CLINICAL TECHNIQUES
Prevalence of Gastric Ulcerations in Horses
with Colic
Tara S. Rabuffo, DVM, ACVS,a Eileen S. Hackett, DVM, MS, ACVS,b
Nora Grenager, VMD,c Raymond Boston, PhD,d and James A. Orsini, DVM, ACVSd
ABSTRACT
The goal of this study was to determine the prevalence of
gastric ulcers in horses with acute abdominal crisis (colic)
and to examine the temporal effect of hospitalization on
ulcer development in equine patients treated for colic. In
addition, other factors that may be associated with gas-
tric ulceration were also explored. The study design
was a prospective original study incorporating 169
horses that presented to the George D. Widener Hospi-
tal for examination. One hundred and twelve horses pre-
senting with the chief complaint of colic were included in
the study group, and 57 horses that presented for non-
colic or nonemergency complaints were evaluated and
included as case controls. Gastroscopy was performed
on equine patients presenting with the chief complaint
of colic or horses presenting for reasons other than colic
(control); mucosal changes were scored 0 to 3. Addi-
tionally, horses presenting for colic were gastroscopically
evaluated twice during a 5-day period. Medical records
were reviewed for history, clinical findings, laboratory re-
sults, and treatment. Seventy-six of 112 horses present-
ing with the chief complaint of colic had gastric
ulceration compared with 41 of 57 horses in the control
group. There was a significant association between age of
the patient and chief complaint (ie, colic vs control) and
between breed and chief complaint. There was no asso-
ciation between gastric ulcer score and chief complaint
(colic vs control). Thirty-eight of the 112 horses present-
ing with colic deteriorated in ulcer score while hospital-
ized. Using a Pearson chi-squared test, there was no
statistically significant association between gastric ulcer-
ation with age, breed, or sex. Horses with gastric ulcer-
ation in the colic group had lower packed cell volumes
compared with horses presenting with colic without
From the Smoketown Veterinary Hospital, Smoketown, PAa; Department of Clinical
Sciences, College of Veterinary and Biomedical Sciences, Colorado State University, Ft
Collins, COb; Steinbeck Country Equine Clinic, Salinas, CAc; and Department of
Clinical Studies, University of Pennsylvania, School of Veterinary Medicine, Kennett
Square, PAd.
Reprint requests: James A. Orsini, DVM, ACVS, University of Pennsylvania, School of
Veterinary Medicine, New Bolton Center, 382 West Street Road, Kennett Square, PA
19348.
0737-0806/$ - see front matter
Ó 2009 Elsevier Inc. All rights reserved.
doi:10.1016/j.jevs.2009.05.005
540
gastric ulcers, and this was statistically significant (P <
.001). The high incidence of gastric ulceration in the
study and control groups supports the reports of other
investigators that gastric ulcers in horses, no matter the
presenting complaint, are widespread. There was a signif-
icant association between breed and chief complaint
(P ¼ .005); however, breed and outcome of gastric
ulceration were not related (Thoroughbreds were the
least likely breed to present for colic). Although a trend
in increasing gastric ulceration was seen in hospitalized
colic patients, it was not statistically significant. This sug-
gests that horses that are hospitalized may be at increased
risk for developing gastric ulcers because of stress, feed
deprivation, and administration of treatment. Thus,
horses that present for colic should be gastroscopically
evaluated if clinical signs raise the index of suspicion for
gastric ulceration.
Keywords: Acute abdominal crisis; Colic; Gastric
ulcers; Gastroscopy; EGUS
INTRODUCTION
Gastric ulceration has been documented to occur in both
adult horses and foals.1-10 The prevalence of gastric ulcer-
ation ranges from 70% to 90% in actively training race-
horses,1,6,7,11-15 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 gas-
tric 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 impor-
tant disease entity.
The high prevalence of gastric ulceration in equids is
thought to be related, in large part, to the functional anat-
omy of the equine gastric mucosa.17,18 The equine muco-
sal lining of the stomach is histologically divided into four
layers.19-24 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 bi-
carbonate. The largest portion of the equine stomach is the
Journal of Equine Veterinary Science  Vol 29, No 6 (2009)
TS Rabuffo et al  Vol 29, No 6 (2009)
fundic gland region. This is the site of the gastric glands in-
cluding 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 com-
prises three different types of cells; G cells, which are a ma-
jor 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 Mur-
ray,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 mu-
cosa than in the squamous mucosa.27 Glandular mucosal
ulcers typically occur because of inhibition of prostaglan-
dins and decreased secretion of mucus and bicarbonate.
Squamous mucosal ulcers are caused by a prolonged expo-
sure 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 protec-
tive factors intrinsic to the glandular mucosa.
Numerous proposed factors are involved in the cause of
EGUS. First and foremost, the horse stomach continu-
ously secretes HC1 with the resultant gastric pH often
below 2.0.16-18,28,29 Furthermore, repeated exposure of
the squamous mucosa to highly acidic fluid can be induced
with feed deprivation.16,30-33 Other described factors in-
clude variable gastric motility and emptying rates, exercise
and training, nonsteroidal anti-inflammatory drug
(NSAID) administration, and stress.11-14,16,19,27,34-38 Hel-
icobacter 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 Addi-
tionally, nitric oxide synthesis may play a role in reduced
ulcer healing and more severe ulceration.40 The pathogen-
esis 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 evi-
dence of gastric ulceration.2 In this study, gastric ulceration
541
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 pre-
senting 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 hy-
pothesized 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 hos-
pitalization on ulcer formation in equine patients present-
ing 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.
MATERIALS AND METHODS
All horses presenting to the George D. Widener Hospital
for Large Animals during a 12-month period were in-
cluded in this study, and the breeds represented Thor-
oughbreds, 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 com-
plaint of acute abdominal crisis (colic). Further refinement
encompassed the randomized selection of study patients,
alternating between those that were treated surgically ver-
sus medically to prevent bias with regard to the type of colic
on admission. Horses were only included as controls if they
were admitted to the hospital without signs of colic or
other clinical signs of gastric ulceration, as has been previ-
ously reported. Controls had to be hospitalized for a mini-
mum of 48 hours before discharge to permit gastroscopic
examination and were matched by the calendar date of
one week before or after a case horse was admitted. Case
horses were matched with control horses in a 2:1 ratio. Po-
tential case and control horses were excluded if there was
not a clear diagnosis of colic or if the horse could not clearly
be determined to be free of gastric ulceration at presenta-
tion based on history and clinical signs.
A complete history, including medications administered,
feeding, exercise level, and past medical problems, and
physical examination with appropriate laboratory evalua-
tion (packed cell volume, total solids, white blood cell
count, fibrinogen and electrolytes) were performed on pre-
sentation and recorded. Every horse in the study was endo-
scopically evaluated within 24 hours of admission. Those
patients in need of immediate surgical treatment were
542
Figure 1. Grade: 0 ¼ normal mucosa, no lesions, upper left; 1 ¼ small single lesion or small multifocal lesions upper
right; 2 ¼ large single or large multifocal lesions lower left; 3 ¼ extensive (often coalescing) lesions with areas of
apparent deep ulceration, lower right.
gastroscopically examined as soon after surgery as allowed
based on clinical status. A second gastroscopic examination
was performed within a 5 day period and the time interval
was recorded. All horses were held off feed for 6 to 8 hours
before examination, sedated with xylazine (0.3 to 0.5 mg/
kg IV) and examined by the same endoscopists.
Gastroscopy examinations were performed using a 9.5
mm diameter, 2.25 meter Olympus (model SIF 100) flexi-
ble videoendoscope (Olympus America Inc., Melville, NY).
The endoscope was passed into the stomach via the nostril,
the stomach was insufflated with air, feed material and saliva
were washed from the gastric mucosa, and the stomach was
systematically examined. The margo plicatus and greater
curvature were identified and examined first, followed by
the fundic portion and the lesser curvature, then the cardia
was examined by retroflexing the endoscope, and finally the
esophagus was examined upon withdrawing the endo-
scope. Images were taken of each of the four areas including
the greater curvature, fundus, lesser curvature, and cardia.
If ulcers were identified in the gastric glandular portion or
the esophagus, additional photographs were recorded.
TS Rabuffo et al  Vol 29, No 6 (2009)
Additionally, all examinations were stored on videotape
for future analysis. Ulcer scores were recorded for each gas-
troscopic examination based on the most severe gastric mu-
cosal lesion, using a scoring system of 0 ¼ no lesions to 3 ¼
severe and extensive ulceration41 (Figure 1).
Hospital procedures, such as feeding and hand walking,
were determined by the attending veterinarian and based
on the primary complaint. All patients were housed in indi-
vidual stalls. Once the case horses were endoscopically ex-
amined twice, treatment with anti-ulcer medication was
instituted. Treatments dictated by the attending clinician,
based on the horse’s clinical diagnosis, were included in
the final analysis.
Statistical Analysis
A data set was established, and statistical analyses were per-
formed using commercially available software (Stata 7.0,
Stata Corporation, College Station, TX). A P-value < 0.05
was considered to be significant, although all P-values were
reported. Comparisons were made at initial examination be-
tween colic (study) and noncolic (control) groups, as well as
TS Rabuffo et al  Vol 29, No 6 (2009)
between colic cases treated medically versus those treated
surgically, using a Fisher’s exact test. Additional comparisons
were made between breed, sex (using Pearson chi-squared),
and age groups, using the Kruskal Wallis test. Furthermore,
ulcer scores were compared in the colic group between the
first and second examinations, and the effects of ulcer treat-
ments were compared by using a Fisher’s exact test.
RESULTS
One hundred sixty-nine horses presenting to the George D.
Widener Hospital for Large Animals during a 12-month pe-
riod were included in this study. Of these horses, 112 pre-
sented with the chief complaint of colic and fit the criteria
for study inclusion out of 405 horses with the same prob-
lem. The remaining 57 horses in the study served as case
controls and presented with non-colic, nonemergency
complaints, which included horses admitted for scinti-
graphic or lameness examination. Of the 112 horses with
colic, 54 horses were treated surgically, and 58 horses
were treated medically. The horses ranged in age from 2
months to 30 years, with a mean age of 7.16 years (median
age, 5 years) and included 60 females, 23 intact males, and
86 castrated males. Horses were grouped by age, with
group 1 including horses 2 years old or younger, group 2 in-
cluding 3-year-olds, group 3 including 4-year-olds, group
4 including 5-year-olds, group 5 including 6-year-olds,
group 6 including 7-year-olds, and group 7 including all
horses 8 years of age or older. The breed distribution con-
sisted of 97 Thoroughbreds, 22 Standardbreds, and 50
other horses of various breeds (including Warmbloods,
Quarter Horses, Appaloosas, miniature horses, draft
breeds, and Arabians). Seventy-six of 112 (67.8%) horses
presented with the chief complaint of colic, versus 41 of
57 (71.9%) horses in the control group that had gastric
ulceration on gastroscopic examination. The Pearson chi-s-
quared value was 0.2941, but this was not significant (P ¼
.588). There was a 6% greater chance for gastric ulceration if
the horse was in the control population as opposed to the
colic group. The horses in the control group had a higher
ulcer score (mean, 1.314) compared with horses in the colic
group (mean ulcer score, 1.153); however, this difference
was not statistically significant (P ¼ .3631).
All 112 horses presenting for colic were examined twice
while hospitalized, and the conditions of 38 of the horses
with gastric ulceration deteriorated (mean, 2.124). The
mean number of days between the first and second examina-
tion was 4. Twenty-eight of the horses had no progression or
improved while in the hospital, and we found no difference
between the colic groups treated medically (n ¼ 58) versus
those treated surgically (n ¼ 54) with the Fisher’s exact
test (P ¼ .735). Fifty-seven controls (noncolic) were exam-
ined gastroscopically one time within 24 hours of admission.
543
Using the Kruskal-Wallis test, there was a significant asso-
ciation between age and chief complaint (P ¼ .0131). The
older horses in the study were more likely to present for colic.
However, there was not a significant association between age
and the prevalence of gastric ulceration (P ¼ .8596) with
Kruskal-Wallis test.
There was a significant association between complaint
and breed (P ¼ .007). Thoroughbreds and Standardbreds
represented 85.7% of the control group and 62.5% of the
colic group. There was no relationship between the preva-
lence of gastric ulceration and breed using the Fisher’s ex-
act test (P ¼ .321). Of Thoroughbreds, 41.2% had gastric
ulceration, and 59.1% of Standardbreds in the study had
gastric ulceration, whereas 46% of horses represented by
the other breed category (Warmbloods, Quarter Horses,
Appaloosas, miniature horses, draft breeds, and Arabians)
had gastric ulceration.
More than half of the horses in this study were geldings
(50.8%); 35.5% were mares; 13.6%, stallions. There was no
association between sex and complaint or sex and the oc-
currence of gastric ulceration (P ¼ 0.710).
Additional analyses were performed to compare hemato-
logic data of the horses presenting for colic and the preva-
lence of gastric ulceration. There was no statistically
significant association between the outcome of gastric ul-
cers and fibrinogen, white blood cell count, total solids,
or electrolytes. However, there was a statistically significant
association between packed cell volume (PCV) and gastric
ulceration (P < .001; mean PCV, 43%). The higher the
PCV, the less likely the horse was to have gastric ulcers.
Horses presenting with the complaint of colic were also as-
signed to groups based on anatomic diagnosis of the lesion,
using either surgical diagnosis or rectal examination find-
ings. They were grouped as follows: group 1 if the lesion in-
volved the small bowel, including anterior enteritis, small
intestine volvulus, ileus, strangulating lipoma, castration
evisceration or inguinal hernia, small intestinal adhesions,
pyloric stenosis, or ileal hypertrophy; group 2 if the lesion
involved the large intestine or descending colon, including
right dorsal colon displacement, large colon volvulus or dis-
placement, large colon tympany, nephrosplenic ligament
entrapment, large colon impaction, small colon impaction,
rectal tear, or strangulating lipoma of the small colon.
There were 13 (7.7%) horses for which an anatomic diagno-
sis could not be determined; these were therefore excluded
from the analysis. There was no correlation between gastric
ulceration and anatomic region of the lesion (P ¼ 0.487).
DISCUSSION
This study confirmed the high incidence of gastric ulcera-
tion in adult horses.1-10 Gastric ulceration was evident in
horses presenting for colic and noncolic complaints at
68% and 72%, respectively; the difference was not
544
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 in-
tended use of the horses may have been a confounder.
Thoroughbreds and Standardbreds (86% of the controls)
were admitted for nonmedical nonsurgical complaints.
Previous reports documenting the incidence of gastric ul-
ceration range from 70% to 90% in Thoroughbreds and
Standardbreds, especially when in training and racing con-
dition.1,6,7,11-15 Gastric squamous mucosal injury in the
Thoroughbred and Standardbred sport horse is believed
to be attributable to the combined result of a number of
factors, including the physiologic changes associated with
training, stress-induced responses, feed management, and
behavior.14,32,33 Although the role of stress in equine gas-
tric ulceration has been postulated, it has been difficult to
document. In stressed foals, gastric lesions were more likely
to occur in gastric glandular mucosa, but the frequency was
not different between stressed and nonstressed foals.3,38
Stress has long been associated with gastric ulceration in
humans; however, how stress affects gastric mucosal de-
fenses leading to gastric ulceration remains unclear.39
Therefore, the stress of hospitalization for horses with
the complaint of colic and those with noncolic complaints
may have induced gastric mucosal lesions. Additionally, the
stress of athletic performance may play a role in the higher
occurrence of gastric ulcers in the noncolic patients.42
The high prevalence of gastric ulceration in this the study
population also may be attributable to periods of feed dep-
rivation, as Murray and Eichorn demonstrated.43 Holding
horses off feed results in prolonged exposure of the gastric
mucosa to acid, with subsequent gastric epithelial mucosa
injury.31 Horses presenting for acute abdominal crisis are
frequently held off feed as part of the treatment regimen,
even when surgical intervention is not indicated. We spec-
ulate that this is one reason why horses presenting with the
complaint of colic could be at increased risk for gastric ul-
cers. Thoroughbreds and Standardbreds constituted
62.5% of the study group, and because the prevalence of
gastric ulceration is especially high in this population of
horses, it is possible that horses in this study group present-
ing for colic may be predisposed to EGUS for that reason as
well. In addition, the slight difference in the prevalence be-
tween the two groups may be attributable to the five horses
of the study population (3%; 3 control, 2 colic) with EGUS
that did not have gastric ulcers. However, these five horses
had decreased gastric emptying, which, as reported by
Murray,25 can be a part of EGUS.
NSAID administration has been associated with in-
creased ulceration of the gastric glandular mucosa, because
a decrease in prostaglandin production is associated with
a decrease in protective mucosal factors. NSAIDs are often
administered to horses as a routine treatment for colic, so
an increase in gastric ulceration might have been expected
TS Rabuffo et al  Vol 29, No 6 (2009)
in the colic group for this reason as well. However, the lack
of a statistically significant increase in gastric ulceration in
horses in the colic group does not correlate with this sup-
position.44
Thirty-eight of the 112 horses (34%) examined twice had
their ulcer score increase while hospitalized, and 66% re-
mained the same or improved. There was an upward trend
in the prevalence of gastric ulceration during hospitaliza-
tion; however, the temporal effects were not statistically
significant. There was a time period of up to 5 days between
the first and second examinations; the interval may be short
enough that a causative relationship between colic and gas-
tric ulcers could not be documented even though gastric
ulceration can develop within 48 hours.30 Therefore, we
were unable to conclude with certainty whether the ulcers
were causal or a contributory factor of the colic complaint.
There was no difference in the prevalence of gastric ulcer-
ation among the horses presenting for colic treated medically
versus surgically. Additionally, we found no association be-
tween the location of the gastrointestinal lesion and the prev-
alence of ulceration. In 13 horses presenting for colic in this
report, no other clinical abnormality was found other than
gastric ulceration. This has been previously reported by Mur-
ray.2 Approximately 28% (31/111) of horses in Murray’s
study had gastric ulceration as the primary cause of colic,
compared with only 12% (13/112) in our study. Further-
more, that study implied that there was a causal relationship
between gastric ulceration and signs of abdominal pain based
on cessation of clinical signs within 24 hours of initiating
treatment with H2 antagonists.2 We were unable to deter-
mine whether gastric ulcers were a causal factor of colic.
However, based on the high number of horses with evidence
of gastric ulceration, it is likely that gastric ulceration in
horses with gastrointestinal disorders may also be a contrib-
uting problem. Therefore, gastroscopy or prophylactic ad-
ministration of anti-ulcer medication seems warranted in
horses presenting with the chief complaint of colic.
Additionally, with the finding of gastric ulceration at the
initial examination, some clinicians opted to treat their
patients with H2 antagonist drugs, including ranitidine
or cimetidine, the proton pump inhibitor omeprazole
(GastroGard, Merial Ltd, Duluth, GA), and gastroprotec-
tants such as sucralfate. Sixty percent of horses treated with
H2 antagonists worsened while hospitalized, whereas only
14% of those treated with omeprazole deteriorated.45,46
Although this difference was not statistically significant,
the apparent magnitude of this supports the reported
evidence that omeprazole is a more effective treatment
for EGUS.46 Omeprazole suppresses gastric acid secretion
by inhibition of the Hþ/KþATPase enzyme system on
the parietal cell, compared with H2 antagonists, which
competitively inhibit histamine to downregulate gastric
acid secretion. Andrews et al47 reported that omeprazole
is five times more potent than H2 antagonists in healing
TS Rabuffo et al  Vol 29, No 6 (2009)
gastric ulcers in horses.47 Age and sex were not associated
with the increased incidence of gastric ulceration in our
study. Proportionally, more horses in the control group
(60%) were less than 4 years compared with 34% in the colic
group.
An important finding in this study was the statistically
significant lower packed cell volumes in those horses with
gastric ulceration versus the control group.48 A relation-
ship between gastric ulcers and hematologic changes has
been previously reported; however, a causal relationship
was not determined.47 Other authors have speculated
that red blood cell counts and hemoglobin concentrations
might be lower because of chronic gastric ulceration.47
Further investigation is necessary to determine the rele-
vance of hematologic abnormalities and their relationship
to EGUS and colic.
CONCLUSION
All hospitalized horses have a high incidence of gastric ul-
ceration. 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 opin-
ion 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 clinical signs reported
to be associated with EGUS.14
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