Stomach ulcers and lesions can be an affliction in horses young and old. The presence of ulcers often causes severe discomfort to the horse and, in radical cases, can result in death. Attempting to describe ulcers is a bit like trying to describe colic. In both cases, one word describes a disorder that is multi-faceted and which varies from case to case. Some horses will have only mild stomach lesions that might heal on their own, leaving little or no scar tissue in their wake. Others will have full-blown ulcers that can cause permanent damage.
Michael J. Murray, DVM, MS, Diplomate ACVIM, Associate Professor and Adelaide C. Riggs Chair in Equine Medicine at the Marion duPont Scott Equine Center at the Virginia-Maryland Regional College of Veterinary Medicine in Leesburg, Va., sums up the complicated ulcer picture this way:
"Gastric ulceration affects large numbers of foals, yearlings, and adult horses, and different clinical syndromes and lesion distribution occur in each group. Ulceration may occur as a primary problem, or may occur secondary to another intestinal disorder. Duodenal ulceration occurs primarily in foals, although it has been diagnosed in yearlings. Duodenal ulceration is a rare finding in adult horses."
First, a look at the stomach, where most of the lesions and ulcers appear.
The stomach in an average horse is about the size of a medium pumpkin. However, it has the potential to stretch to a much greater size and is capable of holding up to eight gallons of fluid, although if the stomach is filled to that extent, there is danger of rupture.
There are two types of lining in the stomach. On top is the non-glandular or squamous lining, and on the bottom is the glandular lining. Most ulcer problems will develop in the non-glandular lining because it has little protection against the hydrochloric acid that is produced in the equine stomach. The glandular lining of the stomach is actually exposed to acid much more--as in constantly--than the non-glandular lining.
"The glandular mucosa is exposed to acid all of the time," says Murray, "because it sets down in the bottom of the stomach where all the juices are, but it has many ways of protecting itself. The non-glandular mucosa is on the top half and generally doesn't have a lot of acid come into contact with it. As a result, it has minimal protection against acid. When acid does come into contact with the non-glandular mucosa damage can occur very rapidly--within hours."
Generally speaking, ulcers occur when there is an imbalance in aggressive and protective factors within the stomach.
Listed as the aggressors in this balancing act are hydrochloric acid and pepsin. The protectors include the mucus/bicarbonate barrier, prostaglandin, mucosal blood flow, cellular restitution, and growth factors that promote development of blood vessels and mucosal proliferation. Also of significance is the stomach's motility. If it does not empty its contents regularly and efficiently, acid can accumulate and ulcers develop.
The squamous mucosa or non-glandular lining at the top of the stomach lacks a mucus/bicarbonate layer, which means that it has little resistance to hydrochloric acid.
One of the significant protection barriers is the food the horse ingests. Because the horse's stomach secretes acid all of the time, the substance is eternally present. However, if the horse is allowed to graze without interruption as nature intended, this does not pose a significant problem because there is always food in the stomach to absorb the acid. Bicarbonate in the saliva also can neutralize some of the acid in the stomach.
When man intervenes with an in-stall feeding regimen, problems can quickly develop. Now, the horse is no longer constantly grazing, but is being fed at intervals. This means that there are times when the stomach is empty and excess acid is coming into direct contact with both the glandular and non-glandular linings.
In an experiment that Murray conducted, the pH of a number of horses' stomachs was measured, both when filled with food and when the horse was fasting. (The symbol pH is used to describe the effective hydrogen-ion concentration or hydrogen-ion activity in gram equivalents per liter. It is used in expressing both acidity and alkalinity on a scale whose values run from 0 to 14. The number 7 represents neutrality, while numbers less than 7 indicate increasing acidity and numbers greater than 7 represent increasing alkalinity. Thus, the lower the pH number, the higher the acidity in the horse's stomach.)
It was found in the experiment that when horses had fasted for 24 hours, their average pH was below 2.
"Each pH number," explains Murray, "has a factor of 10; so a pH of 3 is 10 times less acidic than a pH of 2. We found that in the horses that had fasted for 24 hours, 80% of the pH readings were less than 2."
Horses in the experiment which had free access to hay showed readings where 70% of them had a pH level that was above 2, and the average reading over a 24-hour period was 3.2.
The experiment was carried a step further. This time, the question to be answered was whether increased acidity due to lack of food in the stomach would cause ulcers. The answer was yes.
"We were able to induce ulcers by withholding feed for 24 hours, letting them eat, then withholding it again for 24 hours," Murray says. "Following this feeding and withholding regimen, we were able to induce bleeding ulcers within three to seven days."
So, one might assume, based on this information, ulcers can be prevented by keeping hay in front of horses at all times?
Not necessarily, says Murray.
Research has shown that horses on free-range pasture which are brought into stall confinement frequently will develop lesions in the stomach within a week, even though they have free-choice hay.
Horses which graze get to spend most of their time eating. The horse in a stall spends far less time consuming food. One of the reasons might be that most stalled horses consume grain along with their hay. This means that they receive much of their energy from the grain and, as a result, aren't going to eat as much hay.
It also takes less time to consume grain than it does hay, so the horse spends less time eating. All of this adds up to a stomach that is empty with some frequency and, thus, is susceptible to attacks by the omnipresent acid.
"When you combine less food with more acid in the horse's stomach," says Murray, "you basically have a little ulcer factory functioning."
While feeding management might play a key role as to whether horses will or will not develop stomach lesions, it is only one of the factors involved. The stress of training is also implicated, especially in racing Thoroughbreds.
Murray contends that as many as 90% of Thoroughbreds in training have lesions in the stomach and, in about 40% of that number, the lesions are full-blown ulcers.
There is no brief, definitive answer as to why this is the case, says Murray. Perhaps feeding management plays a significant role. In many cases, the heavier the exercise program, the larger the grain ration.
Or, says Murray, perhaps exercise does have an effect on the gastrointestinal system.
"We do know that in human marathon runners, there is an effect on both the stomach and the duodenum," he says. (The duodenum is the first part of the small intestine into which the stomach empties its contents.)
Contrary to what many have believed through the years, psychological stress does not play a significant role in the development of ulcers in either humans or horses, Murray contends. Psychological stress can cause an upset stomach in man and horse, Murray says, but "there have been many studies which show that psychological stress does not have an effect on ulcers."
However, he is quick to add, there is a strong correlation between physiologic stress and ulcers. Humans and equines which are seriously ill are at an increased risk of developing stomach ulcers.
This type of stress tends to produce ulcers, particularly in foals, Murray says. And, in these cases, the ulcers often are in the glandular lining at the bottom of the stomach rather than in the squamous or non-glandular lining at the top.
"In foals suffering from a serious illness, protection in the glandular part of the stomach apparently is reduced," Murray says.
Ulcers For Young And Old
While ulcers can afflict horses of all ages, the syndromes vary. Foals seem to be more susceptible than adults, though their problems can vary from mild lesions that heal on their own to full-blown ulcers.
"At least half of the young foals develop gastric lesions that heal spontaneously," says Murray. "However, if, during this time, they are under physiologic stress, it can result in that minor lesion turning into an ulcer that doesn't heal--then we have a problem. Because the lining of the stomach is so thin, a relatively minor ulcer can turn into a perforated ulcer very quickly."
A perforated ulcer often leads to peritonitis, which is a death sentence in most cases.
"In some cases where the perforation is minor, we can save the animal," Murray says. "In these cases the small perforation is sealed by the greater omentum, a thin membrane that covers the stomach. This is nature's bandage. If you get the animal on ulcer treatment and antibiotics quickly, it may sometimes be saved."
While most ulcers and lesions occur in the non-glandular lining at the top of the stomach, and, less frequently, in the glandular lining at the bottom of the stomach, they may also appear in the duodenum.
One of the dangers with duodenal ulcers, especially if they are severe, is that they can create scar tissue which, in turn, causes contracture and partial obstruction to the emptying of the stomach into the small intestine. Delayed gastric emptying results in an accumulation of acidic gastric secretions that can yield severe ulceration of the gastric mucosa, particularly to the non-glandular or squamous mucosa at the top of the stomach.
Clinical signs that typically are associated with gastric ulcers in foals include grinding of the teeth, rolling onto the back, salivation, interrupted nursing, and colic.
"These signs, though," says Murray, "are observed in the minority of foals with ulcers and usually are reflective of severe gastric lesions. Signs of salivation or esophageal reflux are indicative of gastric outlet obstruction or pseudo-obstruction, reflecting significant ulceration associated with the pylorus (the rear aperture of the stomach through which the stomach contents are emptied into the duodenum) and/or duodenum.
"These are the foals that will be grinding their teeth and may even be salivating. When we see those signs in weanlings, we are really concerned because it may be a chronic problem that we can't fix because of the scar tissue."
In yearlings, ulcers have been associated with recurrent colic, poor body condition, poor appetite, and intermittent diarrhea.
"In yearlings, most lesions are confined to the squamous mucosa," says Murray. "Normal yearlings do not have gastric ulcers, although mild erosions of the squamous mucosa have been noted. Yearlings have been diagnosed with delayed gastric emptying, resulting in severe bleeding and gastric ulceration. These patients normally have a history of having had signs of gastroduodenal ulceration as foals."
Yearlings so afflicted, Murray says, generally have poor body conditions, poor appetites, and intermittent diarrhea. One animal was observed to belch.
While Thoroughbreds in training seem more prone to stomach lesions and ulcers than other horses, the affliction is not limited to them.
"Gastric ulceration affects a large number of adult horses of all breeds," says Murray, "with clinical signs including poor appetite, poor condition, mild to severe colic, attitude changes, and, in the case of horses on the track, poor racing performance."
As is the case with foals and yearlings, most lesions and ulcers in adult horses occur in the squamous lining at the top of the stomach rather than in the glandular lining at the bottom.
In all cases--horses young and old--clinical signs are rarely enough for a definitive diagnosis. One of the practitioner's best tools in making a diagnosis is the endoscope. In fact, it was the development of the endoscope that made practitioners more aware of ulcers in horses, especially in adults.
The first real mention of ulcers in foals was back in the 1960s, Murray says. Pathologists noted them in post-mortems and reflected that they might have been the result of the youngster eating rocks. In the late 1970s, research papers began to appear, reflecting studies on severe ulcers in foals. By the early 1980s, Murray notes, it was well recognized that stomach ulcers constituted a health problem for many foals.
Ulcers in adult horses, he says, weren't appreciated because it was the mid-1980s before an endoscope was developed that was long enough to enable the veterinarian to literally look into the horse's stomach.
"The long endoscope has made the difference in finding ulcers in adult horses," Murray says.
Needed to examine the stomach of an adult horse is an endoscope that is at least two meters in length. To reach the duodenum, it must be 2.8 meters in length.
Before performing an examination with an endoscope, Murray advises, foals up to 20 days of age can be allowed to nurse, but should not consume solid feed for six to 10 hours prior to the exam. Older foals and mature horses should not have solid feed for six to 10 hours prior to the exam. This time period, Murray explains, is required to ensure adequate emptying of food from the stomach.
As he peers through the endoscope, the veterinarian will see that a healthy squamous or non-glandular lining or mucosa at the top of the stomach appears as a pale to white tissue. In foals, the squamous mucosa is very thin in the first several days of life and appears pale pink to pale white.
By contrast, the glandular mucosa at the bottom of the stomach appears as dark pink to red, with a smooth, glistening texture. The duodenal mucosa, says Murray, should have a uniform pink, velvety appearance.
Once ulcers or stomach lesions are verified, the matter of treatment must be addressed. This is a matter of economic importance as treatment can be very expensive--running into the hundreds, or even thousands, of dollars for an adult horse.
It is for this reason that diagnosis through use of an endoscope whenever possible is highly important, Murray believes.
"If endoscopy is feasible, it should be done. It is cheaper to have the horse examined with an endoscope and find out that it doesn't have ulcers than it is to treat it for ulcers when it may not have them. If the horse does have ulcers, the veterinarian--with an endoscopic examination--can determine how bad the condition is and how long the horse may need treatment."
The problem with relying solely on clinical signs, Murray points out, is that not all horses react to ulcers in the same way.
"In adult horses, many individuals will not demonstrate outward clinical signs. There may be vague indications, such as not eating well, not having as shiny a hair coat as one might desire, or even signs of abdominal discomfort, but no definitive signs such as grinding of the teeth or serious colic."
The only way the practitioner can know what he or she is dealing with is with an endoscopic examination. Once ulcers are diagnosed, treatment is the next order of business.
Often, says Murray, because of the cost, there is pressure to use something less expensive than what the situation might call for.
"The problem is that less expensive often doesn't work, and you must treat the horse longer. Even then, he may have an unfavorable outcome. In those cases, less expensive becomes more expensive."
There are two classifications of drugs used in treating equine ulcers: 1) acid suppressant drugs that decrease acidity in the stomach, and 2) mucosal protective drugs.
The greater use, by far, is made of acid suppressant drugs. The only mucosal protective drug being used, says Murray, is sucralfate (Carafate), and it is only effective for the glandular lining of the stomach and the duodenum, where ulcers and lesions are less likely to occur.
The acid suppressants, he says, are broken down into three categories: 1) antacids, which simply absorb whatever acid is in the stomach, 2) histamine receptor type 2 (H2) antagonists, and 3) a proton-pump inhibitor that blocks gastric acid secretion.
The H2 antagonists are Murray's drugs of choice in most cases.
"Treatment with H2 antagonists," he says, "has been successful in resolving the gastric lesions and in resolving the presenting problem. Cimetidine (Tagamet) and ranitidine (Zantac) are the most frequently used, and both inhibit gastric acid secretion in horses."
The H2 antagonists, he says, can be given orally. The prime disadvantage is cost. Administering ranitidine at the rate of 20 milligrams per kilogram of adult horse body weight on a daily basis can run as high as $60 to $90 per day.
"Because these drugs are expensive," says Murray, "there is pressure to use as little as possible. When deciding on a dose to use, one must recognize that as the dose of an acid-suppressive agent is lowered, the percent of patients that will respond poorly or not at all increases. There is tremendous individual variability in the degree and duration of suppression of gastric acidity by H2 antagonists between horses, presumably as a result of differences of drug absorption and first-pass hepatic metabolism. We have found that 6.6 milligrams ranitidine per kilogram of body weight, given every eight hours, provides adequate suppression of acidity in the greatest percentage of horses. This dosage schedule resulted in a median 24-hour gastric pH of 4.6 in horses with free access to hay, compared to a pH of 3.2 in horses with free access to hay, but not given ranitidine.
"Formulations for intravenous administration of H2 antagonists are available, but are expensive--approximately three times the cost of oral products."
In most cases when using H2 antagonist therapy, a three-week treatment period is required to ensure complete healing. When treated at the above described level, Murray says, 80-90% of the horses studied had complete healing of gastric ulcers within three weeks. Those administered ranitidine for two weeks showed complete healing in only 15-40% of the cases.
The dosage recommended for cimetidine, Murray says, should probably be at the rate of 18 milligrams per kilogram of body weight every eight hours.
For racehorses in training, it is generally necessary to remove them from training in order to effect complete healing, Murray says. If the horse is kept in training, the clinical signs of lesions or ulcers might disappear, but the lesions themselves do not.
Two other H2 antagonists on the market for use in humans are famotidine (Pepsid) and nizatidine (Axid). However, effective dosages for horses have not yet been established.
Why, one might ask, can't we simply give the horse antacids? After all, they are relatively inexpensive and they, too, can be administered orally.
Quite simply put, says Murray, they don't work well because in order to be effective, they must be given in large volume and with frequency. Because of the size of a horse's stomach, he says, one has to administer from eight to 10 ounces of antacid in order for it to be effective. Even at that, the effect will last only about two hours at the most.
"A lot of people will give 30ccs of Maalox twice a day," says Murray, "and that is a complete waste."
The third drug that can be administered--the one which shuts down acid secretion--is omeprazole (Prilosec).
"Because of its potency," says Murray, "once daily treatment is feasible. Research has shown that 0.7 milligrams per kilogram of body weight effectively inhibited gastric acidity, although 1.4 milligrams per kilogram was superior. Administration of omeprazole at a dosage of 1.5 milligrams per kilogram once daily promoted rapid restoration of normal gastric squamous mucosa in a vehicle-controlled study of Thoroughbred racehorses with moderate to severe gastric ulceration."
There are some down sides to the drug. For one thing, Prilosec is even more expensive than the H2 antagonists. For another, it is difficult to administer.
"The drug is difficult to administer because it is manufactured in enteric-coated granules," says Murray. "This is required since the drug is destroyed in an acidic environment."
This means that omeprazole is best administered by stomach tube.
For The Future?
Though much is known today about ulcers, there is still much that is unknown. For example, what about recurrence. Will the treated horse be well for a short time then develop ulcers or lesions again?
In the case of racehorses in training, that could well be the case, Murray says. However, in cases where horses are in pursuits other than racing, treatment often will clear up the ulcers and there is no recurrence, Murray adds.
"Recurrence is not something that is so prevalent that it becomes a reason not to treat. If you have a horse with ulcers and that horse shows clinical signs, it should be treated."
The question isn't so much whether the horse has ulcers, but rather, how much it is bothered by them, Murray believes. Some horses might have ulcers, but because they are more stoic or more pain tolerant, might never show clinical signs. Others might be sorely troubled by them and will show clinical signs.
Why some horses develop ulcers and others don't remains a mystery. In the experiments described earlier, some horses which had feed withheld for 24 hours, were fed, then had it withheld again quickly developed ulcers. Some others in the experiment, though their stomach had as much or more acidity, did not develop significant lesions.
The bottom line remains. If the horse shows clinical signs and an endoscopic examination reveals ulcers, the horse should be treated. If it is not treated, the horse's health and performance will be compromised at best, and, at worst, the ulcer will perforate and the horse will die of peritonitis.
About the Author
Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at www.exclusivelyequine.com or by calling 800/582-5604.
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