The Practitioner 3, 2021

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The Practitioner Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the FVMA

Issue 3 • 2021



The President's Line Greetings fellow practitioners,







I hope this finds you all doing well and enjoying your new year! The weather change is always welcomed by us and our patients. The FAEP/FVMA has experienced many exciting events last year! From the launch of Power of 10 and the rollout of our Membership Assistance Program (MAP) to a return of in-person conferences, we’ve had an exciting year. The 2021 Annual Promoting Excellence Symposium, which took place October 21-24 in Naples, was a resounding success. To those who attended and to those industry partners who have lended support, we thank you! We are also quickly approaching the 2022 Ocala Equine Conference (OEC), to be held January 21-23 in Ocala. OEC promises to be a great meeting with a group of outstanding speakers! If you need continuing education before we get busy in the spring, OEC is an ideal conference to attend. I’m also happy to congratulate Jim Naugle on becoming interim executive director of the FAEP/FVMA. Jim has been with the FAEP/FVMA staff for many years. He and his team are great assets to the FAEP. When you see him at our upcoming events, feel free to introduce yourself. The FAEP/FVMA is eager for us to come forward with our concerns and needs in the industry so they can better understand and provide for the equine veterinary community. As we look forward to 2022, we encourage you to keep up with us and utilize the many benefits your membership provides. To learn more about what we’re up to, follow us on social media, and visit our website–and be sure to renew your membership! Thank you for being a part of our amazing profession.


Armon Blair, DVM FAEP Council President

A NOTE FROM YOUR FVMA TEAM: Your FVMA team thanks you for being a member ANNE L. MORETTA


and values your contributions to helping us progress veterinary medicine. We're proud to present this publication as a part of your membership benefits. If you have questions regarding your membership or your reception of this publication, please contact the FVMA/FAEP at 800.992.3862 or email


If anyone is struggling with mental wellness, please do not hesitate to reach out to colleagues, friends, or the FAEP (call 800.992.3862).

We have instituted our Membership Assistance Program (MAP), which is free for all members. MAP offers personal and professional consultation to help you be your best. For more information, email


Opinions and statements expressed in The Practitioner reflect the views of the contributors and do not represent the official policy of the Florida Association of Equine Practitioners (FAEP) or the Florida Veterinary Medical Association (FVMA), unless so stated. Placement of an advertisement does not represent the FAEP’s or FVMA’s endorsement of the product or service. FAEP | 7207 MONETARY DRIVE, ORLANDO, FL 32809 | PH: 800.992.3862 | FAX: 407.240.3710 | EMAIL: INFO@FVMA.ORG | WEBSITE: WWW.FVMA.ORG

2 The Practitioner

Issue 3 • 2021

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INTRODUCTION Many terms and abbreviations have been used over the years for various inflammatory and hyperreactive airway conditions causing cough in the horse. Most recently in a consensus statement by the American College of Veterinary Internal Medicine, it has been proposed that these various syndromes be characterized under the term equine asthma. Formerly called Recurrent Airway Obstruction (RAO), equine asthma is a naturally occurring respiratory disease characterized by expiratory airway obstruction, bronchoconstriction, excessive mucus production and airway neutrophilia. Two different forms of asthma are recognized in the horse: the barn-associated asthma often seen in stalled horses fed hay, and summer pasture-associated asthma (also called summer heaves and pasture-associated heaves) seen more commonly in horses living on pasture in the Southeast during the summer months. In most horses, the disease is reversible once environmental management changes have been made. Etiology: Most evidence suggests that equine asthma is the result of the lung's hypersensitivity to inhaled antigens, although multiple theories exist. Equine asthma is similar to asthma in people, and has allergic and inflammatory components. The most commonly implicated triggers for asthma include mold, organic dust, and endotoxin present in hay and straw. Commonly implicated mold species include Aspergillus fumigatus and Faenia rectivirgula. Equine asthma occurs worldwide with the highest prevalence in stabled horses fed hay in the northeastern and midwestern United States. The average age of onset in affected horses is 9-12 years, and both genders are commonly affected. Winter and spring appear to be the most common seasons for exacerbation of barn-associated asthma, while pasture-associated appears to have the most severe symptoms during the hot, humid weather of the summer or early fall when grass pollen and mold counts are the highest. There does appear to be a heritable component to the etiology of this condition. The incidence of asthma in horses with healthy parents is approximately 10%, which increases to 44% if two parents are affected. Pathogenesis: There is controversy as to whether asthma represents a Th-2 immune response or whether it simply represents an inflammatory condition similar to farmer’s lung

4  The Practitioner

(grain-dust induced asthma). In affected horses, gene, TNF-α and IL-1β are increased and probably contribute to the pulmonary neutrophilia noted in bronchoalveolar fluid samples. Oxidant stress and increased metalloproteinase production has also been suggested to contribute to the inflammatory response. In rare cases of equine asthma, lung remodeling and structural changes (emphysema) occur.

DIAGNOSIS Clinical signs: The most common signs of equine asthma are chronic cough, nasal discharge, exercise intolerance, and respiratory difficulty. Severely affected horses may also exhibit weight loss, anorexia, and exercise intolerance. Clinical signs are often seasonal in nature. Chronic excessive respiratory effort can lead to hypertrophy of the external abdominal oblique musculatures, resulting in a so-called “heave line.” Most affected horses do not have a fever unless a secondary bacterial pneumonia has occurred. Diagnosis of equine asthma is made on the basis of history and characteristic clinical examination findings in the majority of horses. Additional diagnostic tests to confirm and characterize the lower airway inflammation include upper airway and tracheal endoscopy, bronchoalveolar lavage (BAL), lung function testing, thoracic radiographs, and thoracic ultrasound examination. Routine bloodwork and serum amyloid A (SAA) are usually within normal limits. Inflammatory leukogram changes and/or elevated SAA concentrations should alert clinicians to a potential underlying pneumonia. Upper airway endoscopy reveals excessive tracheal mucous in most horses. Bronchoalveolar lavage (see below) is indicated in horses with poor performance and coughing, but is not compulsory in horses with severe disease and suggestive clinical signs. Excessive concentrations of non-degenerate neutrophils, eosinophils, and/or mast cells in BAL fluid confirms the presence of lower airway inflammation and the diagnosis of asthma. Radiographs are recommended for horses that fail to respond to standard therapy, or to further characterize inflammation in the lungs. Serology-based allergen assays and intradermal allergen testing are not useful for the diagnosis of equine asthma.

Issue 3 • 2021

BRONCHOALVEOLAR LAVAGE (BAL) PROCEDURE The BAL provides a non-sterile fluid sample from the peripheral airways, and is considered superior to the transtracheal wash (TTW) for the diagnosis of diffuse and/or inflammatory pulmonary conditions, e.g. equine asthma and/or equine multinodular pulmonary fibrosis (confirmed via PCR for EHV5). It is also helpful for the diagnosis of exercise-induced pulmonary hemorrhage (EIPH), in which hemosiderin-laden macrophages termed hemosiderophages can be found for at least three weeks following an episode. BAL fluid neutrophil concentrations >15% are considered diagnostic for equine asthma with some horses also exhibiting elevations in eosinophil and/or mast cell concentrations. NOTE: BAL fluid samples are non-sterile, and thus, are not appropriate for bacterial/fungal culture. If both TTW and BAL are to be performed, the TTW should be obtained first to maintain sample sterility. Procedure: Bronchoalveolar lavage may be performed using a commercially available cuffed silicone BAL tube (Figure 1) or two meter

endoscope. With either method, the horse is sedated (a combination of detomidine and butorphanol provide both sedation and cough suppression, respectively), and the tube or endoscope is passed nasotracheally. Upon entry into the trachea, 20cc of 2% lidocaine solution is instilled to desensitize the trachea and carina. The tube or scope is passed into consecutively smaller and smaller airways until resistance is felt. At this point, the horse generally coughs, and another 20cc of lidocaine is instilled. Once the Figure 2. Typical BAL sample coughing subsides, the tube demonstrating a mixture of or scope is confirmed to be fluid and surfactant foam. ‘wedged’ into a terminal airway, Image courtesy of Drs. Amanda and the tube cuff is inflated House and Sally DeNotta. with 5cc of air, if applicable. Four 60cc syringes pre-filled with warm saline are then quickly instilled through the tube or scope into the lower airways. A small amount of air is used to clear any remaining saline from the tube, and gentle suction is immediately applied to retrieve sample. Approximately 50% of the instilled volume should be retrieved (120cc of sample for 240cc of instilled saline). A mixture of foam (surfactant) and fluid indicates a good BAL sample (Figure 2). The cuff is deflated and the tube or scope is removed. All sample syringes should be pooled together and submitted for analysis. The sample need not be kept sterile, but preparing several non-stained, air-dried slides to accompany the fluid sample is helpful for preserving cell morphology and ensuring accurate cytologic evaluation. Normal BAL cytologic values:

Figure 1. Commercially available cuffed silicone BAL tube. Image courtesy of Drs. Amanda House and Sally DeNotta.

ENVIRONMENTAL MANAGEMENT OF EQUINE ASTHMA The most important treatment for equine asthma is environmental and dietary management to reduce exposure to organic dusts and mold. In most cases, asthma is a chronic condition that will require life-long management, and in some cases, periodic pharmacologic intervention. Many horses with mild to moderate disease can be successfully managed with environmental and dietary changes alone, without additional medications.

Neutrophils <10%

Lymphocytes 20-50%

Eosinophils <1%

Mast cells <2%

Macrophages 40-80%

Barn-associated asthma: Affected horses should be housed outdoors and maintained on pasture as much as possible. Round bale hay is high in endotoxin and organic dust content, and the presence of round bale hay is a potential cause of treatment failure in horses on pasture. Soaking hay and feed in water prior to feeding may alleviate the signs in mildly affected individuals. Moderate to severely affected horses should have all hay removed from the diet and be transitioned to a complete pelleted feed. |

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@florida_vma | The Practitioner 5

Pasture-associated asthma: Horses with pasture-associated asthma should be stabled during the summer months when pollen and mold counts are at their peak. While stalled, horses should be kept in a clean, well-ventilated environment, and removed from the barn during aisle sweeping, hay moving, and other activities that increase air particulate concentrations. Straw is not recommended as bedding for asthma-affected horses, and low dust bedding such as chopped paper or cardboard is often helpful. Soaking hay and feed in water prior to feeding reduces dust and often alleviates signs in mildly affected individuals. Moderate to severely affected horses should have all hay removed from the diet and be transitioned to a complete pelleted feed.

PHARMACOLOGIC THERAPY It is important to remember that although medications will alleviate the clinical signs of asthma, respiratory disease will return if the horse remains in a mold/dust-filled environment once the medications are discontinued. Systemic corticosteroids and aerosolized bronchodilators are the most immediately helpful therapy for a horse in respiratory distress. Intravenous administration of dexamethasone (0.1 mg/kg IV) should improve lung function within two hours of administration. Dexamethasone may be continued for one to several weeks at a tapering dose for severe cases. For management of less severely affected cases of asthma, prednisolone is generally considered to be a less potent drug that may have fewer side effects. Oral prednisone is poorly bioavailable and not recommended for treatment of asthma in horses. Rapidly acting bronchodilators such as albuterol are also indicated for treatment of acute asthmatic episodes. Aerosolized albuterol improves lung function and breathing by 70% within five minutes of administration; however, the beneficial effects last only onethree hours. Administration of albuterol will also improve the pulmonary distribution of other aerosolized medications, such as aerosolized corticosteroids, and speed mucus clearance from the lungs. In life-threatening cases, a single dose of intravenous atropine (7-10 mg/500kg horse) or single dose of intravenous N-butylscopolammonium bromide (Buscopan®; 80-150 mg/500kg

horse) can also be given as a rescue bronchodilator. Clenbuterol is an oral bronchodilator that provides long-acting bronchodilation in horses with moderate to severe asthma, but has reduced efficacy if administered for longer than 14 days. Because bronchodilators have minimal to no anti-inflammatory activity, they should not generally be used alone for the treatment of equine asthma. Aerosolized corticosteroids are effective in horses with mild to moderate RAO, and can be used in conjunction with systemic therapy in severe cases. The two most commonly administered aerosolized corticosteroid preparations for administration to asthmatic horses are beclomethasone diproprionate and fluticasone propionate, both of which can be administered via commercial delivery devices (Flexineb 2 Portable Equine Nebulizer System®, Aerohippus Equine® MDI Adapter, Equine Haler®). Inhaled therapies have the added benefit of reduced side effects from the corticosteroid administration (such as laminitis in rare cases on systemic steroids). However, inhaled therapies tend to require an upfront financial investment to purchase the mask and medications. Despite the financial costs, inhaled treatments target inflammation and allergy directly within the lungs, and represent an effective and low-risk method of steroid delivery. Periodic inhalant therapy can also be beneficial for occasional flare ups in horses otherwise well-managed with environmental measures alone. A recently released product, Aservo® EquiHaler®, delivers metered doses of the corticosteroid ciclesonide inhalation spray, and is currently approved for horses with severe equine asthma. The product is sold as a proprietary delivery system and provides a 10-day course of treatment. Preliminary studies show alleviation of clinical signs with minimal systemic drug absorption. Clinical trials are currently ongoing at several institutions in the U.S. and Europe. Omega-3 fatty acids and DHA (docosahexaenoic acid) have also been shown to decrease airway inflammation. These ingredients are commercially available as an oral formulation, Aleira® (http://, and can be administered as a topdressing at a dose of 30 g (1 scoop) per 500 kg (1100 lb), once daily.

Additional Resources • Inflammatory Airway Disease of Horses: Revised ACVIM Consensus Statement. Couetil LL, Cardwell JM, Gerber V, Lavoie JP, Leguillette R, Richard EA. J Vet Intern Med. Mar-Apr 2016;30(2):503-15. doi: 10.1111/jvim.13824. • How to perform a bronchoalveolar lavage in practice. Mansmann RA, King CK. Proceedings: American Association of Equine Practitioners, 1998, p186-188. • Hagyard Pharmacy Online Formulary (contains section dedicated to asthma treatment): formulary-app/

6  The Practitioner

Issue 3 • 2021


■ Dexamethasone (2 mg/mL): The following plan is based on IV or IM administration. The injectable formulation of dexamethasone can also be given orally, simply double the dosage as the drug is 50-60% bioavailable in the horse. • 20 mL IV/IM once daily for 7 days, then • 15 mL IV/IM once daily for 7 days, then • 10 mL IV/IM once daily for 7 days, then • 5 mL IV/IM every other day for 7 treatments. ■ Clenbuterol (Ventipulmin, bronchodilator): • 5mL (362.5 Mcg) by mouth once daily for 14 days.

Nebulization therapy:

■ Albuterol (1.5 mg /3 mL, bronchodilator): Add 2 mL (1mg) to the chamber, and dilute 1:1 with 0.9% saline (2 mL). Administer approximately 15 min prior to administration of the steroid budesonide to improve the efficiency of budesonide delivery to the lower airways. ■ Budesonide (0.5 mg/mL, corticosteroid): This medication also needs to be diluted 1:1 with 0.9% saline. • Add 1.5 mL (0.75 mg) to the chamber (+ 1.5 mL saline) and nebulize twice daily for 14 days, then • Add 1 mL (0.5 mg) to the chamber (+ 1 mL saline) and nebulize twice daily for 7 days, then • Add 0.5 mL (0.25 mg) to the chamber (+ 0.5 mL saline) and nebulize twice daily for 7 days.

Metered Dose Inhaler (MDI) therapy:

■ Albuterol (100 µg/puff, bronchodilator): 8 puffs twice daily for 10 days. Administer approximately 15 min prior to administration of fluticasone to improve the efficiency of fluticasone delivery to the lower airways. ■ Fluticasone (Flovent 220 µg/puff, steroid): • 9 puffs twice daily for 10 days. • 9 puffs once daily for 10 days. • 9 puffs every other day for an additional 5 treatments. ■ Wait approximately 20 sec between each puff for all medications. |

Sally DeNotta, DVM, PhD, DACVIM Sally DeNotta is boardcertified by the American College of Veterinary Internal Medicine and is a member of the clinical faculty at the University of Florida College of Veterinary Medicine. Originally from the rural Oregon coast, she spent time in private practice in Oregon and Colorado before completing an internal medicine residency and PhD at Cornell University. She joined the UF faculty in 2018, where her clinical interests include equine infectious disease and clinical neurology. When not in the hospital, she is the UF equine veterinary extension specialist, serving as the liaison between the College of Veterinary Medicine and the Florida horse industry.

Amanda M. House, DVM, DACVIM (Large Animal) Dr. House is the Associate Dean of Academic and Student Affairs and serves as a clinical professor in the Department of Large Animal Clinical Sciences at the University of Florida College of Veterinary Medicine. Dr. House was the director of the Practice-based Equine Clerkship program from 2010-2020, which enables veterinary students at UF to have a clinical ambulatory rotation with private practitioners. She completed her Bachelor of Science in animal science from Cornell University. After graduating from Tufts University School of Veterinary Medicine in 2001, Dr. House completed an internship and large animal internal medicine residency at the University of Georgia’s Veterinary Teaching Hospital. Dr. House became board certified in large animal internal medicine in 2005. Her professional interests include neonatology, communication training, infectious disease and preventative health care.

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@florida_vma | The Practitioner 7

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Figure 1. Endoscopic view of ulcers in the squamous region (ESGD, left photo) and glandular region (EGGD, right photo). Note ESGD (small and large multifocal squamous ulcers along the lesser curvature) in left photo. Note EGGD (small and linear ulcers with hyperemia near the pylorus) in right photo. Image courtesy of Drs. Frank M. Andrews and Heidi E. Banse.

Equine gastric ulcers (Equine Gastric Ulcer Syndrome [EGUS]) are common in performance horses. The distal two-thirds of the equine stomach is lined with glandular epithelium, and the proximal one-third is lined with non-glandular stratified squamous epithelium, an extension of the esophagus. Recently, to highlight the differences in pathogenesis of EGUS in these two regions, a classification system was created to describe ulcers in the proximal squamous region (Equine Squamous Gastric Disease [ESGD]) and in the glandular region (Equine Glandular Gastric Disease [EGGD].1 The majority of ulcers are observed in the squamous region and are likely caused by exposure to hydrochloric acid (HCl), volatile fatty acids, and bile acids (Figure 1).2-6 However, recently, due to awareness and availability of technically sophisticated endoscopes and experienced clinicians, ulcers in the glandular region (EGGD) have been increasingly recognized as a significant problem in horses (Figure 1).1,7 The pathogenesis of EGGD is less understood and might be due to breakdown of mucosal defenses, bacterial colonization, stress, and inflammation. It should also be noted that both diseases can be primary or secondary to other diseases (inflammatory bowel disease, painful lameness, liver disease, kidney disease, etc.).

PATHOGENESIS Horses are continuous gastric HCl secretors, and HCl (along with other acids) and a low stomach pH is the primary cause of ESGD. Also, performance horses are typically fed low-roughage, high concentrate diets containing a high percentage of water-soluble 10 The Practitioner

carbohydrates (WSCs). A diet high in WSCs provides substrates for gastric fermentation by resident bacteria. Gastric fermentation by-products, such as VFAs (acetic, butyric, propionic, valeric, and lactic acids) might damage the squamous mucosa by disrupting chloride-dependent Na transport within the NG mucosa and cause cell swelling and ulceration.3,4 In addition, HCl (gastric juice pH < 4.0) acts synergistically with VFAs on the squamous mucosa to cause further damage and a low stomach pH is a predictor of ESGD severity.2 Several species of bacteria (Lactobacillus, Streptococcus, E. coli) have been isolated from the stomach of horses and recently from gastric fluid and glandular mucosa, adding credence to this theory.8,9 The pathogenesis of EGGD is less understood. Lesions in this region of the stomach vary widely in appearance (focal flat, depressed or raised, hemorrhagic and fibrinsuppurative) and respond poorly to acid suppression therapy alone (Figure 2).7 Therefore, EGGD is likely related in part to exposure to acids, but more important, by the breakdown in protective factors, such as reduced blood flow, decrease in prostaglandins and decreased mucus and bicarbonate secretion. In addition, stress and inflammation might be important causes of EGGD.7 The role of bacteria in formation or persistence in ESGD and EGGD remains unclear. Helicobacter pylori is a common cause of gastritis in dogs and people; however, current evidence does not support its role in either ESGD or EGGD. However, a diverse population of bacteria was isolated from gastric contents of horses fed various diets.11 In that study, horses with spontaneously occurring ESGD, an antibiotic (trimethoprim sulphadimidine) or a probiotic (Lactobacillus spp. and Streptococcus spp.) administered orally decreased ulcer number and severity compared with untreated control horses.11 These data suggest that resident stomach bacteria are important in maintenance and progression of ESGD in horses. Therefore, probiotics containing Lactobacillus and Streptococcus spp. might protect the squamous mucosa from ulcer formation by colonization of the mucosa and initiating healing.12 Recently, the microbiome of gastric juice and the glandular mucosa of fasted horses with and without EGGD was described.9 Although Helicobacter spp. were detected, there was no association with EGGD lesion severity. However, in that study, a modest difference was detected in the community structure of the gastric glandular mucosal microbiome in association with EGGD score, which supports the presence or absence of specific bacteria that might be associated with EGGD, rather than gastric dysbiosis. Issue 3 • 2021







Figure 2 A. Normal glandular mucosa (Grade 0, all scoring systems). B. and C. Hyperemia (Grade 1, modified EGUS council, Grade 0 MacAllister). D. Grade 2 (modified EGUS council), Grade 1 severity and number (MacAllister), moderate, focal, flat and fibrinosuppurative, antrum (ECEIM). E. Grade 3 (modified EGUS council), Grade 2 severity and number (MacAllister); flat, hemorrhagic, and fibrinosuppurative, antrum (ECEIM). F. Grade 4 (modified EGUS council), Grade 4 severity and number (MacAllister), raised, hemorrhagic and fibrinosuppurative, pylorus (ECEIM). Photo F. courtesy of Ashley Whitehead. Abbreviations: EGUS, equine gastric ulcer syndrome; ECEIM, European College of Equine Internal Medicine. Note: © 2019 Dove Medical Press Limited. Reproduced with permission. From Banse, H and Andrews, F.M. (2019) Equine glandular gastric disease: prevalence, impact and management strategies. Veterinary Medicine: Research and Reports. 10, 69-76.7

A more recent study evaluating the pathogenesis of EGGD, showed that increased stress or sensitivity to stress may contribute to development or persistence of glandular lesions.7 In that study, increased serum cortisol after exercise in both Warmbloods and Thoroughbreds suggests that exercise can be stressful.13,14 Furthermore, Warmblood horses had increased salivary cortisol concentration at competitions, when compared to the same concentrations in the home environment, suggesting competition in unfamiliar environments might be stressful for horses.15 Finally, horses with EGGD had an increased response to ACTH stimulation compared to horses without EGGD.16 The relationship between cortisol, stress, and formation of gastric lesions is complex and remains to be determined. Inflammation appears to be a common finding in the glandular mucosa.17 Preliminary data suggested that inflammation of the glandular mucosa is frequently lymphoplasmacytic.7,18 It could be that EGGD due to inflammatory lesions might be associated with inflammatory bowel disease, suggesting an immune-mediated component as with people.19,20 The relationship between gastric and intestinal inflammation in horses remains to be elucidated.

RISK FACTORS FOR ESGD Horses in training and racing are at high risk of developing ESGD. Previously, horses running on a high-speed treadmill showed

increased abdominal pressure and decreased stomach volume.21 Compression of the stomach allowed acids from the glandular mucosa to reflux into the NG region ("acid splash"), leading to squamous mucosal injury and ESGD. Intense exercise likely increases exposure of the squamous mucosa to acids, which explains the increased prevalence of ESGD in horses in race training and racing. Furthermore, an increase in serum gastrin concentration occurred during exercise; which stimulates HCl secretion resulting in a lower stomach pH. Horses grazing at pasture have a decreased prevalence of ESGD. During grazing, there is a continuous flow of saliva and ingesta that buffers stomach acid and maintain stomach pH > 4 for a large portion of the day. Conversely, when feed is withheld from horses, before racing or in managed stables, gastric pH decreases rapidly and the squamous mucosa is exposed to an acid environment. Intermittent feeding has been shown to cause and increase the severity of ESGD.5 The susceptibility of the squamous mucosa to ulceration is due to its lack of mucosal protective factors. Studies have shown that stomach pH drops six hours after feeding and dry matter (DM) content decreases 12 hours after feeding a mixed-feed diet compared with horses fed a hay diet.2 Thus, horses should be fed hay continuously or every five-six hours to buffer stomach acids. Horses fed alfalfa hay and concentrates had fewer and less severe NSGD when compared to horses fed grass hay alone.2 The protective effects of alfalfa hay fed to exercising horses was confirmed in a more recent study.22 |

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@florida_vma | The Practitioner 11

Stall confinement has been implicated as a risk factor for ESGD (Figure 3a). In a previous study, six of seven horses housed in stalls had ESGD, whereas no horse had ESGD after seven days turn-out to pasture. Stabled horses are typically fed two large meals daily and meals are traditionally high in grains and consumed rapidly, which leads to a decrease in saliva production and less buffering of stomach contents. Thus, confounding factors might be at play in stall-confined horses.

day treatment period.29 Therefore, other factors, including acid exposure, oxidative damage, back diffusion of stomach acids, and/or dietary influences, might be involved in the pathogenesis of EGGD.7

CLINICAL SIGNS Clinical signs associated with EGUS, ESGD, and EGGD, are often vague and include partial anorexia, mild colic, dull and/or rough hair coat, weight loss, poor performance, change in behavior, and halitosis. Lesions are more common in horses showing clinical signs. For example, of horses with a client complaint of conditions associated with gastric ulcers, or showing subtle signs of poor health, gastric ulcers were identified in 88-92% compared to 3752% identified in horses not showing clinical signs. In addition to an increased prevalence of ulcers in clinically affected horses, the severity of ulceration was correlated with the severity of the clinical signs.23 Any horse showing signs of colic (acute or chronic) should be considered at risk for ESGD and EGGD. Stereotypic behavior (crib-biting, etc.) has also been associated with ESGD but not with EGGD.

DIAGNOSIS Figure 3a. Severe ESGD (lesion number and severity score, 4 and 5 respectively, score 4 in ESGD score) in the lesser curvature in a horse after stall confinement and intermittent bolus feeding. Image courtesy of Drs. Frank M. Andrews and Heidi E. Banse.

RISK FACTORS FOR EGGD Unfortunately, the risk factors are not as well worked out for EGGD in horses. To that end, it is recommended that risk factors and management changes described for ESGD should be considered for EGGD. In addition, other factors, including breed (sport horses and Warmbloods) should be considered at higher risk for EGGD.23-28 However, there might have been other confounding factors, such as feeding, stabling, and exercise routines that contributed to their risk. Other risk factors for EGGD, included exercise ≥ 6 days per week, lower performance level and increased number of caretakers and riders, perhaps contributing to stress.24,26 It was also noted that horses performing at lower than expectations (by owner’s survey), were at a higher risk of EGGD, which could mean that EGGD has a negative impact on performance.28 Also, horses with ESGD were at a higher risk of having EGGD. It is not known why Warmblood horses are a higher risk for EGGD; however, higher serum cortisol concentrations after exercise might indicate these horses are more susceptible to stress. EGGD has been associated with treatment of NSAIDs, but the increased risk was associated when higher than therapeutic doses are administered. There is speculation that NSAIDs cause EGGD by inhibiting protective tissue prostaglandins, but a more recent study showed that PGE and PGI levels in the glandular mucosa of horses treated with NSAIDs did not decrease during a seven12 The Practitioner

Diagnosis of EGUS requires a thorough history, identification of risk factors, physical examination, and a minimum data base. Recently, an ulcer risk calculator for horse owners was used, highlighting key questions (Table 1).30 Questions included how many meals the horse’s concentrate provision is divided into per day; how much of the day the horse spends grazing or eating hay; how many days in a row the horse has been given NSAIDs in the past three months; and how many days per week the horse is in intense, high-speed work. Scores were calculated based on provided answers, with a score of zero to five indicating low risk, a score of six to 15 indicating moderate risk, and a score of greater than 15 indicating a high risk for EGUS. The results have not been validated in other studies, but might help clients understand the risk factors for both ESGD and EGGD. Gastroscopy is the only definitive diagnosis for EGUS. Standing gastroscopy procedures have been described in detail elsewhere in the literature and the procedure can be viewed at the following link: and require an endoscope of three meters in length to properly visualize the horse stomach and proximal duodenum in most adult horses.31 Several scoring systems for EGGD and ESGD have been purposed that allow clinicians to compare gastroscopic findings and monitor improvement and healing of ulcers and evaluate efficacy of treatment (Table 2). In scoring gastric ulcers, a clinician can utilize several ulcer scoring systems to keep track of number and severity of ulcers in both regions of the stomach and look for improvement and/or healing. Typically, the scoring systems tend to underestimate the number and severity (depth) of ulcers based on histopathologic findings, as well as some glandular ulcers might be missed as they might be hidden under ventral gastric juice.32 However, EGGD lesions are difficult to score using the scoring systems presented above, so a descriptive system has been utilized Issue 3 • 2021

Table 1. Gastric ulcer risk calculator for clients to determine the risk of their horse for gastric ulcers.

Table 2. Gastric ulcer scoring system for lesions in the squamous region (ESGD) and glandular region (EGGD). Number and severity scoring system can be used to score both ESGD and EGGD.1,31,32

Lesion Number - Grade

0 1 2 3 4

Lesion Number - Grade

Descriptions No lesions 1 - 2 localized lesions 3 – 5 localized lesions 6 – 10 lesions 10 or more lesions or diffuse (very large) lesions Descriptions

0 1 2 3 4 5

No lesions Appears superficial (only mucosa missing) Deeper structures involved (> depth than Number 1) Multiple lesions and variable severity (1,2, and/or 4) Deeper structure involved (> depth than Number 1) and has active appearance (hyperemic and/or darkened lesion crater) Same as Number 4 plus hemorrhage or adherent blood clot

ESGD Scoring


0 1 2 3 4

EGGD Scoring

0 1 2 3 4

No Ulcers, mucosa intact Hyperemia or Hyperkeratosis (no ulcers, record if score > 1) Small focal or multifocal ulcers (<5) superficial Large focal or multifocal ulcers (≥5) focal superficial Extensive, large coalescing multifocal ulcers, deep Descriptions Mucosa intact and no evidence of hyperemia Mucosa intact, areas of hyperemia Small, single or multifocal (<5) superficial ulcers Large single deep or multiple (≥5) focal superficial lesions Extensive lesions with areas of apparent deep ulceration

Continued on Page 16 |

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Continued from Page 13 based on severity, distribution, appearance, and location.1 An example of EGGD lesions and lesion scores seen on endoscopic examination are presented in Figure 2. Of particular interest are raised hyperemic lesions (polyps or polypoid lesions), which have been described during endoscopic examination in horses with EGGD (Figure 4a). These lesions are likely due to hyperplasia of gastric or mucus glands, rather than true gastric ulcers. Recently, transendoscopic electrocautery was used to remove polypoid lesions in standing, sedated horses.34 Histopathologic examination revealed well-differentiated hyperplastic gastric glands supported by fibrovascular stroma with lymphocytes, plasma cells, and few mitotic figures. An adenomatous polyp was the final diagnosis. In humans, adenomatous gastric polyps can be precancerous and surgical excision is warranted. However, the cause and outcome of these lesions in horses has not been determined. In addition, glandular mucosal biopsies should be considered in cases of EGGD that are resistant to treatment. Mucosal biopsy of the glandular region might reveal pathology, such as neoplasia or parasites. In a recent case, a polyp was removed from the glandular region of a horse and a parasite infestation caused by Draschia megastoma was found on histopathologic examination. Habronemiasis, caused by Draschia megastoma to our knowledge has not been reported as a cause of EGGD (Figure 5). The polyp was removed and the horse was treated weekly for three weeks with ivermectin (Ivermectin, 200 mcg/kg, orally, Q1wk X 3 weeks) and omeprazole and sucralfate, and the lesion resolved by six weeks. Clinical signs resolved and the horse was working well under saddle at last examination. Habronema and Draschia spps. spend part of their life-cycle in the horse stomach and can cause inflammation and might be associated or contribute to the pathogenesis of EGGD.

Figure 4a. Moderate, multifocal, raised hyperemic lesions (polyps) located in the antrum and pylorus. Likely a polypoid ademoma. Image courtesy of Drs. Frank M. Andrews and Heidi E. Banse.

RBC counts and hemoglobin concentrations than horses without gastric ulcers.35 Some horses with EGUS might have a decreased packed cell volume (PCV) or total solids over time, but rarely are these values outside normal reference range. Yearly wellness checks including blood work can help clinicians spot decreases in blood parameters that might indicate anemia. Fecal occult blood testing has been proposed in the diagnosis of gastric ulcers in horses. That early study used the human guaiac smear method (gFOBT) to determine hemoglobin in the manure of horses that were euthanatized. The positive predictive value

Figure 5. Endoscopic view of the glandular mucosa of a horse with a polypoid lesion (determined to be caused by Draschia megastoma) and subsequent removal. The horse made a full recovery after removal. Image courtesy of Drs. Frank M. Andrews and Heidi E. Banse.

Figure 3b. The lesser curvature in the same stomach after treatment (4 mg/kg, GastroGard, orally, Q24h, 14 days). There is mild hyperkeratosis (number and severity score of 0 and ESGD score of 1) still present, but no gastric ulcers. Image courtesy of Drs. Frank M. Andrews and Heidi E. Banse.

Currently, there are no hematologic or biochemical markers to diagnose EGUS. However, horses with gastric ulcers had lower 14 The Practitioner

for gastric ulcers was high, but the negative predictive value was low (17%), so the specificity of the test was poor. Since that study, an equine FOBT (SUCCEED® Equine Fecal Blood Test, Freedom Health LLC., Aurora, OH) was developed for horses to aid in diagnosis of EGUS. The FOBT utilizes monoclonal antibodies to measure hemoglobin and albumin in manure. A recent in vitro study showed high sensitivity and specificity in albumin and hemoglobin spiked fecal samples.36 However, the diagnostic accuracy and correlation with gastric ulcer scores Issue 3 • 2021

Habronema muscae Habronema microstoma Habronema megastoma

observed during endoscopic evaluation in at least two studies were low.1,37 Until further evaluation, the FOBT is not currently recommended as a diagnostic test for EGUS.1 False positive FOBT may result if there was a recent rectal examination, rectal biopsy, or other rectal trauma, as well as protein-losing enteropathy, colonic ulcers or acute colitis. When gastroscopy is not available and ulcers are strongly suspected, it may be worthwhile to start empirical treatment and observe for resolution of clinical signs. If the horse does not respond to treatment, further evaluation is indicated.31

PHARMACOLOGIC TREATMENT AND MANAGEMENT The mainstay of pharmacologic treatment of ESGD and EGGD is to suppress hydrochloric acid (HCl) secretion and increase stomach pH > 4.0. Because of the high recurrence rate, effective acid control should be followed by preventative pharmacologic treatment and nutritional and dietary management strategies to prevent ulcer recurrence.

PHARMACOLOGIC THERAPY There is a wide range of pharmaceutical agents used to treat ESGD and EGGD. The name, dose and route of administration of many of the pharmacologic agents used to treat ESGD and EGGD can be found in Tables 3 and 4.



Omeprazole paste (4 mg/kg, PO, q24h; Gastrogard , Boehringer Ingelheim Animal Health, Duluth, GA), FDA approved for horses, significantly inhibits gastric acid secretion for 24 hours and is efficacious in treatment of EGUS.38 In an acid environment, omeprazole is activated to a sulphenamide derivative and binds irreversibly to the H+/K+ ATPase in parietal cells and inhibits transport of hydrogen ions into the stomach. Omeprazole has been shown to be an effective treatment (4.0 mg/kg, body weight) and prevention of recurrence (2.0 mg/kg, body weight) of EGUS. Omeprazole was superior to ranitidine in healing and preventing gastric ulcers in training and racing horses.39 The buffered paste formulation (Gastrogard®) of omeprazole has variable bioavailability and concurrent feeding has been shown to cause decreased absorption. Thus, to improve bioavailability, it should be given before feeding in the morning. Omeprazole should be administered before the morning feeding to increase plasma concentrations. After administration of omeprazole, wait

60 minutes and then feed the hay portion of the diet. This will functionally stretch the stomach and activate the acidic parietal cells. The omeprazole in the blood vascular system will then be attracted to the acidic parietal cells and concentrate inside them resulting in maximal acid suppression. Grain can be fed 30 to 60 minutes after hay feeding. The effectiveness of GastroGard® can be evaluated by aspirating gastric juice from the biopsy chamber of the endoscope or a nasogastric tube and measuring pH using a pH strip or urine dipstick. A gastric juice pH > 4.0, approximately 18 hours after omeprazole administration, is considered effective; however, a lower pH might be effective to heal ESGD.

CO-ADMINISTRATION OF PHENYLBUTAZONE AND OMEPRAZOLE The co-administration of omeprazole (4.0 mg/kg, PO, Q24h) and phenylbutazone (4.4 mg/kg, PO, Q12h) and management changes might lead to intestinal complications. In a recent study, administration of omeprazole ameliorated PBZ-induced EGGD, but was associated with increased intestinal complications, including, colic, diarrhea, cellulitis, necrotic typhocolitis, and colon impaction (days two-12, median six days) during coadministration.40 Thus, caution should be exercised when coprescribing NSAIDs and omeprazole in horses, particularly in association with management changes.

INJECTABLE OMEPRAZOLE A pilot investigation recently reported efficacy of a novel, longacting, injectable formulation of omeprazole in horses and showed acid suppression for up to seven days following a single intramuscular injection. In that study, pharmacodynamics and clinical outcome was similar to oral omeprazole.41 Furthermore, a more recent study showed that four weeks of treatment with that injectable formulation resulted in better rates of ESGD healing than four weeks of oral omeprazole treatment.42 The authors of that study suggested that more robust studies are warranted. It should be noted that the long acting omeprazole injectable is a compounded product and is likely to be highly variable in strength and is not available in the U.S. The product is also not registered by the U.S. FDA for treatment of EGUS and cannot be recommended in the U.S. for use.

HISTAMINE TYPE-2 RECEPTOR ANTAGONISTS CIMETIDINE Cimetidine has been used since the early 1980s to treat and prevent ulcers in horses and foals, but there is little scientific evidence in the veterinary literature showing that it has efficacy in the treatment of EGUS. The author cannot recommend cimetidine for treatment or prevention for EGUS.

RANITIDINE Ranitidine hydrochloride is four times more potent than cimetidine. When given orally (6.6mg/kg, PO, q8h), ranitidine suppresses acid output and significantly improved ulcer scores and increased weight gain, appetite, and decreased frequency |

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of colic episodes.43 A lower dose (4.4 mg/kg, PO, q8h) was not effective for treatment of EGUS.

COATING OR BINDING AGENTS Sucralfate is a hydroxyl aluminum salt of sucrose octasulfate and adheres to the negatively charged particles in the ulcer bed, buffering HCl by increasing local bicarbonate secretion and stimulating prostaglandins production. In the stomach, sucralfate is converted to a sticky amorphous mass, which is thought to prevent back-diffusion of HCl into the ulcer. Sucralfate has been recommended to be used with omeprazole in the treatment of EGGD.1,7

SYNTHETIC HORMONES Misoprostol, a synthetic PGE 1 analogue, is effective in the treatment of gastric and duodenal ulcers in man. Acid suppression, increased mucosal blood flow, increased bicarbonate secretion, and increased mucosal restitution are its mechanisms of action. Misoprostol (5 mcg/kg, PO) was shown to increase gastric juice pH and inhibited gastric acid secretion for eight hours after administration. In a small population of horses, misoprostol was found to be superior to combined omeprazole-sucralfate in the treatment of EGGD and has been recommended as a monotherapy for treatment of EGGD.44 Misoprostol is contraindicated in pregnant and nursing horses due to its effect on increasing uterine contractions. Although there are no reports of side effects in horses in the literature, some treated horses might show mild colic signs and diarrhea 30 to 60 minutes after administration.

PROKINETIC AGENTS Prokinetics agents are a valuable adjunct therapy in horses with EGUS and when there is adynamic ileus and gastroduodenal reflux. Bethanechol (0.25 mg/kg, IV) and erythromycin lactobionate (0.1 and 1.0 mg/kg, IV) have been shown to increase solid phase gastric emptying.45 No adverse effects were seen in healthy horses, however other forms of erythromycin can cause fatal colitis at antimicrobial doses. Both prokinetics increase gastric emptying versus saline, but bethanechol appeared to be superior in increasing solid-phase gastric emptying, where as erythromycin increased liquid-phase gastric emptying. Bethanechol is a synthetic muscarinic cholinergic agent that is not degraded by acetylcholinesterases. The only side effect of the bethanechol administration was increased salivation. Other authors have recommended a dose of 0.025 – 0.030 mg/ kg subcutaneously every three-four hours followed by oral maintenance therapy of 0.3 – 0.45 mg/kg 3-4 time daily. It is also possible that gastroduodenal reflux may worsen after treatment in patients with a proximal small intestinal obstruction.

DURATION OF PHARMACOLOGIC TREATMENT It is difficult to predict how long to treat horses with ESGD or EGGD. Initial recommended treatment time for antiulcer medications is at least 28 days. However, management changes in addition to pharmacologic therapy can affect healing and/or improvement of both diseases. For example, in horses with ESGD, induced by feed-deprivation, lesions were healed or nearly healed after nine days of pasture turnout, whereas, omeprazole-treated (4.0 mg/kg, PO, Q24h) Thoroughbred horses kept in training

Table 4. Selected pharmacologic therapy for Treatment of EGUS. Drug


Dosing Interval

Route of Administration


1.0 mg/kg


Q 24 hrs


4 mg/kg


Q 24 hrs

Omeprazole (prevention)

1 mg/kg


Q 24 hrs


1.5 mg/kg


Q 6 hrs


6.6 mg/kg


Q 8 hrs


0.3 mg/kg


Q 12 hrs


2.8 mg/kg


Q 12 hrs


5 mcg/kg


Q 8 hrs


20-40 mg/kg


Q 8 hrs

AlOH/MgOH antacids

30g AlOH/15 g MgOH


Q 2hrs


0.025 – 0.30 mg/kg


Q 3-4 hrs


0.3-0.45 mg/kg


Q6-8 hrs

Erythromycin lactobionate

0.1 – 1.0 mg/kg



*Cimetidine: Not effective for treatment of EGUS

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Table 5. Selected pharmacologic medication, dose/route, frequency, and mechanism of action for treatment of EGGD. Note: © 2019 Dove Medical Press Limited. Reproduced with permission. From Banse, H and Andrews, F.M. (2019) Equine glandular gastric disease: prevalence, impact and management strategies. Veterinary Medicine: Research and Reports. 10, 69-76.7 Medication


Freqency Mechanisms


4 mg/kg, PO

Q 24 hrs

Proton pump inhibitor


5 mcg/kg, PO

Q 12 hrs

Prostaglandin analogue


20-40 mg/kg, PO

Q 6-12 hrs

Promotes epithelial restitution

Abbreviations: PO, orally; q, every

with ESGD, 77% and 92% healed and improved, respectively, after 28 days.46 Furthermore, pastured horses with spontaneous occurring ulcers showed 86% healing after 28 days of treatment. We recommend endoscopic examination in horses with gastric ulcers after 14 days of omeprazole treatment (Figure 2a and 2b). Over half (57%) of horses with ESGD healed after 14 days of omeprazole treatment.38 This could save the client money and, if lesions have healed or significantly improved, then omeprazole (1.0 – 2.0 mg/kg, PO, q24h) treatment could be reduced, if horses remain in race training. In addition, adding alfalfa hay to the diet might potentiate the effect of omeprazole on increasing gastric juice pH and facilitate healing. If healing has not occurred after 28 days of omeprazole treatment, then further work up may be indicated. It should be noted that clinical signs might resolve before complete ulcer healing has taken place. Duration of treatment in EGGD is more difficult to predict, therefore a longer treatment period might be required to see improvement or healing. For example, poorer improvement and healing rates were seen in horses with glandular ulcers using omeprazole (4.0 mg/kg, PO, Q24h). In that study, overall healing rates were 50% for EGGD, compared to 67% of horses with ESGD.46 In another study, 56% of horses healed and 87% improved, after 28-35 days of misoprostol treatment alone.44 In that study, when compared to omeprazole and sucralfate, healing and improvement in EGGD scores were better when misoprostol was administered alone. Due to the low healing rates in EGGD, a higher dose of omeprazole or co-administration of sucralfate and/or misoprostol might need to be continued for 60-90 days. It has also been shown that chronic severe pyloric lesions can be associated with delayed gastric emptying that can be identified by ultrasonography. It was also found that the prognosis is poor in young horses with severe glandular ulcers.47 Once ulcers have healed or improved to a score of ≤ 1, omeprazole prophylaxis (1.0 – 2.0 mg/kg, PO, Q24h) should be considered in horses actively training. In a meta-analysis study, it was determined that omeprazole prophylaxis was superior to sham treatment in training horses.48 Seven trials were identified involving 566 horses and 95% of horses improved in ulcer scores in the omeprazole prophylaxis group compared to 77.2% in sham. The study concluded, omeprazole prophylaxis in active training horses significantly reduces gastric ulceration compared with no prophylaxis (sham) with the absolute effect of 566 fewer ulcers per 1000 horses treated.

ENVIRONMENTAL, NUTRITIONAL, AND DIETARY MANAGEMENT Pharmacologic therapy may be necessary to heal both ESGD and EGGD. Once pharmacologic therapy is discontinued, ulcers will return within several days if management changes are not instituted. Environmental, nutritional, and dietary management can be initiated during therapy to help facilitate ulcer healing and prevent ulcer recurrence. Adding alfalfa hay to the diet to buffer gastric acid can be helpful. Also, pasture turn-out to facilitate continuous eating will help saliva production.

ANTIBIOTICS VS PROBIOTICS There are a large population of diverse acid-tolerant bacteria (E. coli, Lactobacillus and Streptococcus spp.) in the equine. Because resident bacteria might colonize the ulcer bed and delay healing, trimethoprim suphadimidine or a probiotic (Lactobacillus agilis, L. salivarius, L. equi, Streptococcus equinus, S. bovis) administered orally to horses decreased the number and severity of ulcers compared to untreated controls.11 These data suggest that the resident stomach bacteria are important in maintenance and progression of ESGD in horses and treatment with antibiotic and/ or probiotics might facilitate ulcer healing or prevent ulcers from recurring. Antibiotics and/or probiotics administration might be used in horses with chronic non-responsive gastric ulcers as an adjunct to therapy. Recently, the use of doxycycline (10 mg/kg, PO, Q12h) has been recommended as an ancillary treatment for EGGD. Recent data suggest that there is bacterial colonization of glandular lesions, but treatment with antibiotics is controversial. Doxycycline has antibiotic properties but has also been shown to block gastric ulcers by regulating matrix metalloproteinase-2 and oxidative stress.49 Doxycycline might be an option in horses with chronic non-responsive EGGD; however, bioavailability of doxycycline is poor and adverse responses such as diarrhea have been reported

OILS (CORN OIL, RICE BRAN OIL) Dietary fats delay gastric emptying time in man and other species.50 In contrast to most species, gastric emptying rates were slower in horses fed a high-carbohydrate diet, compared with horses fed a high-fat diet, although these rates were not statistically significant.51 Ponies fitted with gastric cannulas and fed |

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dietary corn oil (45 ml, orally, once daily) had significantly lower gastric acid output and increased prostaglandin concentration (PGE2) in gastric juice.52 Corn oil supplementation could be an economical adjunct approach to the therapeutic and prophylactic management of EGGD. In contrast to positive effects of corn oil, refined and crude rice bran oil (240 ml, once daily, mixed in grain) failed to improve ESGD lesions; however, EGGD lesions were not reported in that study, so there still might be a positive effect on EGGD with other oils.53 In conclusions, general recommendations for treatment and nutritional management of EGUS (ESGD and EGGD) can help minimize the impact on the horse’s health and performance.54

References 1.



Sykes, B.W., Hewetson, M., Hepburn, R.J., Luthersson, N. and Tamzali, Y. (2015) European College of Equine Internal Medicine Consensus Statement—equine gastric ulcer syndrome in adult horses. Journal of Veterinary Internal Medicine, 29(5), 1288. Nadeau, J.A., Andrews, F.M., Mathew, A.G., Argenzio, R.A., Blackford, J.T., Sohtell, M. and Saxton, A.M. (2000) Evaluation of diet as a cause of gastric ulcers in horses. Am. J. Vet. Res. 61, 784-790. Nadeau, J.A., Andrews, F.M., Patton, C.S., Argenzio, R.A., Mathew, A.G. and Saxton, A.M. (2003) Effects of hydrochloric, acetic, butyric and propionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses. Am. J. Vet. Res. 64, 404-412.


■ Provide good quality hay throughout the day and night ■ Feed alfalfa hay to buffer stomach contents (mix with grass hay or feed alone)

Concentrates (grain):

■ Limit high starch grain to ≤ 5 lbs (2.2 kg) every six hours (might be able to feed higher amounts of low starch grain) ■ Weigh grain before feeding to prevent overfeeding ■ Feed grain containing chelated minerals such as Zinc-methionine.


■ Add corn oil to diet to decrease acid secretion and increase prostaglandins ■ Horses with EGGD, especially

Pharmacologic Treatment:

■ Gastrogard® (4.0 mg/kg, PO, Q24h) for initial treatment ■ Consider adding sucralfate (12-22 mg/kg, PO, Q6-8h) with persistent ESGD and for EGGD ■ Consider adding misoprostol (5 mcg/kg, PO, Q12h)


■ SmartGut Ultra® (SmartPak Equine, 40 g, PO, Q12h) mixed with feed during and after Gastrogard treatment • Prevention of rebound hyperacidity after discontinuing omeprazole treatment ■ Outlast® (Purina Animal Health) for horses traveling ■ Seabuck® 7 (Sea Buckthorn berries and pulp) for EGGD

Monitor horses for clinical signs and behavior consistent with recurrence.

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5. 6. 7. 8.



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Nadeau, J.A., Andrews, F.M., Patton, C.S., Argenzio, R.A., Mathew, A.G. and Saxton, A.M. (2003) Effects of hydrochloric, valeric and other volatile fatty acids on pathogenesis of ulcers in the non-glandular portion of the stomach of horses. Am. J. Vet. Res. 64, 413-417. Murray, M.J. (1994) Equine model of inducing ulceration in alimentary squamous epithelial mucosa. Dig. Dis. Sci. 12, 25302535. Berschneider, H.M., Blikslager, A.T. and Roberts, M.C. (1999) Role of duodenal reflux in nonglandular gastric ulcer disease of the mature horse. Equine Vet. J. 31, Suppl. 29, 24-29. Banse, H.E. and Andrews, F.M. (2019) Equine glandular gastric disease: prevalence, impact and management strategies. Veterinary Medicine: Research and Reports, 10, 69-76. Al Jassim, R.A.M., Scott, P.T., Trebbin, A.L., Trott, D. and Pollitt, C.C. (2005) The genetic diversity of lactic acid producing bacteria in the equine gastrointestinal tract. FEMS Microbiol. Lett. 248, 75-81. Paul, L.J., Ericsson, A.C., Andrews, F.M., Keowen, M.L., Morales Yniguez, F., Garza Jr, F. and Banse, H.E. (2021) Gastric microbiome in horses with and without equine glandular gastric disease. J Vet Intern Med 35(5), 2458-2464. Sykes B, Sykes K, Hallowell G. (2015) A comparison of three doses of omeprazole in the treatment of equine gastric ulcer syndrome: A blinded, randomized, dose–response clinical trial. Equine Vet J. 47(3), 285–290. Al Jassim RAM, McGowen, D., McGowen, T., Andrews, F.M. (2008) Rural Industries Research and Development Corporation, Final Report, Australia 2008:1-26. Yuki, N., Shimazaki, T., Kushiro, A., Watanabe, K., Uchida, K., Yuyama, T. and Morotomi, M. (2000) Colonization of the stratified squamous epithelium of the nonsecreting area of horse stomach by lactobacilli. Applied and Environmental Microbiology 66(11), 5030-5034. Freestone J, Wolfsheimer K, Kamerling S, Church G, Hamra J, Bagwell C. (1991) Exercise induced hormonal and metabolic changes in Thoroughbred horses: effects of conditioning and acepromazine. Equine Vet J. 23(3), 219–223. Cayado P, Muñoz-Escassi B, Dominguez C, et al. (2006) Hormone response to training and competition in athletic horses. Equine Vet J. 38 (S36), 274–278. Munk R, Jensen R, Palme R, Munksgaard L, Christensen JW. (2017) An exploratory study of competition scores and salivary cortisol concentrations in Warmblood horses. Domest Anim Endocrinol. 61, 108–116. Scheidegger MD, Gerber V, Bruckmaier R, van der Kolk JH, Burger D, Ramseyer A. (2017) Increased adrenocortical response to adrenocorticotropic hormone (ACTH) in sport horses with equine glandular gastric disease (EGGD). Vet J. 228, 7–12. Martineau H, Thompson H, Taylor D. (2009) Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system. Equine Vet J. 41(7), 646–651. Crumpton S, Baiker K, Hallowell G, Habershon-Butcher J, Bowen I. (2015) Diagnostic value of gastric mucosal biopsies in horses with glandular disease. Equine Vet J. 47(S48):9-9 (Abstract) Sonnenberg A, Melton SD, Genta RM. (2011) Frequent occurrence of gastritis and duodenitis in patients with inflammatory bowel disease. Inflamm Bowel Dis. 17(1), 39–44. Sonnenberg A, Genta R. Low prevalence of Helicobacter pylori infection among patients with inflammatory bowel disease. (2012) Aliment Pharmacol Ther. 35(4), 469–476. Lorenzo-Figueras, M. and Merritt, A.M. (2002) Effects of exercise on gastric volume and pH in the proximal portion of the

stomach of horses. Am. J. Vet. Res. 63, 481-487. 22. Lybbert, T., Gibbs, P., Cohen, N., Scott, B. and Sigler, D. (2007) Feeding alfalfa hay to exercising horses reduces the severity of gastric squamous mucosal ulceration. In Proceedings, Am. Assoc. Equine Pract. 53, 525-526. 23. Mönki J, Hewetson M, Virtala AM. (2016) Risk factors for equine gastric glandular disease: a case-control study in a Finnish Referral Hospital Population. J Vet Intern Med. 30(4), 1270–1275. 24. Luthersson N, Nielsen K, Harris P, Parkin T. (2009) The prevalence and anatomical distribution of equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. Equine Vet J. 41(7), 619–624. 25. Hepburn R. (2014) Endoscopic examination of the squamous and glandular gastric mucosa in sport and leisure horses: 684 horses (2005–2011). Paper presented at and In Proceedings of the 11th International Equine Colic Research Symposium, Dublin, Ireland. 26. Pedersen S, Cribb A, Windeyer M, Read E, French D, Banse H. (2018) Risk factors for equine glandular and squamous gastric disease in show jumping Warmbloods. Equine Vet J. 50, 747–751. 27. Malmkvist, J., Poulsen, J.M., Luthersson, N., Palme, R., Christensen, J.W. Søndergaard, E. (2012). Behaviour and stress responses in horses with gastric ulceration. Applied animal behaviour science. 142(3-4), 160-167. 28. Sykes B.W., Bowen, M., Habershon-Butcher JL, Green M, Hallowell GD. (2019) Management factors and clinical implications of glandular and squamous gastric disease in horses. J Vet Intern Med. 33(1):233–240. 29. Pedersen S, Cribb A, Read E, French D, Banse H. (2018) Phenylbutazone induces equine glandular gastric disease without decreasing prostaglandin E2 concentrations. J Vet Pharmacol Ther. 41(2):239–245. 30. Barakat C. (2016) What’s your horse’s ulcer risk. Equus 454, 6877. 31. Anon. Andrews, F.M., Bernard, W., Byars, D., Cohen, N., Divers, T., MacAllister, C., McGladdery, A., Merritt, A., Murray, M., Orsini, J., Snyder, J. and Vatistas, N. (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet. Educ. 11, 262-272. 32. MacAllister, C.G., Andrews, F.M., Deegan, E., Ruoff, W. and Olovson, S.G., (1997) A scoring system for gastric ulcers in the horse. Equine Vet J. 29(6), 430-433. 33. Andrews, F.M., Reinemeyer, C.R., McCracken, M.D., Blackford, J.T., Nadeau, J.A., Saabye, L., Sötell, M. and Saxton, A. (2002) Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers. Equine Vet J. 34(5), 475-478. 34. Marley, L.K., Repenning, P., Frank, C.B., Hackett, E.S. and Nout‐ Lomas, Y.S. (2016) Transendoscopic electrosurgery for partial removal of a gastric adenomatous polyp in a horse. J Vet Intern Med. 30(4), 1351-1355. 35. McClure, S.R., White, G.W., Sifferman, R.L., Bernard, W., Doucet, M.Y., Vrins, A., Holste, J.E., Fleishman, C., Alva, R. and Cramer, L.G. (2005) Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training. Am. J. Vet. Med. Assoc. 226, 1681-1684. 36. Rebalka, I.A. and Lindinger, M.I. (2021) In vitro Validation Assessment of a Fecal Occult Blood Protein Test for Horses. J Equine Vet Sci. 104, 103695. 37. Andrews, F.M., Camacho-Luna, P., Loftin, P.M., Gaymon, G., Garza, F. Jr, Keowen, M.L. and Kearney, M.T. (2016) Effects of a pelleted supplement fed during and after omeprazole treatment on nonglandular gastric ulcer scores and gastric juice pH in horses. Equine Vet.Educ. 28(4), 196-202. |

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38. Andrews, F.M., Sifferman, R.L., Bernard, W., Hughes, F.E., Holste, J.E., Daurio, C.P., Alva, R. and Cox, J.L. (1999) Efficacy of omeprazole paste in the treatment and prevention of gastric ulcers in horses. Equine Vet. J. 31(S29), 81-86. 39. Lester, G.D., Robertson, I. and Secombe, C. (2007) Risk factors for gastric ulceration in Thoroughbred racehorses. Proc. Am. Assoc. Equine Pract. 53, 529. 40. Ricord, M., Andrews F.M., Yniguez, F.J.M., Keowen, M., Garza, Jr., F. Paul, L., Chapman, A., Banse, H.E. (2020) Impact of concurrent treatment and omeprazole on phenylbutazone-induced equine gastric ulcer syndrome (EGUS). Equine Vet J. 53, 356-363. 41. Sykes, B.W., Kathawala, K., Song, Y., Garg, S., Page, S.W., Underwood, C. and Mills, P.C. (2017) Preliminary investigations into a novel, long‐acting, injectable, intramuscular formulation of omeprazole in the horse. Equine veterinary journal, 49(6), 795801. 42. Gough, S., Hallowell, G. and Rendle, D. (2020) A study investigating the treatment of equine squamous gastric disease with long‐acting injectable or oral omeprazole. Veterinary Med and Sci. 6(2), 235-241. 43. Furr, M.O. and Murray, M.J. (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Veterinary Journal, 21(S7), 77-79. 44. Varley, G., Bowen, I.M., Habershon‐Butcher, J.L., Nicholls, V. and Hallowell, G.D. (2019) Misoprostol is superior to combined omeprazole‐sucralfate for the treatment of equine gastric glandular disease. Equine Vet J. 51(5), 575-580. 45. Ringger, N.C., Lester, G.D., Neuwirth, L., Merritt, A.M., Vetro, T. and Harrison, J. (1996) Effect of bethanechol or erythromycin on gastric emptying in horses. Am J Vet Res. 57(12), 1771-1775. 46. Sykes, B.W., Sykes, K.M. and Hallowell, G.D. (2014) A comparison between pre‐and post exercise administration of omeprazole in the treatment of equine gastric ulcer syndrome: a blinded, randomised, clinical trial. Equine Vet J. 46(4), 422-426. 47. Bezdekova, B., Wohlsein, P. and Venner, M. (2020) Chronic severe pyloric lesions in horses: 47 cases. Equine veterinary journal, 52(2), 200-204. 48. Mason, L.V., Moroney, J.R. and Mason, R.J. (2019) Prophylactic therapy with omeprazole for prevention of equine gastric ulcer syndrome (EGUS) in horses in active training: A meta‐analysis. Equine Vet J. 51(1), 11-19. 49. Singh, L.P., Mishra, A., Saha, D. and Swarnakar, S. (2011) Doxycycline blocks gastric ulcer by regulating matrix metalloproteinase-2 activity and oxidative stress. World journal of gastroenterology: WJG. 17(28), 3310-3321. 50. Sidery, M.B., Macdonald, I.A. and Blackshaw, P.E. (1994) Superior mesenteric artery blood flow and gastric emptying in humans and the differential effects of high fat and high carbohydrate meals. Gut. 35(2), 186-190. 51. Lorenzo-Figueras, M., Preston, T., Ott, E.A. and Merritt, A.M. (2005) Meal-induced gastric relaxation and emptying in horses after ingestion of high-fat versus high-carbohydrate diets. Am J Vet Res. 66(5), 897-906. 52. Cargile, J.L., Burrow, J.A., Kim, I., Cohen, N.D. and Merritt, A.M. (2004) Effect of dietary corn oil supplementation on equine gastric fluid acid, sodium, and prostaglandin E2 content before and during pentagastrin infusion. J. Vet. Intern. Med. 18, 545-549. 53. Frank, N., Andrews, F.M., Elliott, S.B., Lew, J. and Boston, R.C. (2005) Effects of rice bran oil on plasma lipid concentrations, lipoprotein composition, and glucose dynamics in mares. J Animal Sci. 83(11), 2509-2518. 54. Andrews, F.M., Larson, C., Harris, P. (2017) Nutritional management of gastric ulceration. Equine Vet Education. 29(1), 45-55.

20 The Practitioner

Frank Andrews, DVM, MS, DACVIM (LAIM) Dr. Andrews received his BS in bacteriology and public health and a BS in veterinary science from Washington State University in 1979 and 1983 respectively. He also completed his MS and DVM from Washington State University in 1983. He received a residency certificate in equine medicine and surgery from the Ohio State University in 1987. Dr. Andrews is LVMA equine committee professor and head of the department of veterinary clinical sciences at Louisiana State University. His research focus is on treatment and prevention of gastric ulcer disease in horses. His research interests include gastric ulcer disease (pathogenesis, treatment, prevention), endocrine diseases (such as pituitary pars intermedia dysfunction and its treatments), neurologic disease (such as equine protozoal myeloencephalitis and the diagnosis, treatment, and prevention it), and laminitis.

Heidi E. Banse, DVM, PhD, DACVIM Dr. Banse obtained her DVM from Washington State University in 2007. In 2013, she completed a combined residency (equine internal medicine) and PhD program at Oklahoma State University. After four years on faculty at the University of Calgary in Alberta, Canada, she moved to Louisiana State University where she is presently an associate professor of equine medicine and director of education. Her clinical research interests include equine glandular gastric disease and equine endocrine disease.

Issue 3 • 2021



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There’s nothing else like it. For more than 30 years, Adequan® i.m. (polysulfated glycosaminoglycan) has been administered millions of times1 to treat degenerative joint disease, and with good reason. From day one, it’s been 2, 3 the only FDA-Approved equine PSGAG joint treatment available, and the only one proven to. Reduce inflammation Restore synovial joint lubrication Repair joint cartilage Reverse the disease cycle When you start with it early and stay with it as needed, horses may enjoy greater mobility over a 2, 4, 5 lifetime. Discover if Adequan is the right choice. Visit to find a distributor and place an order today. BRIEF SUMMARY: Prior to use please consult the product insert, a summary of which follows: CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian. INDICATIONS: Adequan® i.m. is recommended for the intramuscular treatment of non-infectious degenerative and/or traumatic joint dysfunction and associated lameness of the carpal and hock joints in horses. CONTRAINDICATIONS: There are no known contraindications to the use of intramuscular Polysulfated Glycosaminoglycan. WARNINGS: Do not use in horses intended for human consumption. Not for use in humans. Keep this and all medications out of the reach of children. PRECAUTIONS: The safe use of Adequan® i.m. in horses used for breeding purposes, during pregnancy, or in lactating mares has not been evaluated. For customer care, or to obtain product information, visit To report an adverse event please contact American Regent, Inc. at 1-888-354-4857 or email Please see Full Prescribing Information at 1 Data on file. 2 Adequan® i.m. Package Insert, Rev 1/19. 3 Burba DJ, Collier MA, DeBault LE, Hanson-Painton O, Thompson HC, Holder CL: In vivo kinetic study on uptake and distribution of intramuscular tritium-labeled polysulfated glycosaminoglycan in equine body fluid compartments and articular cartilage in an osteochondral defect model. J Equine Vet Sci 1993; 13: 696-703. 4 Kim DY, Taylor HW, Moore RM, Paulsen DB, Cho DY. Articular chondrocyte apoptosis in equine osteoarthritis. The Veterinary Journal 2003; 166: 52-57. 5 McIlwraith CW, Frisbie DD, Kawcak CE, van Weeren PR. Joint Disease in the Horse.St. Louis, MO: Elsevier, 2016; 33-48. All trademarks are the property of American Regent, Inc. © 2021, American Regent, Inc. PP-AI-US-0629 05/2021