Equine Gastric Ulcer Syndrome (EGUS) PDF

# Equine Gastric Ulcer Syndrome (EGUS) ## Aims - To understand what EGUS is. - To understand the diagnostic criteria for EGUS. - To understand potential differences between adult horses and foals relating to the development of EGUS. - To understand the underlying pathophysiology of EGUS. - To unde...

# Equine Gastric Ulcer Syndrome (EGUS) ## Aims - To understand what EGUS is. - To understand the diagnostic criteria for EGUS. - To understand potential differences between adult horses and foals relating to the development of EGUS. - To understand the underlying pathophysiology of EGUS. - To understand treatment strategies for EGUS. ## Equine Gastric Ulcer Syndrome (EGUS) A picture depicting two horses jumping over a fence next to a picture showing a horse's stomach with a large ulceration. The caption below reads "What's in a name?". ## Prevalence of EGUS - 40% (Quarter Horses) to 93% (Race horses) of performance horses have been shown to have EGUS. - Pregnant (66.6%) and non-pregnant (75.9%) Broodmares. - Affects condition and performance. - 25% to 50% of foals have been shown to have EGUS. - EGUS is potentially fatal in foals. ## Pathogenesis of EGUS - Gastric lining damage occurs when aggressive factors overpower defenses of gastric mucosa. - Squamous mucosal lesions result from increased acid (HCl, bile acids, organic acids such [VFAs]). - Glandular mucosal lesions result from impaired mucosal protection and blood flow which may be related to NSAIDs. ## The Stomach of the Horse A diagram depicting the stomach of a horse. The diagram shows 4 different areas: the esophagus, the nonglandular region (squamous epithelium), the margo plicatus, and the glandular region (glandular epithelium). It also indicates the pylorus and where the duodenum connects to the stomach. ## Prevalence by Region - Squamous (nonglandular) tissue: - Less resistant to acid injury - 80% of equine ulcers - Glandular & mucus-secreting tissue: - More resistant to acid injury - 20% of equine ulcers **Pagan, World Equine Vet Rev, 1997.** ## Risk Factors: Training/Racing - Intensive exercise: - Reduced gastric mucosal blood flow - Increased gastric acidity? - Altered eating behavior? Two pictures: - One shows a horse's stomach on March 25. - The second picture show the same stomach on June 3. ## Acids forced into the proximal stomach A diagram depicting a horse's stomach with arrows pointing from the esophagus to the nonglandular region of the inside of the stomach. The arrows are labeled "HCI, VFAs" and "Bile acids" **Increased intra-abdominal pressure during intense exercise causes gastric compression, pushing acid contents into proximal stomach.** **Lorenzo-Figueras and Merritt, AJVR 2002;63:1481-1487** ## Risk Factors: Feeding - Feeding management: - Low prevalence of ulcers in horses at pasture. - Decreased acid when roughage available. - Increased serum gastrin when fed concentrates. - Intermittent feed deprivation = gastric ulcers. - Stall confinement = gastric ulcers. - Feeding alfalfa hay may help! ## Organic Acids (VFAs or SCFAs) High Concentrate Diets - Acetic, Butyric, Propionic, and Valeric Acids. - Byproducts of carbohydrate fermentation in the stomach. - Synergistic with HCl. - May lead to non-glandular ulcers. - Also, Lactic Acid may be important - Isolation of Lactobacillus from stomach. - Ferment grain and lead to acid damage. ## Clinical Signs in Adult Horses - Poor appetite. - Poor bodily condition. - Attitude changes. - Decrease in performance. - Mild to moderate colic. - Dry poor haircoat. ## Clinical Signs in Foals - Poor appetite or intermittent nursing. - Colic. - Poor body condition. - Frequently lies on back* - Bruxism (grinding of teeth)* - Excessive salivation (Ptylism)* - Diarrhea* (*-Indicates that these signs are also seen in horses with duodenal ulcers)* ## Diagnosis of EGUS - Clinical signs are suggestive of, but not specific for, EGUS. - Response to treatment can be useful. - Gastric endoscopy is only definitive diagnostic tool. - Clinical Pathology (not commonly observed) - Mild anemia, hypoprotenemia. - Increased serum pepsinogen? ## Endoscopic view of the stomach A black and white picture of a horse's stomach taken through an endoscope. The left and right borders of the picture are trimmed. No additional text below the picture ## Endoscopic view of the stomach A black and white picture of a horse's stomach taken through an endoscope. The left and right borders of the picture are trimmed. No additional text below the picture. ## Equine Gastric Ulcer Syndrome (EGUS) Council **Pipers, FS. Recommendations for diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine vet Ed. 10: 122-134, 1999.** A flow chart showing the diagnosis and treatment of EGUS. The flow chart starts with gathering the history, physical exam and minimum database and ends with discontinue therapy if the horse is out of training. ## Endoscopic Evaluation: Adults 3 pictures of a horse's stomach taken through an endoscope. - **Picture 1:** Squamous erosions fundus - **Picture 2:** Squamous ulcer margo plicatus - **Picture 3:** Squamous ulcers lesser curvature ## Endoscopic Evaluation: Adults (cont’d) 3 pictures of a horse's stomach taken through an endoscope. - **Picture 1:** Glandular ulcer rugal fold - **Picture 2:** Erosion, hyperplasia antrum rugal fold - **Picture 3:** Pyloric ulcer ## Treatment: Approaches - Management modifications. - Medical therapy: - Approaches that have been used - Control gastric acid - Mucosal protectants # Traditional Management Modifications - Reduce level of training. - Diet modifications: - Limit periods of fasting. - Increase roughage: - Pasture turnout (green grass) - Free choice hay - Alfalfa hay- dietary antacid** - Reduce grain / concentrates. **( **- Alflafa hay is not always effective and is not a substitute for a true antacid. You should consult with your veterinarian for a proper treatment recommendation. ** )** A graph shows a comparison of the pH of the stomach contents after feeding the horse a diet of alfalfa hay-grain or bromegrass hay. The alfalfa hay-grain diet shows a higher pH than the bromegrass hay diet throughout the day, but the difference is statistically significant at 12 hours. **Figure 1-Mean (SE) pH of the gastric juice when 6 horses were fed a diet of alfalfa hay-grain and when they were fed a diet of bromegrass hay. Time 0 represents sample collected immediately after feed was removed. a,b - Values with different letters differ significantly (P≤ 0.05). - Alfalfa hay-grain diet. A-A = Bromegrass hay diet.** ## Management Modifications (cont’d) - Limit stressful events: - Trailering - Overcrowding - Long-term stall confinement ## Medical Therapy - **Antacid therapy**: - **Neutralizing agents**: - Antacids (MgOH, AIOH) - Approximately 2 hours of effect - **Antisecretory agents**: - Histamine Hz receptor antagonists (Ranitidine) - Prostaglandin analog (Misoprostol) - Acid pump inhibitors (omeprazole) ## Ulcer Treatments: Actions A diagram showing all of the different agents that can affect the gastric mucosa and their interaction with the parietal cells and the mucus/bicarbonate barrier. ## Commonly Used Antiulcer Medications, Routes, and Doses A table showing 8 different antiulcer medications, their dosage, dosing interval, and the route of administration. ## Proton (Acid) Pump Inhibitor - GastroGard® Paste (Merial Limited) - Substituted benzimidazole - Inhibits H-K ATPase parietal Cell - 4 mg/kg, PO, Q24h - Treatment and prevention of recurrence - Can maintain training program - FDA Approved for use in horses ## Prevention: UlcerGardTM - Prevention of ulcers. - Non-prescription strength of Gastrogard™ - Sold through veterinarians. ## Diminishing Returns: **Compounded Omeprazole Products Found to Have Little or No Value** * **Dr. Duane E. Maye, DVM** * **Dr. Frank Pipers, DVM, MS, PhD** * **Dr. Frank S. Hurtig, DVM, MBA** A graph showing the Omeprazole Active vs. Label in Compounded Product. The graph shows that the active compound was between 6% and 74% of the labeled value in the compounded product. **The following chart reviews the analysis of compounded omeprazole samples that Merial has obtained. These compounded products have been sold to owners and trainers, and have delivered sub-standard results.** **The results of this analysis demonstrate that random samples of compounded omeprazole tested between 6% and 74% of their labeled values.** ## Compounded and Generic Omeprazole: Beware!! ## Helicobacter spp. - Helicobacter specific DNA isolated from horse stomachs. - 2 horses with squamous erosions. - 1 horse with glandular erosions. - **ACVIM Forum-Dallas (May 2002)** **Scott DR, Marcus EA, Shirazi-Beechey SSP, et al. Evidence of Helicobacter infection in the horse. Proc Am Soc Microbiology 2001.** ## Antimicrobial Treatment - Amoxicillin, metronidazole, clarithromycin, bismuth compounds, etc. - Primarily used in humans with Helicobacter pylori. - H. pylori has been associated with the stomach of horses, but not EGUS. - Antimicrobials may be used in horses with resistant EGUS. ## Feed Supplements (Neutriceuticals) - **NeighLox® (Kentucky Performance Products)** - Antacid and Coating Agents: - Aluminum Phosphate, Calcium Carbonate - Dihydroxy-Aluminium - Sodium Carbonate - Labeled for prevention of heartburn - No studies in horses to prove or disprove - Probably does not cause any harm. ## Feed Supplements (Neutriceuticals) - **Others: Nutrient Buffer®, G.U.T** ## Conclusions - EGUS is common in performance horses. - Occurs when aggressive factors overpower gastric defenses. - Definitive diagnosis requires gastroscopy; presumptive diagnosis made based on clinical signs following complete diagnostic evaluation. - Effective treatment entails both management and medical interventions. ## Conclusions-Treatment - **GastroGard® (omeprazole, Merial, Ltd.)**: - FDA approved for treatment and prevention of recurrence of EGUS. - Once daily treatment. - **Ranitidine can also be used for treatment**: - Generic for humans. - Must be given 3 time daily. - Feed Supplements/Neutraceuticals are untested. - Beware of compounded omeprazole. ## Duodenal Ulcers/Stricture - Part of EGUS (more commonly in foals) - Similar pathogenesis - Similar clinical signs: - Usually associated with bruxism, ptylism, and diarrhea (occurs most often in foals) - Delayed gastric emptying - Associated with esophageal ulcers ## Duodenal Ulcers/Strictures - Diagnosis - Clinical signs - Duodenoscopy - Radiology - Gastric emptying with barium swallows (liquid meal=30 minutes) - Necropsy 3 pictures of a horse's stomach after being given barium. - **Picture 1:** Shows the stomach after 30 minutes (A). - **Picture 2:** Shows the stomach after 1 hour (B). - **Picture 3:** Shows the stomach after 2 hours (C). ## Duodenal Ulcers/Strictures A picture of a horse's intestine. A diagram of a horse's stomach and small intestines showing the location of a duodenal ulcer. ## Duodenal Ulcers/Strictures - Treatment - **Omeprazole**: - (4 mg/kg, PO, Q24h, 28 days) - **Omeprazole**: - (1.0 mg/kg, IV, Q24h) - **Ranitidine**: - (6.6 mg/kg, PO, Q8h) - Surgery-Gastrojejunostomy (foals only?) Two pictures showing the surgery procedure being performed. ## Ulcers in the Critically III Neonate - It became the standard of care to provide gastric ulcer prophylaxis to foals being treated in NICU's. - Usually an H-2 antagonist and a mucosal protectant such as sucralfate. - The incidence of catastrophic gastric ulceration in foals in NICU's decreased. ## Ulcers in the Critically III Neonate - I stopped treating prophylactically for ulcers in NICU patients in the mid-1990's. - We undertook a retrospective necropsy study of foals in our NICU to determine if: - The overall incidence of ulcers had changed with time in our NICU population. - If prophylactic treatment for gastric ulcers was associated with decreased incidence of ulcers. ## Ulcers in the Critically III Neonate - Despite decreased prophylactic treatment the overall incidence of ulcers had decreased. - Improved overall care and monitoring? - Discontinued use of NSAID's on a routine basis? - I have had only 1 catastrophic gastric ulcer rupture since 1999 that was clearly associated with transmural gastric necrosis and local bacterial infection. The foal was receiving sucralfate. ## Ulcers in the Critically III Neonate - I DO treat all foals with clinical evidence of ulcer disease and those with evidence of gastrointestinal bleeding such as blood in gastric reflux. All critical foals a refluxed routinely and are gradually introduced to enteral feeding. ## Aims - To understand what EGUS is. - To understand the diagnostic criteria for EGUS. - To understand potential differences between adult horses and foals relating to the development of EGUS. - To understand the underlying pathophysiology of EGUS. - To understand treatment strategies for EGUS.