Chapter 21 Regurgitation
Regurgitation is the most important clinical sign of esophageal disease and should be differentiated from dysphagia and gagging of more proximal gastrointestinal disorders, and from vomiting of more distal gastrointestinal disorders. Regurgitation differs from vomiting in that it is characterized by the passive retrograde evacuation of undigested food from the esophagus. Vomiting is characterized by coordinated activities of the gastrointestinal, musculoskeletal, and nervous systems culminating in active evacuation of digested or partially digested food from the gastrointestinal tract.1 Vomiting usually signifies disease caudal to the gastroesophageal sphincter. Severity of clinical signs with esophageal disease is dependent upon the pathogenesis of the disease. For example, animals with vascular ring anomaly may have severe regurgitation, but the appetite is usually excellent because of secondary malnutrition. On the other hand, animals with inflammatory esophageal disease may have anorexia, dysphagia, odynophagia (pain on swallowing), and salivation without much evidence of regurgitation. The latter group clearly presents a diagnostic challenge because of the differing clinical signs. For example, signs referable to aspiration pneumonia, coughing and dyspnea, may be the major presenting complaint in some animals. A good history usually elicits the other signs of esophageal disease in those patients.
Transport of ingested liquids and solids from oral cavity to stomach is the major function of the esophagus. Anatomic structures that permit this function are striated muscle of the cranial esophageal sphincter (cricopharyngeus), striated and smooth muscle of the esophageal body, and smooth muscle of the caudal esophageal (gastroesophageal) sphincter. An important species difference between dogs and cats is in the musculature of the esophageal body. The full length of the canine esophageal body is composed of striated muscle, whereas the distal one-third to one-half of the feline esophageal body is composed of smooth muscle. Striated muscle of the cranial esophageal sphincter and esophageal body is innervated by somatic branches (glossopharyngeal, pharyngeal, and recurrent laryngeal) of the vagus nerve arising from the brainstem nucleus ambiguus. Smooth muscle of the esophageal body and caudal esophageal sphincter is innervated by autonomic branches (esophageal) of the vagus nerve arising from the dorsal motor nucleus of the vagus (see Figure 13-1).2
Anatomic and physiologic differences in canine and feline esophagus have been highlighted in several previous studies.3–6 During fasting elevated pressures of the cranial and caudal esophageal sphincters prevent movement of food and chyme into the esophageal body from the oral cavity and stomach, respectively. When an animal swallows the cranial esophageal sphincter relaxes to permit movement of liquids and solids into the proximal esophageal body. Swallowing also initiates a wave of peristaltic contractions (primary peristalsis) in the esophagus that transports food into the distal esophageal body. Primary peristaltic contractions are reinforced by a secondary wave of contraction (secondary peristalsis) physiologically mediated by intraluminal distention. The caudal esophageal sphincter relaxes in advance of the propagated pressure wave to permit food to empty into the stomach. Once the bolus of food has passed into the stomach, the caudal esophageal sphincter resumes its high resting pressure.
Inflammation (esophagitis, gastroesophageal reflux, esophageal fistulae), hypomotility (idiopathic megaesophagus, dysautonomia, diverticula), and obstruction (stricture, hiatal hernia, neoplasia, intussusception, foreign bodies, vascular ring anomalies) are the major pathophysiologic processes involving the esophagus of dogs and cats.7 With mild esophagitis and hypomotility lesions, the esophagus may undergo healing without further complication. In more severe cases the esophagus may respond with extensive fibrosis, muscular hypertrophy, esophageal narrowing, and/or loss of neural regulation (i.e., flaccidity). Luminal flow is directly related to the fourth power of esophageal radius so that even small diminutions result in significant reductions in esophageal transit.
Esophagitis is an acute or chronic inflammatory disorder of esophageal mucosa that occasionally involves underlying submucosa and muscularis. It most often results from chemical injury from swallowed substances, esophageal foreign bodies, or gastroesophageal reflux. Esophageal mucosa has several important barrier mechanisms to withstand caustic substances, including stratified squamous epithelium with tight intracellular junctions, mucus gel, and surface bicarbonate ions. Disruption of these barrier mechanisms results in inflammation, erosion, and/or ulceration of the underlying structures.8
Gastroesophageal reflux is a disorder of the caudal esophageal sphincter permitting reflux of gastrointestinal fluids or ingesta into the esophagus. Varying degrees of esophagitis result from prolonged contact of gastric acid, pepsin, trypsin, bile salts, and duodenal bicarbonate with esophageal mucosa. The frequency of reflux and composition of the refluxed material determines the severity of the esophagitis. Gastric acid alone produces a mild esophagitis, whereas combinations of acid and pepsin or trypsin, bicarbonate, and bile salts produce a severe esophagitis.9
An esophageal fistula is an abnormal communication between the esophagus and adjacent structures. Most esophageal fistulae involve the lungs or airway structures (e.g., esophagopulmonary, esophagobronchial, or esophagotracheal fistulae). Occasionally, esophageal fistulae expand into the pleural space or cervical tissues.
Idiopathic megaesophagus is the most common cause of regurgitation in the dog.10 Aside from dysautonomia, megaesophagus is a rare finding in the domestic cat. The disorder is characterized by esophageal hypomotility and dilation, progressive regurgitation, and loss of body condition. Several forms of the syndrome have been described, including congenital, acquired secondary, and acquired idiopathic megaesophagus.
Dysautonomia is a generalized autonomic neuropathy that was originally reported in cats in the United Kingdom, but that has now been documented in dogs and cats throughout Western Europe and the United States.11,12 Clinical signs reflect a generalized autonomic dysfunction but megaesophagus, esophageal hypomotility, and regurgitation are fairly consistent findings. Pathologically, degenerative lesions are found in autonomic ganglia, intermediate gray columns of the spinal cord, and some sympathetic axons. No definitive etiology has ever been established despite an intensive search for genetic, toxic, nutritional, and infectious etiologic agents.
Esophageal diverticula are circumscribed sacculations in the esophageal wall that interfere with normal esophageal motility patterns. Both congenital and acquired forms have been described. Congenital diverticula have been attributed to abnormalities in embryologic development that permit herniation of mucosa through a defect in the muscularis. Acquired diverticula are subdivided into either traction or pulsion forms, depending upon pathogenesis. Traction diverticula tend to develop in the cranial and midesophageal body and result from periesophageal inflammation and fibrosis. Adhesions to adjacent tissue (e.g. lung, bronchus, lymph node) distort the esophageal lumen and create sacculations. Abscess development from grass awn migration is a common cause of traction diverticula in the western United States. Pulsion diverticula develop in association with increases in intraluminal esophageal pressure, abnormal regional esophageal motility, or when normal peristalsis is obstructed by a stenotic lesion.13