Any process that causes a thickening of the wall of the large colon may interfere with absorption of fluid and result in chronic diarrhea, weight loss, and sometimes hypoproteinemia. Thickening may be due to neoplasia, inflammatory cells (such as lymphocytes, plasma cells, macrophages, or eosinophils), or scar formation from previous acute colitis.
Rectal palpation may help detect bowel thickening and mesenteric lymphadenopathy. Abdominal fluid cytology may reveal neoplastic cells. Ultrasonography can be used to determine the degree of thickening of the bowel wall (if the affected area of bowel can be imaged) and may reveal masses in the liver or spleen or on the peritoneal surfaces; a percutaneous biopsy could provide a histopathologic diagnosis of neoplasia or inflammatory cell infiltrate. A biopsy of the rectal mucosa and duodenal mucosa (via 3-m endoscope) may be beneficial in diagnosis of inflammatory bowel disease and should also be cultured for Salmonella. Full-thickness jejunal, cecal, and colonic biopsies are more reliable for diagnosis of inflammatory bowel disease ( see Inflammatory Bowel Disease in Horses Inflammatory Bowel Disease in Horses This collection of diseases includes granulomatous enteritis (GE), lymphocytic-plasmacytic enterocolitis (LPE), multisystemic eosinophilic epitheliotropic disease (MEED), and idiopathic focal... read more ) and can be obtained surgically either by standing flank laparotomy or recumbent ventral midline celiotomy. Surgical exploratory laparotomy can provide valuable information but is expensive and involves substantial risks of poor postoperative healing because of hypoproteinemia.
Treatment of abdominal neoplasia or inflammatory bowel disease is often unrewarding, but sometimes remission of clinical signs can be obtained with dexamethasone, especially with inflammatory bowel disease. Improvement of clinical signs and laboratory parameters with high-dose dexamethasone (0.1 mg/kg/day) treatment has been reported in three horses with clinical signs of GI tract lymphoma of T-cell origin. In two horses, the high-dose dexamethasone was followed by a lower dose (0.01–0.95 mg/kg/day) once clinical improvement occurred. Favorable responses persisted for >9 mo. The third horse had to be maintained on the higher dose of dexamethasone throughout treatment, because signs recurred whenever the dose was lowered. Clinical signs recurred despite high doses of dexamethasone, and after 2 mo of treatment the horse was euthanized. The mechanism of action of the steroid is speculated to be control of inflammation associated with the condition, as opposed to glucocorticoid-induced apoptosis.