Difference between revisions of "Gastric Ulceration - Horse"

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NOT associated with ''Helicobacter pylori'' and not typically associated with ''Gasterophilus''
 
NOT associated with ''Helicobacter pylori'' and not typically associated with ''Gasterophilus''
 
==Risk Factors==
 
==Risk Factors==
 +
Exercise
 +
The mechanism for this is that compression of the stomach by abdominal viscera and diaphragm leads to delivery of acid contents into the proximal region of the stomach (Lorenzo-Figueras and Merritt 2002). This mechanism is thought to deliver the acid to the nonglandular mucosa resulting in acid exposure and injury.Other risk factors have surfaced in a variety of recent studies. In one study of horses in Australia, horses trained in urban areas are 3.9x more likely to have gastric ulcers. Also, time in work, crib-biting, difficulty maintaining bodyweight and playing the radio in the barn were identified as other risk factors (Lester et al. 2007). On the other hand, protective factors included training on the property and turnout with other horses. Also, in another study in Standardbred mares, 7/8 horses (Gordon et al. 2006) had gastric ulcers after 8 weeks of training, compared to 0/7 horses housed similarly and not trained.
 +
Although racehorses have a high prevalence of EGUS, 56.5% of horses in endurance competition, show jumping, dressage or western performance and travel, had gastric ulcers (Hartmann and Frankeny 2003) after competition. Thus, even nonrace training and performance horses are at risk of developing EGUS and should be monitored for clinical signs(Nadeau 2009)
 +
J Am Vet Med Assoc. 2007 Jun 1;230(11):1680-2.
 +
Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.
 +
White G, McClure SR, Sifferman R, Holste JE, Fleishman C, Murray MJ, Cramer LG.
 +
OBJECTIVE: To determine the effects of 8 days of light to heavy exercise on gastric ulcer development in horses and determine the efficacy of omeprazole paste in preventing gastric ulceration.). CONCLUSIONS AND CLINICAL RELEVANCE: Results showed that horses in light to heavy training for as short as 8 days were at risk of developing gastric ulcers and that administration of omeprazole paste decreased the incidence of gastric ulcers.
 +
Conclusions: The study confirmed a high prevalence of ulcers in the gastric squamous mucosa of Standardbreds in race training. Of the studied parameters only status of training showed a significant association with gastric ulcers of the squamous mucosa.
  
 +
Housing
 +
Equine Vet J. 2008 Jun;40(4):337-41.
 +
Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach.
 +
Husted L, Sanchez LC, Olsen SN, Baptiste KE, Merritt AM.
 +
REASONS FOR PERFORMING STUDY: Stall housing has been suggested as a risk factor for ulcer development in the equine stomach; however, the exact pathogenesis for this has not been established. OBJECTIVES: To investigate the effect of 3 environmental situations (grass paddock, stall alone or stall with adjacent companion) on pH in the proximal and the ventral stomach. CONCLUSIONS: The change in housing status used in the current study did not affect acid exposure within either region of the equine stomach. The pH in the ventral stomach was uniformly stable throughout the study, while the proximal pH demonstrated a 24 h circadian pattern.
 +
 +
 +
Diet
 +
A high grain low roughage diet is a risk factor in EGUS. High roughage diets provide hours of chewing and the production of salivary bicarbonate that bathes the stomach and protects against gastric ulcers. Metayer et al. (2004), found that small low starch meals empty from the stomach significantly faster than large high starch meals. Since high starch diets are fermented to VFAs and lactic acid, large high starch meals should be avoided in horses prone to gastric ulceration (Taharaguchi et al. 2004; Boswinkel et al. 2007). 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).
 +
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)
 +
In an investigated standardbred population in the Netherlands the amount of concentrate fed is not an important predisposing factor.(Prevalence)
 +
Equine Vet J. 2009 Sep;41(7):625-30.
 +
Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark.
 +
Luthersson N, Nielsen KH, Harris P, Parkin TD.
 +
OBJECTIVES: To investigate the prevalence of EGUS in a population of Danish horses, during winter when the horses had been housed and fed for at least 8 weeks and to analyse the influence of feed, work level and environment on the risk of EGUS of > or = grade 2 in severity. CONCLUSION AND POTENTIAL RELEVANCE: This study has confirmed that components of the diet, readily modifiable, may have an important impact on the risk of EGUS in the nonracehorse. Differences in the multivariable models produced for all ulcers and nonglandular ulcers support differences in the aetiology of ulcers in different locations of the stomach.
 +
Significant factors for the development of gastric ulceration included the feeding of concentrates and faster exercise (Vatistas 1998). In addition, withholding feed before exercise was a modifying factor that, although not causing gastric ulceration, may have decreased time of onset.(Vatistas 2 1999) Murray determined that alternately withholding feed for 24 h followed by feeding for 24 h induced ulceration of the squamous mucosa that appeared endoscopically similar to naturally occurring ulcers (Murray 1994). However, such a severe form of feed deprivation does not occur in horses in training, in which horses may be fasted for 4 h before training exercise, although the period of feed withdrawal may be longer prior to a race. The results of our study tend to support the concept from other studies that feed deprivation is not necessary for the development of gastric ulceration (Vatistas 1998). The stabling of horses from pasture has been documented to increase the severity of gastric ulceration (Murray and Eichorn, 1996). All horses in the present study were stabled and this may have had some influence on the development of gastric ulceration. Evidence for the role grain is predominantly anecdotal, but there has been one study that demonstrated an increased prevalence of gastric ulceration in ponies fed a concentrate diet compared to ponies fed hay alone The results of our study suggest that, rather than training itself, the most stressful event may have been when horses entered their new environment..(Vatistas 2 1999)
 +
It seems reasonable to suggest that any condition
 +
that influences food intake might contribute to the development
 +
of gastric ulcers in horses.(Sandin 2000
 +
 +
Other ailments
 +
Considering the intestinal lesions, gastric ulceration was found in 42% of horses with large bowel lesions and in 31% with small bowel lesions. The association between intestinal lesions and ulcers within the stomach might suggest that gastric ulcers are often part of a larger gastrointestinal disease complex. In man, it is usual to find that disturbed activity in the autonomic nervous system affects both intestine and stomach (Fielding 1977). Murray (1989) reported an association between glandular ulcers and clinical disorders in foals and a similar relationship could also be true for mature horses. It has also been established that colic is associated with gastric ulcers in horses (Murray 1989, 1992; Furr and Murray 1989). In our study, colic disturbances were significantly (P<0.001) associated with gastric ulcers in bivariate analysis. This finding further suggests a relationship between gastric ulcers and clinical signs of colic.  Whether gastric ulceration was the cause or the consequence of colic in our study has not been established. A variety of conditions involving abdominal pain (Murray
 +
1992) have also been associated with gastric ulceration in horses. Abdominal pain or inappetance for any reason probably reduces appetite and, consequently, diminishes feed intake. Feed deprivation generally results in increased stomach acidity (Murray and Schusser 1993), since the absence of protein reduces buffering capacity. Moreover, gastric juice is more readily transported in an empty stomach and, as a consequence, flushed over the vulnerable squamous mucosa resulting in gastric ulceration. Therefore, any condition that considerably influences food intake might, hypothetically, contribute to the development of gastric ulcers in horses.(Sandin 2000)
 +
 +
 +
 +
NSAIDs
 +
Nonsteroidal anti-inflammatory drugs (NSAIDs: phenylbutazone, flunixin meglumine) have been shown to cause gastric ulcers in horses. This is usually related to the use of a high dose or frequent administration of NSAIDs; however, therapeutic doses have been known to cause ulcers in horses. Recently, a study was conducted comparing the ulcerogenic effects of an orally administered prophenylbutazone drug, suxibuzone, to phenylbutazone (Monreal et al. 2004). Horses treated with phenylbutazone had more ulcerated areas and deeper ulcers than those in the suxibuzone treated or placebo groups. The authors concluded that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally at equimolar doses in horses. However, a more recent study in horses given suxibuzone or phenylbutazone at therapeutic doses for 14 days showed no significant difference in gastric ulcer scores when compared to each other and control horses receiving no treatment (Andrews et al. 2009). Thus, therapeutic doses of these NSAIDs did not lead to gastric ulcers more than what was observed in the untreated control group.
 +
Another study evaluated the use of a combination of NSAIDs and gastric ulcers in horses. Phenylbutazone (2.2 mg/kg bwt per os, q. 12 h, for 5 days) or phenylbutazone (same dose) and flunixin meglumine (1.1 mg/kg bwt, i.v., q. 12 h, for 5 days) were administered to adult horses (Reed et al. 2006). In this study, total plasma protein and albumin decreased in NSAID treated horses and nonglandular gastric ulcer scores were significantly higher in horses treated with the 2 NSAID drugs. Thus, NSAIDs and a combination NSAID treatment should be approached with caution in horses.
 +
Recently, firocoxib1, a new cox-2 inhibitor NSAID was approved for treatment of lameness in horses. Gastric ulcers were not detected in horses administered firocoxib (0.1 mg/kg bwt, per os, q. 24 h, 30 days) (Anon 2005). However, firocoxib is FDA approved for the control of pain and inflammation associated with osteoarthritis in horse, thus its efficacy in horses with abdominal pain is unknown. Furthermore, currently there is no i.v. formulation of this product, so it cannot be administered orally in horses with abdominal pain and gastric reflux or dysphagia. (Nadeau 2009)
 +
Vet Ther. 2009 Fall;10(3):113-20.
 +
Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses.
 +
Andrews FM, Reinemeyer CR, Longhofer SL.
 +
These findings suggest that when administered at the recommended label dose for 15 days, neither PBZ nor SBZ causes an increase in the number or severity of gastric ulcers over what would be expected with traditional stabling and intermittent feeding patterns. Also, PBZ-treated horses did not have more severe gastric ulcers than SBZ-treated horses, indicating that SBZ does not appear to offer an advantage over PBZ in preventing gastric ulcers when used at recommended label doses. However, ulcers in other regions of the gastrointestinal tract (e.g., right dorsal colon, duodenum) were not evaluated in horses in this study.
  
  

Revision as of 12:45, 27 July 2010


 This article is still under construction.


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)' is used to describe the disease complex associated with ulceration of the oesophageal, gastric or duodenal mucosa[1] in horses. When such damage is caused by acidic gastric juice, the defect is described as a 'peptic ulcer'.[1] Ulceration of either or both[2] regions of the gastric mucosa is one of the most important conditions of the equine stomach as it may limit performance[3] and compromise welfare.[4] 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[5], adjacent to where most ulcers occur.[1] 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[1](ulceration), full thickness ulceration (perforation)[5] and potentially duodenal stricture.[6] The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.[1]

Prevalence

The prevalence of equine gastric ulceration has increased over the last century.[7] 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.[7] For the squamous region, reported prevalences are:

  • Racehorses 70-100%[8][9][10]
  • Racehorses in active race training 80-90% (incidence 100%)[11][12]
  • Show horses 58%[13]
  • Ponies 78%[14]
  • Endurance 67%[15]
  • Western performance horses 40%[16]
  • Thoroughbred broodmares (67-77%)[17]
  • Nonracing performance horses (17% pre-competition, 56% post-competition)[18]
  • Pleasure horses in full work ~ 60%[3]
  • Pleasure, riding lessons, showing 37%[19]
  • Foals ~25-57%[20][21][22], the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.[1]

The prevalence and severity of ulcers increases with work intensity[6] and duration[23][24], thus racehorses in active training are more often affected[8] and in half of these, the lesions are moderate to severe.[6] In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.[11] Lesions are thought to be chronically progressive during race training, but to regress during retirement.[8] Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.[1]EGUS prevalence is high in horses with bowel, liver and oesophageal lesions.[7] Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers[25] Around 30% of adult horses and about 50% of foals have mild gastric erosions which heal without treatment or clinical signs.[6] 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[26]

Signalment

EGUS develops in horses of all ages[5] but is most common in young horses in training and foals. Gastric ulceration is considered to be rare in horses at pasture.[27]

Pathophysiology

NOT associated with Helicobacter pylori and not typically associated with Gasterophilus

Risk Factors

Exercise The mechanism for this is that compression of the stomach by abdominal viscera and diaphragm leads to delivery of acid contents into the proximal region of the stomach (Lorenzo-Figueras and Merritt 2002). This mechanism is thought to deliver the acid to the nonglandular mucosa resulting in acid exposure and injury.Other risk factors have surfaced in a variety of recent studies. In one study of horses in Australia, horses trained in urban areas are 3.9x more likely to have gastric ulcers. Also, time in work, crib-biting, difficulty maintaining bodyweight and playing the radio in the barn were identified as other risk factors (Lester et al. 2007). On the other hand, protective factors included training on the property and turnout with other horses. Also, in another study in Standardbred mares, 7/8 horses (Gordon et al. 2006) had gastric ulcers after 8 weeks of training, compared to 0/7 horses housed similarly and not trained. Although racehorses have a high prevalence of EGUS, 56.5% of horses in endurance competition, show jumping, dressage or western performance and travel, had gastric ulcers (Hartmann and Frankeny 2003) after competition. Thus, even nonrace training and performance horses are at risk of developing EGUS and should be monitored for clinical signs(Nadeau 2009) J Am Vet Med Assoc. 2007 Jun 1;230(11):1680-2. Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. White G, McClure SR, Sifferman R, Holste JE, Fleishman C, Murray MJ, Cramer LG. OBJECTIVE: To determine the effects of 8 days of light to heavy exercise on gastric ulcer development in horses and determine the efficacy of omeprazole paste in preventing gastric ulceration.). CONCLUSIONS AND CLINICAL RELEVANCE: Results showed that horses in light to heavy training for as short as 8 days were at risk of developing gastric ulcers and that administration of omeprazole paste decreased the incidence of gastric ulcers. Conclusions: The study confirmed a high prevalence of ulcers in the gastric squamous mucosa of Standardbreds in race training. Of the studied parameters only status of training showed a significant association with gastric ulcers of the squamous mucosa.

Housing Equine Vet J. 2008 Jun;40(4):337-41. Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach. Husted L, Sanchez LC, Olsen SN, Baptiste KE, Merritt AM. REASONS FOR PERFORMING STUDY: Stall housing has been suggested as a risk factor for ulcer development in the equine stomach; however, the exact pathogenesis for this has not been established. OBJECTIVES: To investigate the effect of 3 environmental situations (grass paddock, stall alone or stall with adjacent companion) on pH in the proximal and the ventral stomach. CONCLUSIONS: The change in housing status used in the current study did not affect acid exposure within either region of the equine stomach. The pH in the ventral stomach was uniformly stable throughout the study, while the proximal pH demonstrated a 24 h circadian pattern.


Diet A high grain low roughage diet is a risk factor in EGUS. High roughage diets provide hours of chewing and the production of salivary bicarbonate that bathes the stomach and protects against gastric ulcers. Metayer et al. (2004), found that small low starch meals empty from the stomach significantly faster than large high starch meals. Since high starch diets are fermented to VFAs and lactic acid, large high starch meals should be avoided in horses prone to gastric ulceration (Taharaguchi et al. 2004; Boswinkel et al. 2007). 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). 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) In an investigated standardbred population in the Netherlands the amount of concentrate fed is not an important predisposing factor.(Prevalence) Equine Vet J. 2009 Sep;41(7):625-30. Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. Luthersson N, Nielsen KH, Harris P, Parkin TD. OBJECTIVES: To investigate the prevalence of EGUS in a population of Danish horses, during winter when the horses had been housed and fed for at least 8 weeks and to analyse the influence of feed, work level and environment on the risk of EGUS of > or = grade 2 in severity. CONCLUSION AND POTENTIAL RELEVANCE: This study has confirmed that components of the diet, readily modifiable, may have an important impact on the risk of EGUS in the nonracehorse. Differences in the multivariable models produced for all ulcers and nonglandular ulcers support differences in the aetiology of ulcers in different locations of the stomach. Significant factors for the development of gastric ulceration included the feeding of concentrates and faster exercise (Vatistas 1998). In addition, withholding feed before exercise was a modifying factor that, although not causing gastric ulceration, may have decreased time of onset.(Vatistas 2 1999) Murray determined that alternately withholding feed for 24 h followed by feeding for 24 h induced ulceration of the squamous mucosa that appeared endoscopically similar to naturally occurring ulcers (Murray 1994). However, such a severe form of feed deprivation does not occur in horses in training, in which horses may be fasted for 4 h before training exercise, although the period of feed withdrawal may be longer prior to a race. The results of our study tend to support the concept from other studies that feed deprivation is not necessary for the development of gastric ulceration (Vatistas 1998). The stabling of horses from pasture has been documented to increase the severity of gastric ulceration (Murray and Eichorn, 1996). All horses in the present study were stabled and this may have had some influence on the development of gastric ulceration. Evidence for the role grain is predominantly anecdotal, but there has been one study that demonstrated an increased prevalence of gastric ulceration in ponies fed a concentrate diet compared to ponies fed hay alone The results of our study suggest that, rather than training itself, the most stressful event may have been when horses entered their new environment..(Vatistas 2 1999) It seems reasonable to suggest that any condition that influences food intake might contribute to the development of gastric ulcers in horses.(Sandin 2000

Other ailments Considering the intestinal lesions, gastric ulceration was found in 42% of horses with large bowel lesions and in 31% with small bowel lesions. The association between intestinal lesions and ulcers within the stomach might suggest that gastric ulcers are often part of a larger gastrointestinal disease complex. In man, it is usual to find that disturbed activity in the autonomic nervous system affects both intestine and stomach (Fielding 1977). Murray (1989) reported an association between glandular ulcers and clinical disorders in foals and a similar relationship could also be true for mature horses. It has also been established that colic is associated with gastric ulcers in horses (Murray 1989, 1992; Furr and Murray 1989). In our study, colic disturbances were significantly (P<0.001) associated with gastric ulcers in bivariate analysis. This finding further suggests a relationship between gastric ulcers and clinical signs of colic. Whether gastric ulceration was the cause or the consequence of colic in our study has not been established. A variety of conditions involving abdominal pain (Murray 1992) have also been associated with gastric ulceration in horses. Abdominal pain or inappetance for any reason probably reduces appetite and, consequently, diminishes feed intake. Feed deprivation generally results in increased stomach acidity (Murray and Schusser 1993), since the absence of protein reduces buffering capacity. Moreover, gastric juice is more readily transported in an empty stomach and, as a consequence, flushed over the vulnerable squamous mucosa resulting in gastric ulceration. Therefore, any condition that considerably influences food intake might, hypothetically, contribute to the development of gastric ulcers in horses.(Sandin 2000)


NSAIDs Nonsteroidal anti-inflammatory drugs (NSAIDs: phenylbutazone, flunixin meglumine) have been shown to cause gastric ulcers in horses. This is usually related to the use of a high dose or frequent administration of NSAIDs; however, therapeutic doses have been known to cause ulcers in horses. Recently, a study was conducted comparing the ulcerogenic effects of an orally administered prophenylbutazone drug, suxibuzone, to phenylbutazone (Monreal et al. 2004). Horses treated with phenylbutazone had more ulcerated areas and deeper ulcers than those in the suxibuzone treated or placebo groups. The authors concluded that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally at equimolar doses in horses. However, a more recent study in horses given suxibuzone or phenylbutazone at therapeutic doses for 14 days showed no significant difference in gastric ulcer scores when compared to each other and control horses receiving no treatment (Andrews et al. 2009). Thus, therapeutic doses of these NSAIDs did not lead to gastric ulcers more than what was observed in the untreated control group. Another study evaluated the use of a combination of NSAIDs and gastric ulcers in horses. Phenylbutazone (2.2 mg/kg bwt per os, q. 12 h, for 5 days) or phenylbutazone (same dose) and flunixin meglumine (1.1 mg/kg bwt, i.v., q. 12 h, for 5 days) were administered to adult horses (Reed et al. 2006). In this study, total plasma protein and albumin decreased in NSAID treated horses and nonglandular gastric ulcer scores were significantly higher in horses treated with the 2 NSAID drugs. Thus, NSAIDs and a combination NSAID treatment should be approached with caution in horses. Recently, firocoxib1, a new cox-2 inhibitor NSAID was approved for treatment of lameness in horses. Gastric ulcers were not detected in horses administered firocoxib (0.1 mg/kg bwt, per os, q. 24 h, 30 days) (Anon 2005). However, firocoxib is FDA approved for the control of pain and inflammation associated with osteoarthritis in horse, thus its efficacy in horses with abdominal pain is unknown. Furthermore, currently there is no i.v. formulation of this product, so it cannot be administered orally in horses with abdominal pain and gastric reflux or dysphagia. (Nadeau 2009) Vet Ther. 2009 Fall;10(3):113-20. Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. Andrews FM, Reinemeyer CR, Longhofer SL. 

These findings suggest that when administered at the recommended label dose for 15 days, neither PBZ nor SBZ causes an increase in the number or severity of gastric ulcers over what would be expected with traditional stabling and intermittent feeding patterns. Also, PBZ-treated horses did not have more severe gastric ulcers than SBZ-treated horses, indicating that SBZ does not appear to offer an advantage over PBZ in preventing gastric ulcers when used at recommended label doses. However, ulcers in other regions of the gastrointestinal tract (e.g., right dorsal colon, duodenum) were not evaluated in horses in this study.


Housing, stress, boredom, training, diet Feeding practices:

  • Grain and pelleted feed asssociated with increased serum gastrin (Smyth et al 1988)
  • Eating behaviour (grazing vs feeds)
  • Feed constituents (alfalfa)
  • Individual variability

Exercise and training

  • Strenuous exercise stimulates gastrin release which has effects on HCL secretion, gastric emptying, gastric blood flow

Clinical syndrome

Often asymptomatic, may see:

  • Poor appetite
  • Dullness
  • Change in attitude
  • Reduced performance
  • Reluctance to train
  • Poor condition
  • Weight loss
  • Diarrhoea
  • Low-grade colic
  • Excessive recumbency
  • Bruxism (in foals only and almost pathognomonic)

Foals with outflwo obstruction will dveelop reflux after suckling or marked reflux even with limited to no sukcling if the duodenal obstruction is distal to the common biel duct.(Sanhcez)

Diagnosis

Presumptive on clinical signs and response to treatment (Sanchez) Definitive diagnosis requires endoscopy (cannot do in foals as need to starve prior to exam)

Endoscopy

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)

Lesion Grade Description
Grade 0 Intact epithelium with no appearance of hyperaemia or hyperkeratosis
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

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)

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

Abdominal radiography without contrast in foals with outflow obsturction typically rveeals very disticnt enlarged, gas-filled stomach. Liquid barium contrast will either have markedly delayed (with incomplete obstruction) oir no (complete onsbtruction) outflow. (Sanchez)

Biopsy

A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.[28]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.[1] Tests that require further analysis for sensitivity and specificity[5] include:

  • Urine[29] and blood[30] sucrose absorption as an assay of gastric mucosal permeability
  • Serum alpha1-antitrypsin which has been detected more frequently in foals with gastric ulceration[31]

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)

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)

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 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.
  2. ↑ 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.
  3. ↑ 3.0 3.1 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).
  4. ↑ 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.
  5. ↑ 5.0 5.1 5.2 5.3 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.
  6. ↑ 6.0 6.1 6.2 6.3 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial
  7. ↑ 7.0 7.1 7.2 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.
  8. ↑ 8.0 8.1 8.2 Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. Equine Vet J, 18(4):284-287.
  9. ↑ 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
  10. ↑ 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.
  11. ↑ 11.0 11.1 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
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ Bertone, J (2000) Prevalence of gastric ulcers in elite, heavy use western performance horses. Proc Am Assoc Equine Pract, 46:256-259.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. Proc Equine Colic Res Symp 2nd:126-128.
  21. ↑ 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.
  22. ↑ Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc, 195:1135-1141.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ 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.
  29. ↑ 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.
  30. ↑ 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.
  31. ↑ 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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