A handful of common gastrointestinal (GI) diseases in dogs and cats are frequently misdiagnosed, either because they are tricky to diagnose or they are not considered in the first place. Make sure you remember to include the following diseases in your differential diagnoses lists for patients with the appropriate GI signs.

GASTROESOPHAGEAL REFLUX DISEASE

This disease is more common than we think in dogs but can be difficult to confirm. Reflux of gastric or duodenal material into the esophagus can cause esophageal ulceration. Affected patients often salivate, lick their lips, are anorectic, and vomit or regurgitate. The owners may mention halitosis, and the disease is common in brachycephalic dogs, possibly because of increased intrathoracic pressure from upper airway obstruction. Other causes of reflux esophagitis include general anesthesia, hiatal hernia, and persistent vomiting. Endoscopy, which reveals distal mucosal ulceration often with an open lower esophageal sphincter, is needed for a definitive diagnosis.

ATYPICAL ADDISON'S DISEASE

Atypical Addison's disease is thought to be more common than typical Addison's disease is. Suspect atypical Addison's disease in young dogs—especially female large-breed dogs—with unexplained waxing and waning anorexia or GI signs. Most patients present with nondescript signs of anorexia, vomiting, or, occasionally, regurgitation due to megaesophagus.

Complete blood count results in these dogs lack a stress leukogram, but the electrolyte concentrations are normal because of normal mineralocorticoid production. Atypical Addison's disease is diagnosed by performing an ACTH stimulation test and obtaining cortisol concentrations below the reference range pre- and post-ACTH administration, and treatment involves lifelong administration of physiologic doses of prednisone (0.2 mg/kg/day). Since some dogs may become mineralocorticoid-deficient and will require mineralocorticoid replacement, patients with atypical Addison's disease should be checked regularly by noting sodium and potassium concentrations on serum chemistry profiles.

Normal concentrations of endogenous glucocorticoids are important in maintaining gastric mucosal integrity, so an abnormally low glucocorticoid concentration may result in GI ulceration. Hypoadrenocorticism may also cause reversible megaesophagus in dogs. Treat gastric ulceration with H₂-receptor antagonists (e.g. cimetidine, 5 to 10 mg/kg orally or intravenously q.i.d.; ranitidine, 2 mg/kg orally or intravenously t.i.d.; famotidine, 0.5 mg/kg orally once or twice a day; or nizatidine [Axid—Lilly; 5 mg/kg/day orally]) or a proton pump inhibitor (omeprazole, 0.7 mg/kg/day orally), and administer sucralfate (0.5 to 1 g orally t.i.d. or q.i.d.).

BILIOUS VOMITING SYNDROME

This syndrome is seen commonly in dogs and rarely in cats as chronic intermittent vomiting of bile, usually with an empty stomach. Early morning vomiting of bile is often most characteristic. It is considered an idiopathic syndrome, possibly a primary hypomotility disorder, although it has been associated with giardiasis and inflammatory bowel disease.¹

Most patients respond to symptomatic treatment, often requiring only a late-evening meal. A gastric mucosal protectant (e.g. H₂–receptor antagonist, sucralfate, or antacid) or a prokinetic agent (e.g. metoclopramide, 0.2 to 0.4 mg/kg orally; cisapride, 0.1 mg/kg orally; or erythromycin, 0.5 to 1 mg/kg orally) given once in the evening can also be considered.

CLOSTRIDIAL DIARRHEA

Clostridial diarrhea is thought to be a common cause of antibiotic-responsive diarrhea in dogs. Clostridium perfringens is a normal enteric inhabitant, but some strains can produce an enterotoxin that causes GI signs. Affected dogs can have chronic, intermittent diarrhea, usually typical of large bowel diarrhea, though some may exhibit small bowel diarrhea.

Clostridial diarrhea can be difficult to diagnose since it is a normal enteric inhabitant. But examining a fecal sample at the onset of clinical signs may reveal large numbers (> 5/HPF) of clostridial spores (the spores are larger than most bacteria and are shaped like safety pins), and detecting fecal clostridial enterotoxin with a fecal ELISA may help confirm the diagnosis.

Long-term to lifelong antibiotic therapy may be needed for chronic cases. Tylosin (10 to 25 mg/kg orally once or twice a day) is a good choice and can be used long-term, if needed. Diets high in insoluble fiber or fermentable fiber may be beneficial as well. Prebiotics (containing fructooligosaccharides) and probiotics may also help.

DIETARY SENSITIVITIES

Dietary sensitivities are common in dogs and cats and may result from food allergy or food intolerance. Food allergy is an immunologically mediated reaction to a specific dietary antigen. Food intolerance results from an inability to digest food adequately or from a nonallergic-based reaction to a dietary substance (e.g. glutens). Diet-related diarrhea appears to resolve quickly—usually within one or two weeks with appropriate diet correction.

In cases of food allergy, eliminating the offending protein from the diet resolves the clinical signs, although it can be difficult to identify the offending protein.

Gluten enteropathy is classified as an intolerance to food. Gluten, which is found in cereal grains such as rye, wheat, barley, and oats, damages the intestinal mucosa in some dogs. Eliminating cereal grains from the diet resolves the clinical signs.

A conceptually ideal diet to use in animals with dietary sensitivities would be hypoallergenic; highly digestible; gluten-free; and low in fat, fiber, and lactose. In reality, low-fiber, highly digestible diets are usually recommended. High insoluble fiber diets often reduce digestibility and increase fecal bulk. However, adding a soluble fiber such as psyllium may help resolve small bowel diarrhea because it has water-holding properties and because fiber fermentation may alter the enteric flora.

David C. Twedt, DVM, DACVIM

REFERENCE

1. Twedt DC. Bilious vomiting syndrome. In: Tilley LP, Smith FKW, eds. The 5-minute veterinary consult. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2003;155-156.