Equine Gastric Ulceration Syndrome (EGUS)
EGUS is a very common disease of the stomach of foals and adult horses, and has a reported prevalence of up to 50% in foals and over 75% in adult horses. These percentages do heavily depend on habitat, breed, performance, age and population.
The horse’s stomach is divided into two very distinct areas, the non glandular/squammous and glandular region separated by a sharp demarcation called the margo plicatus.
The non glandular portion is an extension of the oesophagus and contains no glands. The glandular portion covers over one half of the stomach and contains multiple glands which secrete varying amounts of hydrochloric acid, mucus, enzymes and bicarbonate.
Gastric ulceration in foals ( up to 6 weeks) and adult horses are commonly found in the non glandular portion of the stomach, however foals having concurrent disease or have been treated with long term NSAIDS (e.g. bute) may have ulcers in the glandular portion of the stomach. Foals can initially develop duodenal ulceration which can progress to more proximal secondary ulceration.
The stomach secretes hydrochloric acid (HCl) continuously even without food being present. Foals secrete this acid as early as 2 days of age. It is this acid which predisposes the animals to EGUS. Adult horses secrete 1.5 litres of gastric juice per hour, which contains the HCl. The pH of gastric contents range from 1.5 to 7.0, being lower (more acidic) at the margo plicatus and glandular mucosa. A near neutral pH is found at the area of the cardiac sphincter. Gastric emptying occurs within 30 minutes for a fluid based meal whereas emptying a hay content meal would take 24 hours. EGUS in foals and horses results from an imbalance of mucosal aggressive factors ( HCl, pepsin, bile acids) with the mucosal protective factors (mucus, bicarbonate).
The mucosal protective factors are more developed in the glandular mucosa when compared with the non glandular portion, so ulceration in the squammous mucosa is primarily due to the HCl, bile acids and pepsin, by splashing or refluxing across the margo plicatus. Ulcers in the glandular portion are due to blood flow disruption and decreased production of the mucosal protective factors which results in a relative increase in HCl which damages the underlying submucosa. Inhibition of prostaglandins at this time have a major involvement.
The causes of ulceration include fasting reduced gastric motility and emptying. Fasting or anorexia is an important cause of squammous ulceration in both foals and horses. Anorexia and recumbency leads to low pH of the gastric juices especially in foals. Milk is thought to have a buffering effect on the gastric acid and recumbency tends to increase the slashing of the acid across the margo plicatus. Feed deprivation in horses can cause squammous ulceration by the exposure of the non glandular portion of the stomach to HCl. Horses fed hay continuously had less acid compared with fasting horses. Alfalfa hay is also thought to stimulate less acid production. High roughage diets stimulate saliva which is rich in bicarbonates this has a buffering effect on the gastric acids.
EGUS is especially high in performance horses and is thought to be due to the constant splashing of acidic contents across the margo plicatus. Mechanical aspects of exercise and abdominal pressure are thought to increase this splashing effect. Also maximum exercise levels reduce gastric motility and emptying which when combined exacerbate the condition. Performance horses are also fed diets high in fermentable by-products of carbohydrates which produce volatile fatty acids, generated by resident bacteria,these are thought to induce acid damage to the squammous mucosa of the stomach.
Prostagandins maintain the well being of the stomach mucosa by stimulating the production of surface active protective phospho-lipids which stimulate mucosal repair and stimulate sodium transport which prevents cellular swelling. Stresses in foals and horses e.g. dystocias, training, confinement and illness can release excessive amounts of endogenous corticosteroids which inhibit prostaglandin release. The decrease in prostaglandin leads to breakdown of mucosal protective factors and is the primary cause of glandular ulceration. NSAIDS, such as bute or flunixin can also block prostaglandin synthesis which causes decreased mucosal blood flow, stimulates gastric acid secretion and inhibits bicarbonate production by the glandular mucosa.
Diagnosis...this is based on the clinical signs. In foals there is intermittent colic (especially after eating or suckling) frequent recumbency often with dorsal positioning, poor appetite, not sucking out the mare and diarrhoea. Teeth grinding (bruxism) and excessive salivation also occur but can suggest pyloric obstruction. Older horses show poor appetite, dullness in the coat, rough hair coat, poor athletic performance, depressed attitude and low grade colic. The definitive diagnosis is by use of a long (3metre) scope.
The isolation of EGUS has led to a grading system
Grade 0.. Epithelium intact throughout. No hyperaemia. No hyperkeratosis
Grade I.. Mucosa intact. Areas of hyperaemia and/or hyperkeratosis
Grade II.. Small single or multifocal erosions or ulcers
Grade III.. Large, single or multifocal ulcers or extensive erosions and sloughing
Grade IV.. Extensive ulceration. Submucosal penetration
|EGUS grade grade II||EGUS grade III||EGUS grade IV|
Treatment….The bottom line in effective treatment of this condition is the inhibition of gastric acid secretion. There are a myriad of products on the market which are perpetrated to have excellent efficacy, but usually only have a soothing or coating effect over the stomach mucosa. One product ,OMEPRAZOLE, is the only really effective medication by being an “acid pump inhibitor” which inhibits the gastric acid stimulus, regardless of cause.