Gastrointestinal motility disorders (Proceedings)

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Gastrointestinal motility disorders (Proceedings)

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Aug 01, 2008

Primary motility disorders of the gastrointestinal (GI) tract in the dog and cat are not well studied. We know how to identify the specific syndromes and in some cases provide treatment but the etiology of the problem is still a mystery. Primary causes of motility disorders of the GI tract include congenital and idiopathic megaesophagus, gastric retention/delayed emptying and idiopathic megacolon. There is genetic predisposition to some of these disorders as certain breeds are over-represented. Secondary motility disorders of the GI tract in the dog and cat are due to mechanical or functional causes. Causes of mechanical dysfunction include GI obstructions such as intussusceptions, strictures, tumors, foreign bodies and vascular ring anomalies. Functional causes include severe inflammation of the intestinal wall, reflux esophagitis, esophagitis, acquired megaesophagus, endocrine disorders such as Addison's and Hypothyroidism, metabolic disease, neuromuscular disorders, paraneoplastic syndrome, toxins, and drugs such as anticholinergics and narcotics. Diagnosis and treatment of these disorders varies with each different syndrome with secondary motility disorders having a better prognosis if the primary cause can be improved or resolved. Motility drugs can be of benefit but are still limited in ability to completely reverse GI motility disorders.

GI Motility Disorders of the Esophagus

Megaesophagus (congenital and acquired)

Congenital

Esophageal hypomotility is suspected as the cause of congenital megaesophagus. Dogs by far present with this syndrome more commonly than cats. Some patients have hypomotility due to delayed maturation of esophageal function that may or may not improve with age. Congenital myasthenia gravis may cause congenital megaesophagus however congenital myasthenia gravis does not usually respond to treatment. Breeds predisposed to congenital megaesophagus are Newfoundlands, Jack Russell terriers, Samoyeds, Springer spaniels, smooth fox terrier and the Shar pei. Most puppies and kittens begin to show signs of regurgitation at weaning when they are started on solid food about 4 weeks of age. Diagnosis is by thoracic radiography and/or an esophagram (barium study) showing a diffusely dilated esophagus throughout the cervical and thoracic esophagus. Other congenital conditions such as vascular anomalies (persistant right aortic arch) can also cause megesophagus and diagnosis is a dilated esophagus cranial to the heart.

Acquired

Most patients with acquired megaesophagus are idiopathic with no underlying cause identified. Mostly this disease is seen in the dog although the cat with dysautonomia syndrome can present with megaesophagus. Although the exact etiology of acquired megaesophagus is unknown it is suspected that there is a defect in the afferent neural pathway causing reduced responsiveness of the esophagus to distention thereby limiting peristaltic contraction. Most patients present as adults although acquired forms can occur in the young. Acquired megaesophagus with primary causes include acquired myasthenia gravis, hypothyroidism, hypoadrenocorticism, neuromuscular disorders such as botulism, polymyositis, polyradiculoneuritis, dysautonomia, bilateral vagal nerve damage, brainstem disease, lead toxicity and organophosphate toxicity. The most common and most treatable primary causes of acquired megaesophagus are acquired myasthenia gravis, hypoadrenocorticism and hypothyroidism. In all cases of acquired megaesophagus these diseases should be investigated with proper diagnostics to rule out a treatable condition. Diagnosis of acquired megaesophagus is thoracic radiograph and/or esophagram showing a diffusely dilated esophagus throughout the cervical and thoracic esophagus. Further diagnostic tests should include basic bloodwork (CBC, chemistry panel) and testing for myasthenia gravis (acetylcholinesterase receptor antibodies), hypoadrenocorticism (ACTH stimulation test) and hypothyroidism (TSH, TT4, FT4).

Treatment of Congenital and Acquired Megaesophagus

A common complication of megaesophagus is aspiration pneumonia due to frequent regurgitation of food and water. Aspiration pneumonia should be treated aggressively with intravenous broad-spectrum antibiotics, intravenous fluid therapy, nebulization and coupage. Megaesophagus without a primary cause is treated with elevated feedings of either gruel or meatball consistency of canned food giving small amounts frequently depending on the individual patient response and holding the dog in an upright position for 15 minutes after each feeding. Severe cases that regurgitate in spite of these feedings can have a permanent low profile gastrotomy tube placed and used for the rest of the dogs life. The most common cause of death in these patients is repeated aspiration pneumonia and owner request for euthanasia.