CHAPTER 95 Right Dorsal Ulcerative Colitis
Many horses with right dorsal ulcerative colitis (RDUC) are performance animals with a history of treatment with one or more nonsteroidal anti-inflammatory drugs (NSAIDs). No predilections associated with age, sex, or breed have been identified. The prevalence of RDUC in horses is unknown, but it appears to be low.
Right dorsal ulcerative colitis primarily affects the right dorsal segment of the colon, but it can affect other segments. It is characterized by mucosal ulceration of variable severity with thickening, inflammation, and edema of the underlying submucosa and lamina propria. Depending on the duration of disease, fibrosis may be evident and may be accompanied by development of intestinal strictures. Right dorsal ulcerative colitis has been associated with NSAID administration at higher than recommended doses but may also be seen in horses treated with appropriate doses of NSAIDs. Other factors that may increase the risk of RDUC in horses treated with NSAIDs include underlying inflammation of the colon, dehydration, and sepsis-endotoxemia. Individual variation in NSAID sensitivity may also affect the risk of developing RDUC. Although treatment with any NSAID may cause RDUC, most reported cases have been associated with phenylbutazone treatment. It is unclear whether this reflects a propensity for phenylbutazone to cause RDUC or the relatively common and often chronic use of this drug for musculoskeletal conditions in the horse.
The mechanism by which NSAIDs cause mucosal ulceration is via inhibition of cyclo-oxygenase (COX) activity and suppression of intestinal prostaglandin production. Nonselective NSAIDS such as phenylbutazone and flunixin that inhibit both COX-1 and COX-2 are more damaging to the gastrointestinal tract in general and likely to be a causative factor in RDUC than are selective COX-2 inhibitors such as firocoxib that spare the homeostatic and reparative prostaglandins produced by COX-1–dependent pathways. Prostaglandins are critical for maintaining epithelial integrity and repair following damage. Treatment with NSAIDs disrupts epithelial barrier function in both healthy and healing colon, resulting in increased permeability to microbial products, such as endotoxin. Absorption of microbial molecules potentiates an inflammatory reaction that worsens mucosal injury. Administration of NSAIDs may cause ulceration throughout the alimentary tract, and it is not clear why the right dorsal colon is a particularly susceptible site.
The most prominent clinical signs of RDUC are inappetence, lethargy, diarrhea, and colic. Moderate to severe colic, inappetence, signs of depression, diarrhea, fever, and signs of sepsis-endotoxemia characterize acute RDUC. Chronic RDUC is associated with weight loss, chronic intermittent colic and diarrhea, lethargy, inappetence, and ventral edema. Ventral and limb edema secondary to hypoproteinemia is a hallmark of the disease.
Clinicopathologic findings, although characteristic, are not often helpful in diagnosing RDUC. Peritoneal fluid analysis and cytologic examination may reveal nonspecific evidence of inflammation. Complete blood count may reveal neutropenia, neutrophilia, or hyperfibrinogenemia. Anemia is common, associated with either blood loss or chronic inflammation. Hypoalbuminemia is a hallmark of the disease and may be severe (serum concentration less than 1.5 g/dL). Hypocalcemia may be evident but usually reflects hypoalbuminemia; ionized calcium may be normal.
Presumptive diagnosis is usually made on the basis of clinical signs, laboratory findings, and a history of NSAID administration. Transabdominal ultrasonography (performed with a 3.5- to 5-MHz transducer in the right 12th to 15th intercostal spaces, below the margin of the lung and axial to the liver) may reveal mural thickening of the right dorsal colon (to greater than 0.5 cm) and evidence of colonic edema (Figure 95-1