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Gastric Ulceration - Horse

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Also known as: Gastroduodenal ulceration

Gastrointestinal ulceration
 Equine Gastric Ulcer Syndrome
 Peptic ulcer disease
 Equine Gastric Ulcer

See also: Gastric Ulceration - all species


Description

The term 'Equine gastric ulcer syndrome (EGUS)' encompasses a number of disease complexes[1] associated with ulceration of the oesophageal, gastric or duodenal mucosa[2] in horses. When such damage is caused by acidic gastric juice, the defect is described as a 'peptic ulcer'.[2] Ulceration of either or both[3] regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance[4] and compromise welfare.[5] The non-glandular (proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion. The two regions meet abruptly at the margo plicatus[6], adjacent to where most ulcers occur.[2] Damage to these regions occurs via differing pathophysiological routes and varies in severity from inflammation, to cellular death and sloughing causing disruption of the superficial mucosa (erosion), penetration of the submucosa down to the level of the lamina propria[2](ulceration), full thickness ulceration (perforation)[6] and potentially duodenal stricture.[7] The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.[2]

Prevalence

The prevalence of equine gastric ulceration has increased over the last century.[8] In a retrospective study of 3715 Swedish horses, ulcers were most often found in the squamous mucosa along the margo plicatus, then the glandular body, proximal squamous mucosa and antrum.[8] For the squamous region, reported prevalences are:

  • Racehorses 66-93%[9][10][11]
  • Racehorses in active race training 80-93% (incidence 100%)[12][13]
  • Show horses 58%[14]
  • Ponies 78%[15]
  • Endurance horses 67%[16]
  • Western performance horses 40%[17]
  • Thoroughbred broodmares (67-77%)[18]
  • Nonracing performance horses (17% pre-competition, 56% post-competition)[19]
  • Pleasure horses in full work ~ 60%[4]
  • Pleasure, riding lessons, showing 37%[20]
  • Foals ~25-57%[21][22][23], the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.[2]

The prevalence and severity of ulcers increases with work intensity[7] and duration[24][25], thus racehorses in active training are more often affected[9] and in half of these, the lesions are moderate to severe.[7] In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.[12] Lesions are thought to be chronically progressive during race training, but to regress during retirement.[9] Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.[2]EGUS prevalence is high in horses with bowel, liver and oesophageal lesions.[8] Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers[26] Around 30% of adult horses and about 50% of foals have mild gastric erosions which heal without treatment or clinical signs.[7] In 201 clinically normal horses in Denmark, 53% had EGUS with severity score >2 and older horses were more likely to have lesions in both regions of the stomach[27]

Signalment

EGUS develops in horses of all ages[6] but is most common in young horses in training and foals. Gastric ulceration is considered to be rare in horses at pasture.[28]

Pathophysiology

Risk Factors

Exercise

There appears to be a high prevalence of gastric ulcers in horses performing in most disciplines including racing, endurance, show jumping, dressage and western performance.[29] Although this may be related to exercise, other confounding factors associated with these disciplines such as travel, diet, feeding regime, NSAIDs and stress may be significant. However, Vatistas and co-workers (1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise.[12] There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.[30] Furthermore, the higher prevalence of gastric ulcers at post mortem in racehorses in training compared to those in retirement adds weight to the hypothesis that exercise is an important risk factor for EGUS.[9] Strenuous exercise is known to stimulate gastrin release which has effects on HCl secretion, gastric emptying and gastric blood flow. It is also thought that exposure of the squamous mucosa to acid is increased as the stomach is compressed by the abdominal viscera and diaphragm during excercise.[31]

Housing and Transport

Housing in stables has been proposed as a risk factor for gastric ulcers, with more lesions being found in confined horses compared to those out at grass.[32] However, when comparing solitary stable confinement with stabling next to a companion, and finally turn out in a paddock, Husted and colleagues (2008) found that the environmental situation had no effect on mucosal acid exposure in the equine stomach.[33] Transport has also been shown to induce squamous mucosal ulceration in horses.[34]

Diet

Feed deprivation encourages gastric ulceration in two ways: (1) it precludes the buffering capacity of protein leading to a reduced gastric pH[35] and (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice.[8] It is unsurprising, therefore, that an alternating feed-fast protocol would produce a consistent model of ulcer induction in the equine squamous mucosa.[36][37] Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse.[38] Diets that are plentiful in roughage prolong the mastication process and the production of salivary bicarbonate that protects the gastric mucosa. A diet of high grain and low roughage thus predisposes to EGUS.[39] This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses.[40] Ponies fed a concentrate diet had a greater prevalence of gastric ulcers than ponies fed hay alone.[12] and this may be because grain and pelleted feeds are asssociated with increased serum gastrin.[41] High starch meals are also a risk because they are fermented to volatile fatty acids (VFAs) and lactic acid and are emptied from the stomach relatively slowly.[42][43][44]

Other ailments

Conditions that produce abdominal pain and/or inappetance are likely to reduce food intake and predipose to gastric ulcers.[8] This may be the reason that colic and other gastrointestinal disorders have been associated with EGUS.[45] Alternatively, EGUS may be part of a more general gastrointestinal disease complex.[12] Stress induced by other clinical disorders has been reported to increase the prevalence of EGUS in neonatal foals[46] and a similar mechanism may exist for adult animals.[12]

NSAIDs

As in other species, nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to cause gastric ulcers in horses. Typicaly this is associated with high doses or frequent administration of phenylbutazone or flunixin meglumine. However, although there is evidence to the contrary,[47]therapeutic doses of NSAIDs may be sufficient to induce EGUS. Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally[48]and that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.[49] The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa[50][51][52], they may look different endoscopically from ulcers that occur naturally,[53] and they appear to heal spontaneously.[54][55] Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.[56][57][38]

Temperament

A nervous disposition has been linked with gastric ulcers[58]but the same association was not seen in another study.[59] The physiological and psychological stresses of training, housing, boredom, travel, mixing, hospitalisation and entering new environments[12] may increase the risk of developing EGUS. In foals hypoxia may also be a risk factor.

Clinical syndrome

The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.[60] In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.[20] The significance of gastric ulceration in horses thus remains questionable. However, there have been instances where ulcer treatment has preceded an improvement in clinical status and/or racing perfomance, suggesting that in some horses, ulcers are a considerable burden.[60] Cases gastric ulceration are often asymptomatic, but signs that have been attributed to these lesions in mature horses include:

  • Poor appetite (particularly decreased consumption of concentrates)[6]
  • Poor condition
  • Rough hair coat
  • Weight loss
  • Excessive recumbency[2]
  • Mild to severe colic
    • Mild, recurrent colic signs post-prandially[61]
    • In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.[62]
  • Changes in attitude (dullness or depression)[60]
  • Poor racing performance and reluctance to train
    • Performance improved in 4 Thoroughbred racehorses after antiulcer treatment[63]
    • Gastric ulcers have adversely affected physiological indices of performance in horses.[64]


Clinical signs in foals vary depending on age and severity:

  • Neonatal foals: many ulcers are silent, some foals only exhibit signs when ulceration has become severe. Glandular ulcers are considered the most significant[6]
    • Poor appetite
    • Diarrhoea
    • Intermittent colic
    • Frequent dorsal recumbency
  • Sucklings and weanlings:[6]
    • Diarrhoea
    • Poor appetite (off suck or partially off suck)
    • Poor growth, failure to thrive
    • Poor body condition
    • Rough hair coat
    • Potbelly appearance
    • Bruxism (almost pathognomonic)
    • Colic after feeding or tubing
    • Chewing straw
    • Dorsal recumbency
  • Signs of gastroduodenal ulcer disease (GDUD):[6]
    • Bruxism
    • Colic
    • Gastrooesophageal reflux after suckling
    • Ptyalism (secondary to gastric outflow obstruction and gastroesophageal reflux)[7]
    • Diarrhoea

In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.[6] GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and Candida infection.[7]

Diagnosis

A presumptive diagnosis can be based on clinical signs and response to therapy,[6] however, a definitive diagnosis requires visualisation of the stomach. This can be achieved in the live horse using endsocopy or, alternatively, at post-mortem.(Nadeau 2009)

EGUS was recently discussed at the 2010 Annual meeting between the Equine Insurers Forum (EIF) and the British Equine Veterinary Association (BEVA). The EIF maintained that in order to support claims for the long term costs associated with treatment of EGUS, there would be a requirement for veterinary surgeons to make a definitive diagnosis prior to prescribing omeprazole.(BEVA)

Endoscopy

(cannot do in foals as need to starve prior to exam)

ante mortem using a 2.5–3.0 m endoscope and utilising an established scoring system (Nadeau 2009)

Endoscopic equipment can be grouped into 2 categories: fibreoptic and video. Flexible endoscopes: for mature equine gastric endoscopy, a minimum working length of 200 cm is required. However, a 280-300 cm long endoscope is required to perform duodenoscopy in mature individuals. A working length of 110 cm with an outer diameter of 10 mm (human gastroscope) is sufficient to reach the stomach of foals up to age 30-40 days. Fibreoptic endoscopic equipment uses glass-fibre bundles to transmit light to the area to be viewed and transmit this image to an eyepiece. The image is magnified by a lens system within the eyepiece. This is important in alimentary endoscopy, since 150 W lamps used in most portable light sources provide poor illumination of a horse’s stomach. More powerful light sources are available (up to 300 W) but become larger and less portable as the lamp intensity increases. The quality of the fibreoptic instrument is determined largely by its image resolution, which is related directly to the number of optical fibres. Videoendoscopic systems use glass-fibre bundles to transmit light, but use a charge-coupled device (CCD) chip to transmit the image. Generation of the light source (300 W) and processing of the CCD-generated electronic signal occurs in the endoscope’s processor.


A diagnosis can be made only by endoscopy (oesophagogastroscopy). Oesophagogastroscopy may be performed at the facility where the horse is normally housed. The horse must be held off feed for 6-8 h before oesophagogastroscopy to allow time for the stomach to empty and permit visualisation of the mucosa. The procedure is usually performed approximately 5 min after i.v. sedation with xylazine (Rompun), 0.6-0.8 mgkg bwt. (Orsini)

Minimum endoscope length of two metres and 2.8-3.0 metre instruments are required for duodenoscopy A 3 mtre endoscope allows visualization of stomach, pyrlorus and proximal duodenum (Sanchez) Shorter scopes permit investigation fo gastric body and fundus only (Sanchez) Maximum external diameter of 9mm for neonates (Sanchez) Foals - lesions mainly in glandular epithelium Adults - margo plicatus and squamous epithelium

Performed under mild sedation in standing horse or foal (Sanchez) Duodenoscopy is most specific diagnostic method but is technically me chanllenegng than gastrocopy EGUS Lesion Scoring System publsihed based on consens by Equine Gastric Ulcer Council(2 in Sanchez) The EGUS Council has adopted a lesion grading system that: 

Is simple and straightforward
Can be applied to the squamous and glandular mucosal linings of the equine stomach

Note that no mention of bleeding is made in assigning lesion grades, because bleeding does not determine lesion severity. Small superficial erosions (Fig 3) may bleed, whereas deep ulcers may not have active haemorrhage at the time of endoscopic examination.(EGUC)


Lesion Grade Description
Grade 0 Intact epithelium with no appearance of hyperaemia (reddening) or hyperkeratosis (yellowing of the squamous mucosa)
Grade 1 Intact mucosa with areas of reddening or hyperkeratosis (squamous)
Grade 2 Small single of multifocal lesions
Grade 3 Large single or multifocal lesions or extensive superficial lesions
Grade 4 Extensive lesions with areas of deep ulceration

While these systems are useful for assessing the extent of disease and monitoring response to treatment, little work has been done to correlate gross observations with the histological picture. Lesions that appear alike grossly and receive similar numerical scores may have dissimilar histological appearances and underlying pathogeneses.(Martineau 2009) The endoscopist may underestimate the n u m b e r of gastric ulcers and may not be able accurately to p redict the severity or depth of those ulcers present in the n o n g l a n d u l a r equine stomach. Furt h e r m o re, the endoscopist may miss glandular gastric ulcers. (Andrews 2002

Diffuse reddeing or inflammation may be only lesion seen in cases of early duodenal disease In older foals with GDUD, detection ofgastrci outflow obsturction is critical to therapeutic plan and appropriate prognosis (Sanchez)

Radiography

In foals, abdominal radiography can be used to highlight gastric outflow obstruction. Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction. Without contrast medium, a large, gas filled stomach will be obvious.[6]

Biopsy

A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.[65]Unfortunately this technique failed to produce samples of squamous mucosa that would be suitable for histopathological analysis.

Laboratory tests

The detection of occult blood in faeces has proven unreliable in the horse and currently, useful laboratory markers for EGUS are lacking.[2] Tests that require further analysis for sensitivity and specificity[6] include:

  • Urine[66] and blood[67] sucrose absorption as an assay of gastric mucosal permeability
  • Serum alpha1-antitrypsin which has been detected more frequently in foals with gastric ulceration[68]


In a recent study, a faecal occult blood test was found to be helpful in diagnosis of EGUS (Pellegrini 2005). The positive predictive value of the faecal occult blood test (FOBT) in horses with EGUS was 90%; however, the negative predictive value was only 17%, which suggests that a horse with a positive FOBT islikely to have a gastric ulcer. In an attempt to improve the negative predictive value of the FOBT, investigators developed another test (SUCCEED Equine Fecal Blood Test)2 that utilises specific equine monoclonal antibodies to both albumin and haemoglobin in an easy to use kit (Carter and Pellegrini 2006; Pellegrini and Carter 2007). Recent reports showed an improved predictive value of a negative test (72%), but the predictive value of a positive test was slightly lower (77%). Thus, this new test may be helpful in diagnosing EGUS in horses, but should be used as part of a complete work-up. A false positive FOBT may result if a recent rectal examination, rectal biopsy or other rectal trauma has occurred or if the horse has a protein-losing enteropathy. Furthermore, serum 1-antitrypsin was present in 44/47 foals with gastric ulcers compared to only 3/22 healthy foals (Taharaguchi et al. 2007). 1-antitrypsin may be released into serum from damaged gastric tissue, but more research is needed to validate this serum marker as a diagnostic test for EGUS.(Nadeau 2009)

Other diagnostic methods include measuring urine and plasma sucrose concentration (sucrose permeability tests) (O’Conner et al. 2004; Hewetson et al. 2006). However, methods for measuring sucrose require sophisticated analysis equipment, which may not be practical for clinicians in the field. (Nadeau 2009)

Pathology

Treatment

Proton pump inhibitors: only omeprazole (Gastroguard) is licensed for horses. Given PO once daily (4mg/kg) for 3-4 wks, most effective drug at controlling HCl secretion (decreases basal and stimulated release). Expensive and not absorbed in foas with diarrhoea Histamine H2 receptor antagonists:

  • ranitidine 7mg/kg TID for 3-4wks
  • cimetidine 25mg/kg QID for 3-4wks (cheaper but less effective so must be given more frequently)

Gastric protectants: sucralfate 10-20mg/kg TID for 2-4wks Antacids: magnesium and aluminium hydroxides (NOT recommended as have massive rebound effect)

Foals: Omeprazole 4mg/kg PO SID (preferred) Ranitidine (Zantac, Zeneca, UK) 6mg/kg TID PO, 1-2mg/kg IV BID (second choice) Sucralfate (Antepsin, Wyeth Labs, Maidenhead, UK)(intestinal mucosal protective), 2-4g total dose or 50kg per foal QID PO (in theory best effect of this compound is in acid medium so should not be given at the same time or after H2 blockers btu latest research shows it appears to work just as well if given at the same time and this reduces stress of handling), NB nto a good prophylactic Antacids not good - rebound effect Metocloprmade, gastrci decompression (foals with severe gastor0duodenal stenosis), analgesia (butorphenol or pethidine or morphine NOT NSAIDs) Supportive nursing by reducing stressors, milk and saliva have preventative effects so good feeding habits should be encouraged Corn oil (50ml q6h) reportedly anti-ulcerogenic (increases PG production) PG analogues (Misoprostenol) 5microgram/kg PO q8h

Prognosis

Complications:

  • Recurrence if management not altered
  • Perforation and peritonitis (rare - foals)
  • Pyloric stenosis (rare - foals)

Complications related to gastric ulcers are most frequent and severe in foals and include perforation, delayed gastric emptying, gastroesophageal reflux and oesophagitis, and megaoesophagus secondary to chronic gastroesophageal reflux. Sudden gastric perforation without prior signs occurs sporadically in foals.[7]Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. The latter complication is seen in both foals and adult horses. In rare cases, severe gastric ulceration causes fibrosis and contracture of the stomach.[7]

Prevention

Gastroguard at lower dose (1-2mg/kg) daily for 3-4wks (100, 107-109 in Sanchez) Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation (Sanchez). It may be beneficial in foals receiving substantial doses of NSAIDs for orthopaedic pain (Sanchez) Management: diet, training, exercise, stress (company, toys) Pasture turnout and continuous access to high quality forage especially alfalfa (Sanchez) Furthermore, recent information suggests that feeding a diet that contains 0.5 kg of grain per 100 kg bwt no more frequently than 6 h apart can reduce the risk of EGUS (Andrews et al. 2006). It has been suggested that a high-grain, low-hay diet would increase the incidence of ulcers (Hammond et al. 1986). In another study, alfalfa hay was shown to protect horses against EGUS, by increasing stomach pH. Gastric juice pH and ulcer scores were lower in horses fed a diet containing alfalfa hay compared to the same horses fed dietary brome or costal Bermuda hay (Nadeau et al. 2000; Lybbert et al. 2007). The authors concluded that alfalfa hay may be useful in addition to antiulcer treatment for prevention and treatment of squamous gastric ulcers.(Nadeau 2009)

References

  1. ↑ Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric ulcer syndrome. Equine Vet J, 41(7):616.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 11(5):262-272.
  3. ↑ Andrews, F.M, Bernard, W.V, Byars, T.D et al. (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 1:122-134. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  4. ↑ 4.0 4.1 Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. N Z Vet J, 55(1):1-12).
  5. ↑ Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.
  6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial
  8. ↑ 8.0 8.1 8.2 8.3 8.4 Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
  9. ↑ 9.0 9.1 9.2 9.3 Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. Equine Vet J, 18(4):284-287.
  10. ↑ Vatistas, N.J, Snyder, J.R, Carlson, G, et al (1994) Epidemiological study of gastric ulceration in the thoroughbred racehorse:202 horses 1992-1993. Proc Am Assoc Equine Pract, 40:125-126
  11. ↑ Murray, M.J, Schusser, G.F, Pipers, F.S, Gross, S.J (1996) Factors associated with gastric lesions in thoroughbred racehorses. Equine Vet J, 28:368-374.
  12. ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  13. ↑ Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthruy, R.M, Thurmond, M, Zhou, H, Lloyd, K.L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J, Suppl 29:34-39.
  14. ↑ McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Assoc, 215:1130-1133.
  15. ↑ MacAllister, C.G, Sangiah, S, Mauromoustakos, A (1992) Effect of a histamine H, type receptor antagonist (WY 45, 727) on the healing of gastric ulcers in ponies. J Vet Int Med, 6:271-275.
  16. ↑ Nieto, J.E, Snyder, J.R, Beldomenico, P et al. (2004) Prevalence of gastric ulcers in endurance horses: a preliminary report. Vet J, 167:33-37.
  17. ↑ Bertone, J (2000) Prevalence of gastric ulcers in elite, heavy use western performance horses. Proc Am Assoc Equine Pract, 46:256-259.
  18. ↑ LeJeune, S.S, Nieto, J.E, Dechant, J.E, Snyder, J.R (2009) Prevalence of gastric ulcers in Thoroughbred broodmares in pasture: a preliminary report. Vet J, 181(3):251-5.
  19. ↑ Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In:Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  20. ↑ 20.0 20.1 Murray, M.J, Grodinsky, C, Anderson, C.W, Radue, P.F, Schmidt, G.R (1989) Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. Equine Vet J Suppl, 7:68-72.
  21. ↑ Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. Proc Equine Colic Res Symp 2nd:126-128.
  22. ↑ Murray, M.J, Grodinsky, C, Cowles, R.R, et al.(1990) Endoscopic evaluation of changes in gastric lesions of Thoroughbred foals. J Am Vet Med Assoc, 196:1623-1627.
  23. ↑ Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc, 195:1135-1141.
  24. ↑ Orsini, J.A, Pipers, F.S (1997) Endoscopic evaluation of the relationship between training, racing, and gastric ulcers. Vet Surg, 26:424. In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
  25. ↑ Murray, M.J (1994) Gastric ulcers in adult horses. Comp Cont Educ Pract Vet, 16:792-794. In:Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
  26. ↑ Murray, M. (1992) Gastric ulceration in horses: 91 cases (1987-1990). J Am Vet Med Assoc, 201:117-120. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.
  27. ↑ Luthersson, N, Nielsen, K.H, Harris, P, Parkin, T.D (2009) The prevalence and anatomical distribution of equine gastric ulcer syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):619-24.
  28. ↑ Murray, M.J (1994) Characteristics of gastric ulcer pathophysiology. Proc Am Coll Vet Intern Med, 12:610-612. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
  29. ↑ Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  30. ↑ White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. J Am Vet Med Assoc, 230(11):1680-2.
  31. ↑ Lorenzo-Figueras, M, 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, 63:1481-1487.
  32. ↑ Murray, M.J, Eichorn, E.S (1996) Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Am J Vet Res, 57:1599-1603.
  33. ↑ Husted, L, Sanchex, L.C, Olsen, S.N, Baptiste, K.E, Merritt, A.M (2008) Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach. Equine Vet J, 40(4):337-41.
  34. ↑ McClure, S.R, Carithers, D.S, Gross, S.J, Murray, M.J (2005) Gastric ulcer development in horses in a simulated show or training environment. J Am Vet Med Assoc, 227:775-777.
  35. ↑ Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
  36. ↑ Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  37. ↑ Murray, M.J (1994) Equine model of inducing ulceration in alimentary squamous epithelial mucosa. Dig Dis Sci, 39:2530-2535. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  38. ↑ 38.0 38.1 Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred. PhD Thesis. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  39. ↑ In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  40. ↑ Luthersson, N, Nielson, K.H, Harris, P, Parkin, T.D (2009) Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):625-30.
  41. ↑ Smyth, G.B, Young, D.W, Hammond, L.S (1988) Effects of diet and feeding on post-prandial serum gastrin and insulin concentrations in adult horses. Equine Vet J Suppl 7:56-59.
  42. ↑ Mètayer, N, Lhôte, M, Bahr, A, Cohen, N.D, Kim, I, Rousell, A.J, Julliand, V (2004) Meal size and starch content affect gastric emptying in horses. Equine Vet J, 36:434-440. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  43. ↑ Taharaguchi, S, Okai, K, Orita, Y, Kuwano, M, Ueno, T, Taniyama, H (2004) Relation between amounts of concentrated feed given mares and gastric ulcers in foals. J Japan Vet Med Ass, 57:366-370. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  44. ↑ Boswinkel, A.M, Ellis, A.D, Sloet van Oldruitenborgh-Oosterbaan, M.M (2007) The influence of low versus high fibre haylage diets in combination with training or pasture rest on equine gastric ulceration syndrome (EGUS). Pferdeheilkunde, 23:123-130. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  45. ↑ Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Vet J Suppl, 7:77-79.
  46. ↑ Furr, M.O, Murray, M.J, Ferguson, D.C (1992) The effects of stress on gastric ulceration, T3, T4, reverse T3 and cortisol in neonatal foals. Equine Vet J, 24:37-40.
  47. ↑ Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. Vet Ther, 10(3):113-20.
  48. ↑ Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses. Res Vet Sci, 76:145-149. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  49. ↑ Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses. Am J Vet Res, 67:398-402. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  50. ↑ MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses. J Am Vet Med Ass, 202:71-77. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
  51. ↑ Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Vet J Suppl, 7:77-79. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  52. ↑ Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion. Cenfaur Mylapore, 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  53. ↑ Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
  54. ↑ Jones, W.E (1983) Gastrointestinal ulcers [foal]. Equine Vet Data, 4:305-308. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  55. ↑ MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies. Am J Vet Res, 54:1103-1107. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  56. ↑ Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses. Proc Am Ass Equine Pract, 39:125-126. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  57. ↑ Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses. Equine Vet J, 28:368-374. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
  58. ↑ McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Ass 215:1130-1133. In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
  59. ↑ Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J Suppl, 29:34-39. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
  60. ↑ 60.0 60.1 60.2 Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
  61. ↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract, 25(2):283-301.
  62. ↑ Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain. Equine Vet J, 38:347-349.
  63. ↑ Franklin, S.H, Brazil, T.J, Allen, K.J (2008) Poor performance associated with equine gastric ulceration syndrome in four Thoroughbred racehorses. Equine Vet Educ, 20:119-124. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
  64. ↑ Nieto, J.E, Snyder, J.R, Vatistas, N.J, Jones, J.H (2009) Effect of gastric ulceration on physiologic responses to exercise in horses. Am J Vet Res, 70(6):787-95.
  65. ↑ Rodrigues, N.L, Dore, M, Doucet, M.Y (2009) Validation of a transendoscopic glandular and nonglandular gastric biopsy technique in horses. Equine Vet J, 41(7):631-5.
  66. ↑ O'Connor, M.S, Steiner, J.M, Roussel, A.J, et al. (2004) Evaluation of urine sucrose concentration for detection of gastric ucleration in horses. Am J Vet Res, 65:31-39. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  67. ↑ Hewetson, M, Cohen, N.D, Love, S, et al. (2006) Sucrose concentration in bood: a new method for assessment of gastric permeability in horses with gastric ulceration. J Vet Intern Med, 20:388-394. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
  68. ↑ Taharaguchi, S, Nagano, A, Okai, K, et al. (2007) Detection of an isoform of alpha(1)-antitrypsin in serum samples from foals with gastric ulcers. Vet Rec, 161:338-342. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.


Gastric Ulceration - all species

  • Affects the pars oesophagea (margo plicatus) in adults and foals.
  • Due to parasites - Gasterophilus (Bots).
  • Bots are not as common as they once were.
  • Look like big pink maggots.
  • Killed by Ivermectin.
  • Gasterophilus leave large ulcers in glandular regions of the stomach.
    • Ulcers / erosions are quite deep.
  • The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth.
  • Carcinoma can also produce ulceration in the stomach of the horse as, in other species.
  • In foals, the glandular area may sometimes be affected.
    • This may be e.g. stress-related, or due to used of NSAIDs.
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