Introduction. Introduction. Equine Gastric and Pyloric Ulcer Syndrome. Equine gastric ulcer syndrome (EGUS) First described in 1986

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1 Equine Gastric and Pyloric Ulcer Syndrome Jenifer R Gold DVM, DACVIM-LA Assistant Professor-Colorado State University Colorado Veterinary Medical Association September 22, 2013 S Introduction Equine gastric ulcer syndrome (EGUS) First described in 1986 Common in all types of horses Introduction Clinical signs are variable and often vague Can easily be diagnosed via history, PE, and confirmed via gastroscopy Will discuss etiology, risk factors, approach

2 Gastric Anatomy Single chamber compound stomach Orad 1/3 lined with stratified squamous epithelium No glands Minimal protective mechanism No functional role Ends abruptly at margo plicatus Gastric Anatomy Glandular portion 2/3 s of stomach Compound columnar epithelium Numerous gastric glands-contain proton pumps responsible for HCL secretion Gastric Anatomy Glandular epithelium also produces an acid-retarding bicarbonate A mucous layer that protects entire surface Horse continuously secretes hydrochloric acid Acid secretion predominantly stimulated by histamine Histamine stimulated by gastrin

3 Anatomy Gastric Anatomy A dorsoventral ph gradient exists Ranging from the squamous mucosa being the least acidic (ph 5 to 7) Through the glandular fundus (ph 4 to 5) Pyloric glandular mucosa (ph 2 to 4) Gastric juice (ph 1 to 2) Anatomy

4 Gastric Anatomy Similar dorsoventral layering of gastric contents occurs with dense acid liquid Trapped ventrally by the more fibrous material found dorsally This stratification is vital to normal gastric health Gastric Anatomy Gastric emptying is continuous at a speed that varies by stomach content Liquid contents reduce in volume by half every 30 minutes Solid contents take about 1-5 hours Gastric Physiology The oxyntic portion of the glandular mucosa is in the body of the stomach Acid secreting parietal cells pepsinogen secreting chief cells, histamine secreting cells somatostatin releasing cells These cells are aligned vertically from the lumen to the muscularis mucosa Secreted hydrochloric acid is transported along channels toward the luminal surface

5 Gastric Physiology As the glandular mucosa transitions from the body of the antrum fewer oxyntic glands exist. In the antral region of the stomach: Mucus and mucin secreting cells Endocrine cells Gastrin secreting G cells Equine Stomach Previously it was thought to be sterile Evidence of a diverse population of mucosal bacteria Lactobacillus, Streptococcus, Escherichia coli Increasing evidence of equine gastric-adapted Heliobacter species Less pathogenic than human form Mechanisms of Gastric Injury Increased acid exposure (ph < 4) is predominant cause of ulceration Squamous ulceration occurs rapidly due to minimal defenses Reflects increased mobility of acid gastric juice

6 Mechanism of Injury Glandular ulceration forms more slowly after breakdown of mucous and bicarbonate barrier Involvement of bacteria has been implicated 3 Types of EGUS Primary squamous ulceration Increased acid exposure Alteration in gastric ph gradient and content stratification Primary glandular ulceration Acid exposure occurs Failure of mucosal defenses Secondary squamous ulceration Delayed gastric emptying (pyloric disease) Increases residual gastric fluid volume Dorsal movement of acid Factors Affecting Ulcer Formation Horses on pasture and light exercises-low prevalence of ulcers Starvation produces prolonged high gastric acidity (ph < 2) Squamous ulceration occurs typically within 96 hours

7 Ulcer Formation Ulceration more common in horses fed twice daily (75%) than those fed 3x daily (58%) Forage deprivation of more than 6 hours increase the risk of ulceration by a factor of 4. Ulcer Formation Continuous forage access the most important during day time. Consistent fresh water is also important Water deprivation increases risk of EGUS by a factor of 3 Ulcer Formation Fermentation of soluble carbohydrates within the stomach produces lipid soluble VFA VFA penetrate squamous epithelium and cause cellular damage Most evident with high carbohydrate, rather than roughage diets Concentrate diets also produce higher serum gastrin concentrations

8 Factors Would expect greater acid production High starch diets (> 1 g starch /kg bw per meal) Increase risk of ulcers by a factor of 2 Dietary focus should be on consistent roughage feeding Exercise Intragastric ph falls rapidly to < 4 during treadmill exercise Intra-abdominal pressure increases which compresses the stomach Push gastric acid past margo plicatus onto squamous mucosa Exercise Duration of acid exposure is obviously related to the duration and intensity of exercise Can lead to splash ulcers

9 Stress Show horses that have a nervous demeanour have predisposition to ulcers Experimentally ulcers can be created via travel, unknown stable, exercise Weaning is a risk factor for mare and foal NSAIDS While experimental overdose studies induce EGUS Alteration of protective prostaglandin metabolism and direct topical toxicity This effect is not seen clinically with normal dosing regimens Epidemiological studies in Demark and the US have not shown NSAIDS to increase risk of EGUS Standard doses of phenylbutazone did not induce ulceration Gastric Inflammation-Study A variable degree of lymphocytic/plasmacytic inflammation in most tissue sections from the antrum Lymphocytes were more prevalent in the deeper portions of the mucosa than in superficial mucosa Often were concentrated adjacent to muscularis mucosa. Mike Murray-Unpublished Data

10 Gastric Inflammation-Study Some cases found large numbers of lymphocytes Accompanied proliferation of smooth muscle Proliferation of stromal tissue at the interface of the mucosa and muscularis mucosa. In contrast to the antral mucosa-lymphocytes were sparse in tissue sections taken from the oxyntic mucosa in the corpus of each horse. Mike Murray-Unpublished data Gastric Inflammation This may relate to the pathogenesis of lesions in the glandular mucosa HCl can certainly exacerbate tissue injury, Not the primary instigator. Unlike the gastric squamous mucosa where HCl is the primary instigator. Thus, acid suppression therapy will often provide more satisfying results for squamous lesions than lesions in the antrum Mike Murray-Unpublished data Gastric Bacteria Two types gastric bacteria may be involved in the development of EGUS Opportunistic pathogens Gastric-adapted bacteria An Australian study found reduced bacterial diversity in ulcer beds compared with normal mucosa Suggestive of colonization by opportunistic bacteria Significant healing occurred after prolonged use of antibiotics and specific probiotic therapy

11 Diagnosis History Physical examination Confirmation with gastroscopy Clinical Signs Poor haircoat Girthing pain Variable appetite/slowed eating Poor performance Weight loss/inability to maintain condition Clinical Signs Excessive recumbency Behavioral/attitude change Frequent stretching to urinate Acute colic Recurrent colic

12 Clinical Signs Relevant ulceration can occur in asymptomatic cases Prevalence is significantly lower than with symptomatic cases No consistent clinicopathological abnormalities Slight anemia and lower hemoglobin are reported Appetite changes are the most useful identifying sign as ulceration is significantly more prevalent when these are reported Colic is rare as a primary complaint of EGUS Diagnosis Fecal occult blood and albumin test Suggested for presumptive diagnosis of EGUS Effect of hindgut fermentation on these variables not understood Sensitivity and specificity of this test is poor compared with gastroscopy Diagnosis Gastroscopy is the gold standard diagnostic technique Grading system created

13 Prevalence Varies with breed and level of training % of racehorses in full training of ulcers 55% out of work have ulcers Ulcer severity increases with training intensity Sport horses in training 58% prevalence 36-53% leisure horses have ulcers

14 Prevalence Values just mentioned refer to presence of any form of gastric ulcers Gastric and glandular have similar prevalence, No association between presence or severity Not possible to postulate on glandular mucosa based on appearance of squamous mucosa Treatment Spontaneous healing can occur Combination of pharmacological therapy and risk reduction usually vital Treatment duration depends upon severity of ulcers Squamous ulcers heal more rapidly than glandular ulcers Repeat endoscopy to confirm healing recommended Treatment All cases important to prevent re-occurrence in the short and long term Institute changes to create acid-neutralization therapy as well as management changes Glandular ulcers may need antimicrobial therapy and misoprostal to help with healing Nothing proven however Studies on-going

15 Environmental Strategies Limitation of stress associated with exercise Stabling and transport are important when managing EGUS No ideal housing or management scheme has been identified Allowance for foraging even if not on pasture Within a population it appears no advantage of turnout versus stabling Cater for individual preferences ideal Dietary Strategies Historically main dietary emphasis has been on safe concentrate feeds However this is erroneous as relative risk of high concentrate feed is two times compared with lack of adequate fiber (4x the risk) In reality: difference between individual concentrates feeds is likely to be minimal Effect on gastric acid mobility easily reduced by addition of chopped fibre Dietary Strategies Maximize consistent day time fiber intake an constant provision of water are essential Establishment of a consistent feeding order may also be helpful

16 Dietary Strategies Traditionally feed has been withheld before exercise BUT gastric emptying continues during exercise Leads to reduced stratification and increased mucosal acid contact Giving small meals 30 minutes before exercise should reinforce stratification and limit splash lesion development Dietary Strategies Supplementation with corn or rapeseed iol ( ml x2 daily) can increase protective gastric prostaglandin production Improving glandular ulcer healing potentially No effect on squamous ulceration Pharmacological Management Acid suppressive therapy is mainstay Prolonged intragastic ph>4 is vital for healing Two classes of acid suppressant assessed in the horse Histamine type 2 antagonist Proton pump inhibitors

17 Pharmacologic Management Currently only omeprazole is the only licensed product for treatment and prevention of EGUS Gastrogard effective formulation 4 mg/kg inhibits gastric acid production for 24 hours Should be administered 30 minutes prior to feeding to increase bioavailability Gastrogard Horses in full training endoscopically confirmed ulcer resolution rates of 77-86% Significant improvement rates over 90% have been reported clinically and experimentally Improved weight gain, appetite, appearance and performance occur before ulcer resolution Usually within 10 days Not all horses have to be on for a full 28 days Gastrogard Resolution can be seen in 57-67% after respectively Possible to repeat gastroscopy at 14, 21 or 28 days If repeat gastroscopy NOT available a full 28 day course should be given IV omeprazole at 1 mg/kg can be used in dysphagic patients

18 Gastrogard Lower dose 1-2 mg/kg to prevent ulcer recurrence 1 mg/kg has 82% response in most cases 2 mg/kg has 89% response No adverse effects of long term therapy or overdose Legal with FEI H-2 blockers Rantidine blocks HCl production Less support to show healing of ulcers occurs At least 40 days of treatment may be needed to get a positive response Along with reduced exercise and increased forage access. Low efficacy reflects the variable oral availability of these drugs Mucosal Protectants Sucralfate (20 mg/kg g 8 to 12 hours per os) In combination with acid suppression Potential for increasing speed of mucosal ulcers Binds to ulcer bed provides physical barrier against acid Increases blood flow via prostaglandin stimulation Not effective when used alone

19 Antacids Most commercial preparations are based on calcium carbonate, magnesium and aluminium hydroxides Minimal evidence to support use Efficacy in the horse where gastric acid secretion and gastric emptying are continuous poor compared to humans Neighlox may be the exception to help with prevention not heal ulceration Antibiotic Use Study in naturally occurring ulceration showed TMS (15 mg/kg orally q 12 hours) Or Live culture of Lactobacillus and Streptococcus species can produce squamous healing over 4-6 weeks 1 Antibiotics tend to be used in cases of ulceration that persist or worsen with acid suppressive therapy Doxycycline has also been used Take Home Message Variety of causes of EGUS in horses Treatment is multifactorial Glandular ulcers take quite a bit longer to heal May be up to 3-6 months These tend to respond to tx with antimicrobials Mucosal protectants

20 Take Home Message Glandular ulceration much more complex Acid suppression and combination therapy best Treatment is multifactorial Still much to learn

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