Gastric Ulceration - Horse

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

Prevalence

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

• Racehorses 66-93%
• Racehorses in active race training 80-93% (incidence 100%)
• Show horses 58%
• Ponies 78%
• Endurance horses 67%
• Western performance horses 40%
• Thoroughbred broodmares (67-77%)
• Nonracing performance horses (17% pre-competition, 56% post-competition)
• Pleasure horses in full work ~ 60%
• Pleasure, riding lessons, showing 37%
• Foals ~25-57%, the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.

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

Signalment

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

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. 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. There is also evidence that training for just 8 days is suffcient to induce gastric ulcers. 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. 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.

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. 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. Transport has also been shown to induce squamous mucosal ulceration in horses.

Diet

Feed deprivation encourages gastric ulceration in two ways: (1) it precludes the buffering capacity of protein leading to a reduced gastric pH and (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice. It is unsurprising, therefore, that an alternating feed-fast protocol would produce a consistent model of ulcer induction in the equine squamous mucosa. Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse. 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. This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses. Ponies fed a concentrate diet had a greater prevalence of gastric ulcers than ponies fed hay alone. and this may be because grain and pelleted feeds are asssociated with increased serum gastrin. 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.

Other ailments

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

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,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 orallyand that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone. The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa, they may look different endoscopically from ulcers that occur naturally, and they appear to heal spontaneously. Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.

Temperament

A nervous disposition has been linked with gastric ulcersbut the same association was not seen in another study. The physiological and psychological stresses of training, housing, boredom, travel, mixing, hospitalisation and entering new environments 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. In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation. 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. 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)
• Poor condition
• Rough hair coat
• Weight loss
• Excessive recumbency
• Mild to severe colic
  • Mild, recurrent colic signs post-prandially
  • 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.
• Changes in attitude (dullness or depression)
• Poor racing performance and reluctance to train
  • Performance improved in 4 Thoroughbred racehorses after antiulcer treatment
  • Gastric ulcers have adversely affected physiological indices of performance in horses.

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
  • Poor appetite
  • Diarrhoea
  • Intermittent colic
  • Frequent dorsal recumbency
• Sucklings and weanlings:
  • 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):
  • Bruxism
  • Colic
  • Gastrooesophageal reflux after suckling
  • Ptyalism (secondary to gastric outflow obstruction and gastroesophageal reflux)
  • Diarrhoea

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

Diagnosis

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

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.

Endoscopy

Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine) in the standing horse. Of these, duodenoscopy is the more specific but more technically demanding method. Endoscopic examination requires preparatory starving of the patient for 6-8hours, eliciting a certain degree of stress. As such, it is preferable not to carry out this technique in foals. In adult horses, a minimum endoscope length of two metres is essential to visualize the gastric body and fundus. A 2.8-3.0 metre endoscope is needed to observe the gastric antrum, pylorus and proximal dudoenum. In either case, fibreoptic or videoendoscopic equipment can be used.

Based on a consensus, the Equine Gastric Ulcer Council (EGUC) published an EGUS Lesion Scoring System which they claimed to be simple and applicable to both regions of the equine gastric mucosa. This last point has been debated, since most of the acquired data on gastric lesions refers only to the squamous mucosa. At the time of writing however, the EGUC system appears to be the most well established and useful in practice:

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

Diffuse inflammation may be the only lesion observed in foals with early GDUD. In contrast to other scoring systems, the EGUC approach does not include bleeding when assigning lesion grades. The justification is that the 'snapshot' provided by endoscopy may by chance identify bleeding of superficial erosions whilst missing the intermittent haemorrhage of more severe lesions. Endoscopy may assist in understanding the severity of the disease and assessing the therapeutic response, but it is not without disadvantages. Ulcer severity may be underestimated, particularly in the squamous region and glandular ulcers may be missed altogether. Lesions that appear grossly similar may have different grades on histopathology. This is important as varying lesions may have different causes, requiring a range of treatment approaches.

Radiography

In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis. 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.. The need to perform contrast radiography must be weighed against the stress it would place upon the foal.

Biopsy

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

Laboratory tests

Currently, useful and reliable markers for EGUS are lacking. The SUCCEED® Equine Fecal Blood Test™ uses specific equine monoclonal antibodies to albumin and haemoglobin to detect occult blood in faeces.The test has a positive predictive value of 77% and a negative predictive value of 72% and thus cannot be relied upon alone to diagnose EGUS. False positive results may arise from rectal trauma (e.g. recent biopsy or rectal examination) or protein losing enteropathy. Other tests that require further analysis for sensitivity and specificity include:

• Urine and blood sucrose absorption as an assay of gastric mucosal permeability
• Serum alpha1-antitrypsin may be released from damaged gastric tissue and has been detected more frequently in foals with gastric ulceration

Pathology

Martineau and co-workers (2009) demonstrated that in a mixed population of horses, a wide range of lesions associated with EGUS could be found at post-mortem. These included hyperkeratosis, punctate scars, diffuse erosions or ulcerations and margo injuria in the squamous region and hyperaemia, focal erosions and ulcerations in the glandular region. A novel finding was glandular metaplasia which may be evidence of a protective mechanism developing in response to acid exposure. The authors then devised a pathological scoring system - the Equine Gastritis Grading (EGG) system - which uses 5 samples of gastric mucosa taken from specific regions of the equine stomach. For each of these, the inflammatory infiltrate is graded by type, density and location, reactive changes are classified in both squamous and glandular samples and the presence or absence of infectious agents and lymphoid follicles is noted. From their findings, a pathogenesis for the development of lesions in the squamous region was proposed:

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.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.

Prevention

Prophylaxis

• Omeprazole paste at lower dose (1-2mg/kg) daily for 3-4wks (100, 107-109 in Sanchez)
  • Prevented ulcers in horses maintained under ulcerogenic conditions (White et al. 2003; McClure et al. 2005a,b,c;White et al. 2007).
  • Treating ulcers in asymptomatic performance horses may lead to improved performance.(Orsini)
  • Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation (Sanchez).
  • May benefit foals receiving substantial doses of NSAIDs for orthopaedic pain (Sanchez)

Management

Diet, training, exercise, stress (company, toys) Free access to good quality pasture and feeding alfalfa or other high calcium or high protein forages may help to prevent gastric ulceration (Nadeau et al. 2000; Lybbert et al. 2007; Ralston 2007). Since a large quantity of VFAs are produced in the stomach of horses fed high concentrate diets, it has been suggested that concentrates should be fed at ≤ 0.5 kg/100 kg bwt not more frequently than every 6 h and horses that are prone to EGUS should be feed concentrates with caution. Also, horses at risk of ulceration, performance horses, horses confined to stalls, and horses that are ill should be fed concentrates sparingly and roughage should be fed continuously.(nadeau 2009) 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). 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)

Pasture turnout has been recommended as the most natural and least ulcerogenic environment (Murray 1994). Horses that must be kept in a stall should have continuous access to hay and should eat it; stall confined horses may eat less often than grazing horses, and may also eat less hay if all calorific requirements are met by concentrates or grains. The practical requirements of race training may make most of these recommendations difficult or impossible to achieve.(Orsini)

References

• 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.