INTRODUCTION

Gastrointestinal (GI) motility disorders are common and are challenging to diagnose and treat in both humans and animals. Therapy is directed toward correcting predisposing factors and utilizing prokinetic drugs to promote normal GI motility.

MEGAESOPHAGUS

Congenital megaesophagus is seen in a number of breeds of dogs, including Wirehaired Fox Terriers, Miniature Schnauzers, German Shepherds, Great Danes, Irish Setters, Labrador Retrievers, Newfoundlands, and Chinese Shar Peis. It is rare in cats, but Siamese cats may be predisposed. Congenital megaesophagus in dogs is due to organ-specific sensory dysfunction, whereby the distention-sensitive vagal afferent system innervating the esophagus is defective, but other contiguous and physiologically similar distention-sensitive vagal afferent systems are unaffected.¹ Acquired megaesophagus can develop in association with a number of primary diseases in dogs and cats, but most adult-onset cases are idiopathic.² Myasthenia gravis accounts for most cases with a known cause. Other causes of acquired megaesophagus include hypoadrenocorticism, lead poisoning, lupus erythematosus, and severe esophagitis. Inflammatory myopathies associated with megaesophagus in dogs include immune-mediated polymyositis, infectious and preneoplastic myositis, and dermatomyositis. Dogs with peripheral neuropathies, laryngeal paralysis, myasthenia gravis, esophagitis, and chronic or recurrent gastric dilation with or without volvulus are at an increased risk of developing megaesophagus. German Shepherds, Golden Retrievers, and Irish Setters are at increased risk for acquired megaesophagus.² Although often cited as a cause, a clear link between hypothyroidism and megaesophagus can not be demonstrated.

Regurgitation is the predominant symptom associated with megaesophagus, and a careful history can help distinguish between passive regurgitation and active vomition. The frequency of episodes and relation to time of feeding vary considerably. Puppies with congenital megaesophagus typically begin regurgitating when started on solid foods. Emaciation from malnutrition and aspiration pneumonia are the most common complications of megaesophagus.

Plain survey radiographs are often diagnostic, but contrast radiography may be useful to confirm the diagnosis and evaluate motility. Endoscopy also confirms the diagnosis and can identify esophagitis, which often occurs in dogs with megaesophagus. Routine hematology, serum biochemistries, and urinalysis should be performed to investigate primary disorders that can result in secondary megaesophagus. Additional diagnostic tests for acquired megaesophagus include serology for nicotinic acetylcholine receptor antibody and antinuclear antibody, adrenocorticotropic hormone stimulation, serum creatine phosphokinase activity, electromyography and nerve conduction velocity, and nerve and muscle biopsies.

Treatment of congenital megaesophagus is symptomatic, because traditional prokinetic drugs such as metoclopramide and cisapride have no effect on the striated muscle of the canine esophagus. Because the incidence of esophagitis is high, affected animals should be treated with sucralfate (1 g q8h for large dogs, 0.5 g q8h for smaller dogs, and 0.25 g q8-12h for cats) or a histamine-2 blocker (cimetidine 5 to 10 mg/kg PO q8-12h; ranitidine 1 to 2 mg/kg PO q12h; famotidine 0.5 to 1 mg/kg PO q12h). Animals with secondary megaesophagus should be treated for the primary disease. Myasthenia gravis in dogs is managed with pyridostigmine (1 to 3 mg/kg PO q12h), prednisone (1 to 2 mg/kg PO q12h), or azathioprine (2 mg/kg PO q24h initially). Affected animals should be fed small amounts of a high-calorie diet at frequent intervals from an elevated position to allow gravity to assist passage into the stomach. The Bailey Chair (http://www.geocities.com/bailey_chair/) is an example of a positioning device that may be helpful. If unable to maintain adequate nutritional intake in this manner, a temporary or permanent gastrostomy tube can be placed.

GASTRIC EMPTYING DISORDERS

Dog and cats frequently have gastric emptying disorders from mechanical obstruction or defective propulsion.³ Defective propulsion is caused by abnormalities in myenteric neuronal or gastric smooth muscle function or antropyloroduodenal coordination. Primary problems associated with defective propulsion include infectious and inflammatory diseases, ulcers, and postsurgical gastroparesis. Delayed gastric emptying also occurs secondarily to electrolyte imbalances, metabolic derangements, drugs (cholinergic antagonists, adrenergic and opioid agonists), and peritonitis. In critically ill animals, delayed gastric emptying limits enteral nutrition, and the effects of severe disease further deplete caloric reserves, impairing wound healing, decreasing immune function, and increasing morbidity and mortality.⁴

The most common presenting complaint is chronic intermittent vomiting that occurs more than 8 hours after eating. Gastric distention may be discernible after eating and is relieved by vomiting. Additionally, some patients may have lost weight.

Although diagnosis and treatment of mechanical obstruction are straightforward, disorders of propulsion are more challenging. Other causes of chronic vomiting should be ruled out. Imaging studies are used to confirm delayed gastric emptying, the most common gastric motility disorder. Survey films, barium contrast studies, and fluoroscopy may all be used to document abnormal gastric emptying. Barium-impregnated polyspheres can be administered to measure the passage of various-sized beads. Endoscopy is used to rule out gastritis or obstructive disease. If no underlying cause is determined, a functional disorder of gastric emptying is diagnosed presumptively. Treatment consists of dietary modification and gastric prokinetic agents.³ Animals should be fed frequent small meals that are low in fat and protein and high in carbohydrates (e.g., cottage cheese, rice, pasta).

SMALL INTESTINAL TRANSIT DISORDERS

Causes of small intestinal transit disorders include enteritis, postsurgical ileus, nematode impaction, intestinal sclerosis, and radiation enteritis.⁵ Pseudoobstructions are functional obstructions caused by hypomotility and ileus; most are idiopathic. Intestinal stasis can result in bacterial overgrowth, and the absorption of endotoxin and bacteria can lead to endotoxemia and septicemia. Clinical signs depend on the location and cause of the disorder but typically include vomiting, diarrhea, and weight loss. Abdominal pain and distention may be noted.

With pseudoobstruction, survey radiographs show dilated bowel loops without evidence of a physical obstruction. Contrast studies or barium-impregnated polyspheres can demonstrate delayed transit through the small intestine. The hemogram findings are typically normal, but changes in the serum biochemical profile may be seen with protracted vomiting or diarrhea. Mechanical obstructions should be ruled out before treatment with prokinetic drugs. Additional therapy will be based upon the cause of the transit disorder and may include glucocorticoids and antimicrobial agents.