Gastric Ulceration - Horse

Also known as:

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

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 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 conditions 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 70-100%
• Racehorses in active race training 80-90% (incidence 100%)
• Show horses 58% (McClure et al 1999) (12 in Sanchez)
• Ponies 78% (MacAllister et al 1982)
• Endurance 67% (Pieto et al 2004) (13 in Sanchez)
• Western performance horses 40 % (14 in Sanchez)
• Thoroughbred broodmares (67-77%) (15 in Sanchez) (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.
• Nonracing performance horses (17 % precompetition, 56% postcompetition)
• Pleasure horses in full work ~ 60% (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).
• Pleasure, riding lessons, showing 37 % (Murray et al 1989 in Orsini)
• Foals – 25-57% (20-22 in Sanchez) unknown, probably common, increasing or diagnosing more? Overall, the currently accepted prevalence estimates is 30-50%, increasing sharply in foals demonstrating signs of disease, especially gastrointestinal signs.

The prevalence and severity of ulcers increases with work intensity and duration(Murray 1994; Orsini and Pipers 1997 in Orsini), thus racehorses in active training are more often affected (Hammond et al. 1986; Johnson et al. 1994) 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. (Vatistas 2 1999). Lesions are thought to be chronically progressive during race training, but to regress during retirement.(Hammond 1986). Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.(EGUC)Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers (Murray 1992a). 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 (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.

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.

Pathophysiology

NOT associated with Helicobacter pylori and not typically associated with Gasterophilus

Risk Factors

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)

Laboratory tests

No known laboratory markers, attempts to detect occult blood in faeces unreliable in horse. Other tests need further evaulationfor senstivty and sepcificity (Sanchez): Urine (93) and blood (94) sucrose absorption testing have been evauated a sameasure of gastric mucosal permeability (Sanchez) Serum alpha1-antitrypsin was detectable more frequnetly infoals with gastrci ulceration (95 in Sanchez)

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)

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

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.