion of mucus and bicarbonate. Squamous mucosal ulcers are caused by a prolonged exposure to HCI, pepsin, and bile acids (the aggressive factors). The gastroesophageal reflux disease syndrome that occurs in humans is believed to be similar to ulcers occurring in the equine squamous mucosa, because both the human esophagus and equine squamous mucosa lack the protective factors intrinsic to the glandular mucosa.
Numerous proposed factors are involved in the cause of EGUS. First and foremost, the horse stomach continuously secretes HC1 with the resultant gastric pH often below 2.0.16, 17, 18, 28, 29 Furthermore, repeated exposure of the squamous mucosa to highly acidic fluid can be induced with feed deprivation.16, 30, 31, 32, 33 Other described factors include variable gastric motility and emptying rates, exercise and training, nonsteroidal anti-inflammatory drug (NSAID) administration, and stress.11, 12, 13, 14, 16, 19, 27, 34, 35, 36, 37, 38 Helicobacter pylori has been documented to both contribute to and exacerbate ulcer disease in humans, but it has not been demonstrated to be a consistent factor in EGUS.39 Additionally, nitric oxide synthesis may play a role in reduced ulcer healing and more severe ulceration.40 The pathogenesis of EGUS is thus likely to be multifactorial, with several of the causative factors associated with daily management. This helps explain why the disease is so common in the equine population.
A previous study found a large variability in the severity and duration of abdominal discomfort in horses with evidence of gastric ulceration.2 In this study, gastric ulceration was determined to be the primary cause of colic in 31 of 111 cases (28%).2 This diagnosis was based primarily on endoscopic evidence of gastric ulceration, response to treatment, and improvement in clinical signs. Horses presenting with the chief complaint of colic are thought to be at increased risk of development of gastric ulcers because of the stresses of hospitalization, feed deprivation, possible administration of NSAIDS, and stall confinement. We hypothesized that horses admitted for colic would have a higher incidence and severity of gastric ulceration than horses hospitalized for reasons other than gastrointestinal disease.
The objectives of this prospective clinical study were to evaluate the prevalence of gastric ulcers in horses with acute abdominal crisis and to examine the temporal effect of hospitalization on ulcer formation in equine patients presenting with the complaint of colic. Also, other factors that may be associated with gastric ulceration including age, sex, breed, clinical laboratory data, and anatomic site of lesion for colic were examined.
Section snippets
Materials and Methods
All horses presenting to the George D. Widener Hospital for Large Animals during a 12-month period were included in this study, and the breeds represented Thoroughbreds, Standardbreds, Warmbloods, Quarter Horses, Appaloosas, miniature horses, draft breeds, and Arabians. The case horses were included if the history and physical examination supported the presenting complaint of acute abdominal crisis (colic). Further refinement encompassed the randomized selection of study patients, alternating
Results
One hundred sixty-nine horses presenting to the George D. Widener Hospital for Large Animals during a 12-month period were included in this study. Of these horses, 112 presented with the chief complaint of colic and fit the criteria for study inclusion out of 405 horses with the same problem. The remaining 57 horses in the study served as case controls and presented with non-colic, nonemergency complaints, which included horses admitted for scintigraphic or lameness examination. Of the 112
Discussion
This study confirmed the high incidence of gastric ulceration in adult horses.1, 2, 3, 4, 5, 6, 7, 8, 9, 10 Gastric ulceration was evident in horses presenting for colic and noncolic complaints at 68% and 72%, respectively; the difference was not statistically significant. The high number of horses with gastric ulcers in the control population is likely a reflection of the equine hospital population, although breed and intended use of the horses may have been a confounder. Thoroughbreds and
Conclusion
All hospitalized horses have a high incidence of gastric ulceration. A surprising finding from this study was that we found no statistically significant increased risk in horses with colic developing EGUS. Our results support the opinion that hospitalized horses are at increased risk for gastric ulcers because of multiple factors, including confinement, feed management, and treatment regimens. Diagnostic gastroscopy should be performed in hospitalized horses if they are symptomatic or have the
References (48)
- et al.
Prevalence of non-glandular gastric ulcers in horses involved in a university riding program
J Equine Vet Sci
(2006) - et al.
Oesophageal peristaltic dysfunction in peptic esophagitis
Gastroenterology
(1986) The role of prostaglandins in the regulation of gastric mucosal blood flow
Prostaglandins
(1981)- et al.
Peptic ulcer pathophysiology
Med Clin North Am
(1991) - et al.
The effect of exercise on equine gastric ulcer syndrome in the Thoroughbred and Standardbred athlete
J Equine Vet Sci
(2009) - et al.
Gastric ulceration in mature Thoroughbred horses
Equine Vet J
(1986) Gastric ulceration in horses: 91 cases (1987–1990)
J Am Vet Med Assoc
(1992)Endoscopic appearance of gastric lesions in foals: 94 cases (1987–1990)
J Am Vet Med Assoc
(1989)- et al.
Gastric ulcers in foals
J Am Vet Med Assoc
(1982) - et al.
Prevalence of gastric lesions in foals without signs of gastric disease: an endoscopic survey
Equine Vet J
(1990)