The horse’s stomach is divided into two main areas, each with a different lining (mucosa). The top part, called the squamous or non-glandular portion, has a mucosa similar to skin, and although it has a thin surfactant layer, it doesn’t have a protective mucous coating and it has a poor blood supply so its healing capacity can be variable. The bottom two thirds is the glandular area, which is responsible for acid secretion. It also secretes a thick layer of mucous as well as bicarbonate to buffer acid. The blood supply to this area is better, and is one of the main protective mechanisms.
This gastroscopy image clearly shows the demarcation between the paler pink squamous mucosa of the nonglandular portion and the darker pink glandular mucosa. This line is called the Margo Plicatus. The black tube you can see is the scope entering the stomach at the oesophagus
Gastric ulceration in horses can be divided into two kinds, squamous ulceration (ESGD) and ulceration of the glandular region (EGGD). ESGD is the more common condition. EGGD can be more difficult to treat and its causes are less well understood. Medications that decrease gastric blood supply and some of the hormonal protective mechanisms of this area, such as phenylbutazone (bute) can potentially contribute. However, it takes a prolonged course of high doses to have a clinically significant effect.
The photo on the left shoes a normal pyloris, the lower valve of the stomach before it empties into the intestine, showing healthy pink lining. The photo on the right shows ulceration of this area.
Horses, unlike humans, secrete gastric acid continuously. When horses have continuous access to feed, particularly roughage, the presence of feed buffers the acid, protecting the vulnerable squamous portion. Eating also causes saliva to be produced, and this is high in bicarbonate which also helps to neutralise acid. When the stomach is full, the pH at the squamous part, is much less acidic than lower down. Exposure to acid is thought to be the cause of ulcers in the squamous part of the stomach. Certain feeds can also be broken down into acidic by-products. High starch feeds create more acidic conditions than roughage or fat.
When horses exercise, the pressure in the stomach increases, and causes acid to splash onto the squamous mucosa, causing damage. The more strenuous the exercise, the more pronounced this effect is. Added to this is the fact that many horses are held off feed before exercise, so there is more acid, and less feed and saliva to neutralize it. Even when horses aren’t exercising, periods of feed restriction put them at a higher risk of ulcers. This can even happen at pasture if grass is short and insufficient hay is to allow continuous supply is fed.
The type of diet also contributes to ulcer risk. High starch, grain diets increase acid production and can directly injure cells in the squamous part of the stomach. Higher fibre feeds are eaten more slowly, and also form a ‘mat’ that sits on the acid to reduce splashing. Lucerne is a particularly good feed because the high calcium content assists in buffering the acid, and it also has a low sugar and starch content.
Stall confinement and stress can also increase the likelihood of ulcers developing.
Nonsteroidal anti-inflammatories (NSAIDs) such as phenylbutazone (bute), can contribute to ulcers, because they can reduce benefical prostaglandins which make up part of the defence mechanism of the gut. However, in most cases it takes a prolonged period of quite high doses to have a measurable effect. Newer, selective NSAIDs such as meloxicam have less detrimental effect (among other advantages), but this feature must be balanced in individual cases by its higher cost and reduced efficacy for significant orthopaedic pain, especially for laminitis.
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