How to cite this article: [627354]

How to cite this article:
Parrah JD, Moulvi BA, Gazi MA, Makhdoomi DM, Athar H, Dar S and Mir AQ (2013) Gastric ulceration in dog: A review,
World 6(7):449-454, doi:10.5455/vetworld.2013.449-454Vet
Introduction perforating ulcers. And on the basis of clinical
presentation, ulcers may be acute or chronic [4].In narrow sense, gastric ulcer is a defect in the
mucosa that penetrates the muscularis mucosa [1]. But Incidence of gastric ulcerations
in real sense gastric ulceration and gastrodudonal Gastric ulcers are found both in young and adult ulceration describe a clinical finding, the cause of animals, but higher percentage is found in mature which is likely to be multifactorial and to differ from animals. Likewise athletic animals do suffer more from one case to another, and are anatomical circumscribed gastric ulceration compared to the canine population as breaks in the surface of gastrointestinal mucosa. The large. Endoscope studies have revealed gastric ulcer of the stomach or the proximal duodenum is also ulceration is 48.5% into canine athletes. Some called peptic ulcers, because these ulcers are bathed by incidence of gastric ulcers is also reported in foals-25 to acid pepsin [2].50% [4].However, higher incidence of gastric ulcers Gastrodudonal ulcers can occur independently or 60% has been reported in mature horses. [4]. as a complication of many systemic diseases or Gastroendoscopy has revealed gastric ulceration in following administration of various drugs to treat many horses as well as in animals with associated symptoms diseases, hence have paramount significance for any like poor appetite, poor body conditions or signs of clinician to understand its etiological factors, abdominal discomfort [5]. However, the incidence of pathophysiology for their effective treatment and early gastric ulceration in relation to the exciting cause also prophylaxis.varies significantly from species to species. Unlike
Classification of gastric ulcershumans with renal failure in whom gastric ulcer
predominates, gastric necrosis and ulceration appear to A classification of gastric ulcers is very important
be uncommon in dogs with renal failure-3.6% [5,6]. to know for the clinician as the treatment regimen
varies widely for each class of gastric ulcer. The gastric Etiology
ulcers are classified according to their depth in the
Gastric ulcer may be caused by various factors and gastrointestinal mucosa, anatomical location in the
these factors may range from inflammatory conditions gastrointestinal area and the severity of the clinical
of non steroidal and steroidal (glucoco-rticoid) anti- presentation.
inflammatory drugs for treatment of various diseases Gastrodudenal ulcers may be glandular mucosal
besides primary and secondary tumors of stomach, ulceration, generalized gastritis, focal duodenal
systemic disease and ingestion of poisonous and other ulceration, duodenal erosions or duodenitis [3].
harmful substances. Ulcers have been reported in dogs, Depending upon the depth of the ulcer, gastric ulcers
rodents, horses and human secondary to admini- can be superficial or deep and range from simple
strations of a variety of non-steroidal anti-inflammatory epithelial erosion to full thickness bleeding or
drugs piroxicam [6] including, aspirin, ibuprofen [7],
naproxen [8], endomethacine [9], ketrolac [10]. Steroidal
anti inflammatory drugs are also incriminated as cause
of gastric ulceration [11], for the treatment of other
www.veterinaryworld.org 449doi:10.5455/vetworld.2013.449-454
Gastric ulceration in dog: A review
J. D. Parrah, B. A. Moulvi, Mohsin Ali Gazi, D. M. Makhdoomi, H. Athar, Shahid Dar and A. Q. Mir

Faculty of Veterinary Sciences and Animal Husbandry
Sher-e-Kashmir University of Agricultural Science and Technology, Kashmir, India
Corresponding author: Mohsin Ali Gazi, email:mohsingazi9975@gmail.com
Received: 24-10-2012, Accepted: 20-11-2012, Published online: 01-05-2013
Abstract
The common acid related diseases of the upper gastrointestinal tract could be considered as primarily due to the defect in
barrier function either of the gastric mucosal or duodenal epithelium leading to the formation of gastric or duodenal ulcers. An
attempt was made in this review to discuss the classification, pathophysiology, diagnosis and treatment of gastric ulcer in dogs.
Early surgical advances in the management of peptic ulcers are emphasized that were then subsequently replaced by
pharmacological treatment (histamine H2-receptor antagonists, proton pump inhibitors) and considered as the major strategy
against the acid disorders.
Keywords: dog, gastrointestinal tract, stomach, ulcer
This article is an open access article licensed under the terms of the
Creative Commons Attribution License (http://creativecommons.
org/licenses/by/2.0) which permits unrestricted use, distribution
and reproduction in any medium, provided the work is properly cited.

www.veterinaryworld.org 450doi:10.5455/vetworld.2013.449-454
primary diseases like spinal insult like intervertebral prostaglandin, which also increases mucous and
disk disease [12], primary neoplastic condition of the bicarbonate production. Mucous has high viscosity,
stomach carcinoma , gastric intestinal lymphoma [13], adhesive, and readily forms a film effectively coating
gastrinoma and disseminated mast cell disease [14] are the epithelium which can be assessed on radiograph
also responsible for gastric ulceration. Gastric ulcers [24]. This mucous layer is not digested by pepsin. It has
have been noticed after the dogs have suffered from selective permeability and traps alkaline fluid, creating
systemic diseases like hepatic, renal, Addison's a buffer zone against noxious or acid environment.
disease; shock [15]. A range of exogenous toxins may Bicarbonate ion, produced by oxyntic cells and
cause gastric ulceration. Ingestion of household, actively secreted into the luminal surface also acts as a
cleaning chemical, lead and various plants may directly chemical buffer.
damage the gastric mucosa [16]. Three dogs following Mucosal defense mechanism can be impaired by
administration of phenol (total dose of 2430 mg of many means. Non-steroidal anti inflammatory drugs
phenol) experienced severe oral and gastric ulceration generally inhibit the cycloxygenase pathway (COX-1
[17]. A lead salt mixture (Chloride Br, Sulfate, 1:1:2) and COX-2) through which prostaglandins are formed
when given orally to nine dogs at different dose rates from Arachidonic Acid. Prostaglandins that are
ranging from 5-60 mg/kg body weight/day for 14-152 beneficial to the stomach are created through the COX-
days induced gastric ulceration [18]. Gastric ulceration, 1 pathway [25]. Without these beneficial PG's blood
as complication has been recorded following auto flow and gastric mucous and bicarbonate production
transplantation of the ovary to the portal vein drainage are reduced. Corticosteroid increases gastric acid
as a possible method of preventing obesity in ovariectomized production and reduce PG's formation thereby
bitches [19]. promoting development or persistence of gastric ulcers
[26]. Spinal insult may contribute to the development Pathophysiology of gastric ulceration of diseases through altered gastric circulation and
There are multiple pathophysiological mechanisms motility [26].
for the developments of ulcer in each of the disorders. Shock reduces blood supply to the stomach and
However, the common underlying pathophysiological results in acidosis because of poor perfusion, both
mechanism is stimulation of gastric acid secretion and reduce delivery of bicarbonate ion to the surface cells.
inhibition of the gastric mucosal barrier properties. In animals, with renal failure, uraemia has been
Acid secretary disorders are uncommon in companion postulated to result in diffuse vascular injury to the
animals but mucosal barrier disorders are fairly common. mucosal lamina propria with subsequent epithelial cell
In dogs, the multifactorial pathophysiological damage from anoxia [27,28].
mechanism of gastric ulceration, thus stem from any Chemical insult to the gastric mucosa comes from
processes, including physical damage to the gastric endogenous compounds (HCl, bile acids, and
mucosa, impaired mucosal defense and chemical pancreatic enzymes) or exogenous HCl. In Dogs,
alteration to the mucosa and its repair process. Physical Helicobacter pylorus experimentally increases gastrin
disruption of the mucosa that occurs normally with the production by endocrine G cells, which increases
passage of the particulate debris is rapidly corrected. production of the HCl by oxyntic cells. Whether
After superficial insult, the damaged necrotic cells Helicobacter pylori infection is clinically significant in
initially slough, become trapped in the superficial dogs and cats is debatable. [28]. Histamine like gastrin
mucous layer and cover the lesion, tripping alkaline is another primary messenger that stimulates HCl
rich fluid leaking from exposed capillaries in and production by oxynitc cells through a cyclic adenosine
around the lesion. Superficial mucosal epithelial cells monophosphate mediated secretary process. Animals
begin migrating immediately under this protective with mast cell tumor and mastocytosis have increased
covering to reform the mucosal barrier within hours circulating histamine concentration and are predis-
[20]. Ulcers develop from physical disruption only posed to gastric ulcer formation. Disease processes that
with sustained or significant trauma (Gastric foreign decrease the removal of circulating gastrin or histamine
bodies, surgical implants) [21]. Gastric mucosa has a such as renal or hepatic failure or that pathologically
variety of defense mechanisms that protect and increase circulating gastrin levels [29], such as
maintain epithelial integrity [22]. The gastric epithelial gastrinomas increase HCl production. Various positive
layer is in a continuous state of renewal, surface feedback mechanisms may also increases gastric acid
mucous cells are renewed in 3 days, whereas deeper production. When the epithelial barrier is disrupted by
neck mucous cells are renewed in 7 days [22]. Surface any means, HCl is absorbed across the mucosa (acid
mucous cells, ingrate within 30-60 min to cover the back diffusion) and through stimulation of the intrinsic
small defects in the gastric epithelial lining of the basal nervous system; it triggers release of more HCl and
lamina are intact. The mucosa receives 70 % or more pepsin. HCl also directly stimulates tissue mast cells to
gastric blood flow to maintain protective and digestive release histamine, resulting in further HCl secretion.
functions [23]. Physiological levels of corticosteroids The duodenum plays a role in suppressing pathological
may be critical in maintain adequate blood flow during gastrin and HCl release in normal animals. If gastric
streaming. In addition, blood flow is supported by outflow is surgically altered e.g. (gastojejunostomy),

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ulcers are more likely to develop [30]. Duodenal of orthopedic problem [35].
contents (bile acids and pancreatic enzymes) may irritate III. Laboratory finding: These are rarely specific for gastric mucosa [31], although evidence suggests that gastric ulcers. Results are evaluated for indicators of these compounds without altered mucosal cellular severity of clinical abnormality (anemia or septic metabolism do not induce ulceration. Exogenous toxins abdominal fluid sample) and predictors of inciting like lead may directly damage the gastric mucosa [32].cause e.g. (renal failure). Fecal occult blood is a Systemic diseases like hepatic dysfunction may difficult test to interpret, positive findings may be from result in the decreased excretion of various xenobiotics bleeding in the stomach or small intestine of the patient and resulting in their producing side effects. Ketorolac is receiving a non-meat diet. Serum gastrin may be is conjugated by the liver to an inactive metabolite and elevated in the patients with gastrinomas or decreased excreted by the kidney. Concurrent hepatic diseases renal or hepatic clearance. Serum histamine levels may may have prolonged its duration of activity thereby be increased if a mast cell tumor or mastocytosis is increasing the severity of side effects including gastro present. intestinal ulceration.Some diagnostic kits are also available for testing
gastric juice. Gastro diagnose (Merck) is a preparation Diagnosis
of pentagastrin, when injected IM @ 6 microgm/Kg The diagnosis of gastric ulceration is based on the body weight. increases the gastric secretion (hyperacidity) following consideration;in a dog suffering from gastric ulceration and perforation.
The degree of endoscopically detected damage correlates I. Signalment and history: No breed, age or sex
well with sucrose permeability. Sucrose permeability predilections are reported for gastric ulcer disease.
decreases more rapidly than disappearance of the gastric History of the patient may indicate non-steroidal anti-
ulcer. Sucrose permeability test is more sensitive to inflammatory drug (NSAID) therapy, ingestion of
generalized mucosal damage than to discrete usual poisons and any other systemic disease like
ulceration [36]. Neutrophilic leucocytosis was hepathopathy, tumor pregnancy gastric or secondary
prominent laboratory finding in piroxicam associated metastases.
gastric ulceration in dog. Dog suffering from gastric
II. Physical and clinical findings: Like the historical ulceration following phenol poisoning revealed findings, physical findings at presentation range from hematological abnormalities including neutropenia non existent to severe. The animal might simply appear with the presence of toxic neutrophils, thrombocyto-underweight or it could have a pale mucous membrane penia and increased muscle enzyme [37].
and tachycardia from severe anemia or shock. Pain on
IV. Radiography: Radiography (plain and contrast) are palpation may be apparent in the generalized if
beneficial in determining potential cause of abdominal perforation with significant peritoneal contamination
pain (gastric foreign bodies) but may be unrewarding has occurred. The commonest clinical sign of gastric
in fetching evidence of gastric ulceration [37,38] Could ulceration are vomiting, haemoptesis, melena, weight
not find any gastrointestinal lesion in drug induced loss and anemia. Acute or chronic vomiting with or gastric ulceration, which were later confirmed by without hematemesis is the most common clinical sign endoscopy. Focal, increased soft tissue density associated with gastric ulcer or erosion formation not associated with traction of gastric wall may indicate all animals with gastric ulcer vomit, however, and not perforation with an associated abscess. Generalized all animals that vomit blood have gastric ulcers [32].loss of serosal detail may indicate peritonitis secondary Other clinical signs observed include anorexia, to perforation. For contrast radiography, barium abdominal pain, melena, anemia, edema (from sulphate produces a better study than iodine contrast hypoproteinemia related to elementary hemorrhage) agent, and requires multiple positions to identify and septicemia. (From perforation). Other signs may lesions. Barium may adhere to mucosal defect or be related to the underlying cause (liver disease, penetrate into urater. Small ulcers or larger defects neurologic disease). Perforation of the stomach or the filled with blood or debris may not be seen.duodenum may result in the sudden onset of severe
weakness, severe abdominal pan, fever, shock V. Ultrasonography : Ultrasonography is a useful
abdominal distension and death caused by peritonitis noninvasive tool to detect the gastric ulceration in
[33]. Rarely animals with perforated gastric ulcer have dogs. Ultrasonographic features of gastric ulcers
only mild signs of abdominal discomfort. [34] includes local thickening of the gastric wall, possible
Reported diarrhoea, progressive anorexia, 23-39% loss of the 5- layer structure the presence of the wall
body weight loss, vomition, depression and lethargy defect or crater fluid accumulation in the stomach and
associated with primary gastrointestinal lymphosar- diminished gastric motility. The localized gastric
coma induced gastric ulceration in 3 male Shepard thickening usually varies from 9-16mm. The ulcer
dogs and one Boxer dog. Almost similar signs but with crater is often localized in the center of the thickened
addition of melena and pallor of the tongue has been site and appears as a mucosal defect associated with
reported in dogs associated with gastric ulceration persistent accumulation of small echoes, most likely
secondary to the use of NSAIDS used for the treatment representing micro bubbles. However, there is no

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definitive distinction between benign and malignant drug such as sucralfate is important for protecting
ulcers, and gas within the gastric lumen may interfere ulcerated tissue.
with imaging. The H antagonists: The H antagonists suppress Hcl 2 2No biopsy of the center of the ulcer bed should be secretion through competitive inhibition of the parietal obtained as it can be easily perforated by the biopsy cell histamine receptors. Gastroscopic examination has forceps and no blood should be inspired from the ulcer, suggested that the degree of suppression of acid as there are chances of renewed bleeding. Biopsy secretion required to heal lesion is greater than that samples are collected from the edge of the ulcer to rule required to produce relief from discomforts.H 2 out neoplasia. Multiple biopsies of the same location antagonist therapy should continue for 14-21 days; are taken because superficial inflammation often however in some cases healing will occur in 30-40 accompanies neoplasia. Non lesioned biopsies are days.taken to identify diffuse gastritis. Perforation may be
difficult to direct endoscopically because small lesion Prostaglandin E analogs: Prostaglandin analogues (eg.
may seal over with omentum and perforation. Perfo- misoprostol) may improve ulcer healing or prevent
ration is suspected if the stomach remains distended ulcer formation by increasing mucosal circulation,
after the stomach is deflated or if abdominal vascular permeability or mucosal cell turnover and
radiographs reveal free gas in the abdomen after the migration. There drugs inhibit adenylate cyclase,
procedure. If perforation is known to exist, endoscopy reducing cyclic AMP production and thereby reducing
is contraindicated because examination increases the protein kinase activity essential to hydrogen ion
contamination of the abdominal cavity with gastric generation. Misoprostol is a analogue of prostaglandin
contents. E that that is administered in doses of 0.5 to 2.3µg/lb 1
two or three times per day. It is the drug of choice for TreatmentNSAID- induced ulceration and so more effective than
Medical therapy: Medical therapy is directed towards-sucralfate or H receptor antagonists in preventing 2a) Removing or attenuating is directed toward hepatic NSAID –induced ulceration [40]. Some patients failure, hepatic bacter infection, non steroidal anti-develop diarrhoea, which is usually self limiting. inflammatory drug or corticosteroid therapy.Prostaglandin E is not used in hypotensive animals 2b) Supporting ulcer healing by:because gastric damage may be increased. i) Maintaining mucosal perfusion
Cimetidine: Cimetidine was the first H receptor ii) Decreasing gastric acidity, 2
antagonist used in dogs. It is available in injectable, iii) Protecting ulcer
liquid and tablet forms. Inhibition of histamine iv) Correcting secondary conditions (anaemia,
stimulated acid secretion peaks at 75% within 1.5 dehydration, weight loss).Fluid therapy is important in
hours, and 50% inhibition of acid secretion lasts about dehydrated patients with gastric ulcers or maintains
2 hours after an oral dose. Drug effects are gone after 5 mucosal perfusion. Dehydration is quantities and
hours. Thus cemetidine is administered 3-4 times daily corrected over an appropriate period. Acute life
at a dose of 2.5-5 mg/lb to suppress gastric acid threatening haemorrhage from gastric ulcer is treated
secretion in dogs [41]. Even so, there is only mild to with blood transfusion, appropriate synthetic and
moderate inhibition of acid secretion over a 24 hours natural colloid fluids where efforts to stop the
period. The fact that it works clinically for ulcer haemorrhage are underway. If perfusion is imminent or
therapy suggests that even partial suppuration of confirmed, blood spectrum antibiotics or antibiotic
gastric acid secretion is beneficial for the healing of combination are instituted [39].
most gastrodudenal ulcers. Food is withheld at least initially to avoid stimulation
of gastric acid and pepsin secretion. Subsequently Ranitidine: It is more potent and lasts longer than
dietary managements is similar to that recommended cemetidine. Inhibition of acid secretion peaks at 90%
for acute gastritis. Patients, vomiting are given antiemetic within 1.5 hours, and 50% inhibition of acid secretion
as recommended for treatment of acute gastritis. last about 4 hours after an oral dose. Ranitidine is
Systemic acid reducing drugs fall into the categories of usually effective clinically when administered at a
histamine (H ) – blocking agents (Cimetidine, ranitidine, 2 1mg/lb twice a day. Ranitidine is available in injectable
fomitidine) and proton pump inhibitors (omeprazole, and tablet forms, and as syrup. Ranitidine can cause
lansoprazole, rabeprazole). H blocking agents reduce vomiting if rapidly administered I/V . 2 –
hydrochloric acid production that is stimulated at
Fomitidine: It is more potent than either ranitidine or histamine receptors. Proton pump inhibitor decrease cemetidine. It is administered twice or once daily at hydrochloric acid production from oxyntic cells by 0.25 to 0.5mg/lb. + +inhibiting the H , K -ATPase and work independently
of specific receptors and thus may be more effective. Nizatidine: This H receptor antagonist is like 2
Besides this, acid reducing drugs include those drugs ranitidine and has prokinetic activity, hence may be
that act on cellular metabolism to inhibit hydrogen on preferable in patients with gastric ulcers co-existing
secretion (e.g. prostaglandins) [40]. A Cytoprotective with a motility disorder hypersensitive like reactors

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such as drug eruption or acute interstitial nephritis or be administered at least 6 times per day in doses
poliomyelitis, hyperpyrexia, diarrhoea, granulocyto- sufficient to titrate gastric acid. Cisapride may be
penia and central nervous system aberrations. helpful if the ulcer patient has concurrent motility
problems resulting in the delayed gastric emptying Protom pump blockers: Omeprazole: it is a substituted [49].benzimidazole, blocks hydrogen ion secretion in the
+ +Surgical interventions: Gastric surgery is less parietal cell by inhibiting H , K – ATPase located on
commonly performed to treat the gastric ulceration of the apical membrane. It is a weak base, accumulates in
erosion [50]. Surgical intervention is resorted to as the the acid compartments of the parietal cell, hence
treatment of gastric ulceration when perforation is administered once daily at dose of 0.33 to 1mg/lb.
suspected or if severe bleeding is discovered. Serial Omeprazole is indicated for disease states that are not
evaluation of the haematocrit and cardiovascular responsive to H receptor antagonist therapy, such as 2
assessment are necessary to determine whether blood non respectable gastrinoma and systemic mast cell
loss is sufficient to warrant surgery. Surgery i9s also disease.
indicated if the patient has not responded to appropriate
Aspirin: Administration of aspirin twice daily reduces medical therapy that has been administered at least for periods of fecal blood volume [42].5-7 days.
Lesions are resected during exploratory Lansoprazole: it does not differ significantly from
laparotomy. Sometimes it is difficult to locate mucosal omeprazole in potency or duration of action.
lesion when examining the serosal surface [50]. A Cytoprotective drugs: Cytoprotective drugs such as thickening gastric wall may be detected resulting from sucralfate protect healthy and denuded mucosa from inflammatory infiltrate around the lesion so that if further harm and promote gastric mucosal epithelia-multiple ulcers are present they can all be located.lization [43].
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