Updated: Jan 25
Colonic ulcers are different than gastric ulcers, and 45% of nonperformance and 63% of performance horses have them. Most of us know that horses can suffer from equine gastric ulcer syndrome (EGUS), a condition where horses develop ulcers in their stomachs. Horses can also develop ulcers in their large intestines. This condition is referred to as colonic ulcers or right dorsal colitis (RDC). In a recent study of 545 horses tested for RDC, 45% of nonperformance horses and 63% of performance horses had colonic ulcers. Although they are not as prevalent as gastric ulcers, colonic ulcers are still a significant problem, especially in performance horses.
RDC seems to be closely associated with stress. When horses become stressed, their bodies release natural steroids that can over time irritate and damage the lining of the intestine. The more stress a horse is under, the more damage occurs. The administration of non-steroid anti-inflammatory drugs (NSAIDs) such as phenylbutazone (bute) and Banamine has also been connected to the development of RDC for much the same reason; they irritate the lining of the intestine and leave it open to further erosion.
In the early stages of RDC, a horse will present with several nonspecific symptoms, such as recurring episodes of colic, poor appetite, dull hair coat, and lethargy. As the problem gets worse, an owner might see a complete loss of appetite, fever, colic, and diarrhea. Horses who are left untreated can develop dehydration, ventral edema (swelling under the belly and legs), and weight loss. Since these symptoms can be similar to other illnesses, such as Potomac horse fever and salmonellosis, it is best to contact your veterinarian as soon as possible so that they can rule out infectious causes and properly identify your horse’s illness.
An accurate diagnosis of colonic ulceration cannot be made without visualizing the colonic mucosa, however, a presumptive diagnosis could be made based on a combination of the following findings:
History of NSAID administration (if there is no NSAID exposure, colonic ulcers cannot be ruled out, especially if the following signs are present).
Intermittent colic, especially if combined with diarrhea, weight loss and/or peripheral edema.
Positive result to fecal blood and albumin test (see below)
Abdominal ultrasound finding of a thickened mural wall in the right dorsal colon (see below), or other parts of the colon.
Ruling out of more common diseases, that have a similar presentation, i.e. gastric ulcers, salmonellosis, intestinal parasitism, etc.
Gastric ulcers can occur concurrently with colonic ulcers, however, gastric ulcers are unlikely to cause hypoalbuminemia or diarrhea.
The fecal test can detect the presence of hemoglobin and albumin in horse feces; this indicates damage to the intestinal mucosa with protein and/or blood leakage. If both hemoglobin and albumin (or only albumin) are present in the feces, the test has a high specificity for large colon disease. If only hemoglobin is present in the feces, then bleeding from the foregut is more likely. The test has a relatively low sensitivity for colonic disease, which means it may not detect all cases of colonic ulceration.
Current research indicates that diet plays a significant role in the health of the equine intestinal tract. Many performance horses are fed diets that are high in grain and low in roughage. This feeding practice may lead to abnormal patterns of fermentation in the large bowel and to alterations of the intestinal microbiota. Readjusting feeding regimes to better mimic more natural feeding habits (high roughage diets) may go a long way to preventing colonic ulcer formation, and may also help treat low-grade ulceration. This is an area in which more research is required.
Horses with moderate-to-severe colonic ulceration may benefit from the following treatments (Jones, Andrews 2009):
Discontinue NSAID medication If pain medication is required, consider alternatives such as opioids (butorphanol or fentanyl), lidocaine/lignocaine infusions or epidural anesthesia.
Decrease bulk in the diet in order to give the colon time to heal.
Feed frequent small meals at regular intervals (4-6 times daily).
Use a pelleted complete feed that is alfalfa (lucerne) based and contains at least 30% dietary fiber.
Allow short periods of grazing fresh grass (10-15 minutes, 2-3 times per day) – this is also good for stress minimization.
Corn oil, 1 cup given 1-2 times daily. Corn oil helps increase caloric intake without adding bulk to the diet. Other Omega-3-rich oils can also be used.
Psyllium mucilloid, 5 tablespoons given 1-2 times per day. Psyllium mucilloid is an amylase-resistant fermentable fiber that is hydrolyzed by colonic bacteria into short-chain fatty acids (SCFAs). The SCFAs are an important energy source for colonocytes and can help improve the function of the cells and promote faster colonic healing (Jones et al. 2009).
Sucralfate may bind to the ulcer bed and act as a protective cover over the ulcer. Once bound, sucralfate can stimulate the release of protective prostaglandins. Sucralfate is known to work for gastric ulceration, however, is not clinically proven with colonic ulcers. Sucralfate has very few side effects in horses and is worth considering.
Plasma infusions for severe hypoproteinemia and edema. Replacing the albumin deficit increases the plasma oncotic pressure, which improves tissue perfusion and helps reduce edema, both peripheral edema, and edema in the colon, which will benefit colonic healing. Hetastarch is a cheaper alternative than plasma for increasing the plasma oncotic pressure, but Hetastarch will not improve the hypoalbuminemia.
Water. Encourage regular water intake to maintain hydrated intestinal contents.
Improvements in clinical signs should be seen within 1-2 weeks, however, the colon will take longer to heal – on average 3-4 months, sometimes longer. Blood work can be monitored regularly, as improvements in blood albumin concentrations will indicate that the treatment is working.
Medications used to treat gastric ulcers, such as antacids and ranitidine, have not been found to be beneficial in treating colonic ulcers. Proton-pump inhibitors, such as Omeprazole, also have no known effect, as there are no gastric-acid-producing proton pumps in the large colon.
Misoprostol, a synthetic form of prostaglandin E1, theoretically may prevent the worsening of clinical signs due to its cytoprotective and help the healing process.
Omeprazole/Misoprostol paste can treat both gastric and colonic ulcers at the same time.
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