Swallowing Disorders

Swallowing is a coordinated process consisting of three phases - oropharyngeal, esophageal, and gastroesophageal [1]. Swallowing disorders can be caused by a mechanical or anatomic lesion either intrinsic to the alimentary tract or by compression from adjacent structures, by a functional or neurologic disturbance, or secondary to pain (Table 25-1) [2]. The interruption to the normal coordinated sequence of swallowing may involve one or more of the contributing structures, including the muscles of the tongue, hyoid apparatus, soft palate, pharyngeal muscles, cranial esophageal sphincter, esophagus, and gastroesophageal junction [2].

Oropharyngeal Phase

The oropharyngeal phase of swallowing involves the prehension of food and formation of a bolus in the mouth and passage of the bolus into the cranial cervical esophagus. The oropharyngeal phase is subdivided into oral, pharyngeal, and cricopharyngeal stages [1]. These stages occur in rapid succession and can only be reliably differentiated by careful analysis of fluoroscopic studies. The oral stage is a voluntary process involving prehension and mastication of food, the formation of a bolus at the back of the tongue, and the delivery of the bolus into the pharynx. The pharyngeal stage is the first step of the involuntary phase of swallowing and is initiated by the delivery of a food bolus into the oropharynx. Pharyngeal constrictor muscles propel the bolus aborally to the cricopharynx. Contraction of the palatal and pharyngeal muscles closes the nasopharynx and prevents nasal reflux, while the epiglottis and adduction of the vocal folds close the larynx and prevent laryngotracheal aspiration. No obvious thickening occurs of the esophageal wall at the pharyngoesophageal junction to form a true cranial (or upper) esophageal sphincter. However, the cricopharyngeus and thyropharyngeus muscles and associated elastic tissue serve the function of a cranial esophageal sphincter. The cricopharyngeal stage of swallowing involves the relaxation of the cricopharyngeus and thyropharyngeus muscles and the delivery of the bolus into the cranial cervical esophagus. The oropharyngeal phase of swallowing is coordinated by cranial nerves V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), and XII (hypoglossal).

Oral dysphagia is caused by abnormalities in prehension or interference in the voluntary process of bolus formation at the base of the tongue. The tongue plays the dominant role during the oral phase of swallowing, milking fluid aborally against the hard and soft palates. Food should be maintained in midline; oral dysphagia often results in lateral deviation of food into the buccal folds and loss of food from the mouth. The diagnosis can normally be made on the basis of the history, physical examination, and evaluation of swallowing. Fluoroscopy is not usually required for diagnosis. When performed, the dynamic study will show a reduced ability to form a bolus, with normal transport of the bolus after it reaches the oropharynx. Many animals with oral dysphagia learn to compensate by modifying their eating behavior.

Pharyngeal and cricopharyngeal dysphagia produce similar clinical signs. Affected animals are able to prehend and chew normally; these actions are followed by several, partially successful attempts to swallow. The animals then become anxious, gag, and expel the food from their mouth by forward motion of the tongue. The cycle is then repeated until the entire meal is swallowed. The animals may have an associated nasal discharge and coughing caused by aspiration of food material into the nasal cavities and trachea. Homogenized food is usually easier to swallow than chunks; although, oddly, water may be more difficult to swallow than food [3].

Fluoroscopic examination of swallowing is needed to differentiate pharyngeal and cricopharyngeal dysphagias. In pharyngeal dysphagia, fluoroscopy demonstrates the absence of a strong aboral pharyngeal peristaltic contraction, resulting in incomplete bolus transport across the pharynx [4]. Associated reflux of contrast medium into the nasopharynx and laryngotracheal aspiration may occur. Cranial esophageal sphincter relaxation is proportionate to the size and consistency of the bolus delivered; therefore, pharyngeal dysphagia may result in a less pronounced relaxation of the sphincter compared with that in a normal animal. The deficient relaxation of the cricopharyngeal sphincter could result in an erroneous diagnosis of cricopharyngeal dysphagia. However, cricopharyngeal dysphagia is associated with vigorous contraction of the pharyngeal muscles, which causes distortion of the cricopharynx and/or transient pharyngeal outpouchings [4].

Cricopharyngeal dysphagia is characterized by either cricopharyngeal asynchrony or achalasia. Cricopharyngeal asynchrony is caused by an incoordination between contraction in the dorsal cranial and middle pharyngeal constrictor muscles (hyopharyngeus, pteryopharyngeus and palatopharyngeus muscles) and relaxation of the cranial esophageal sphincter. In dogs with cricopharyngeal asynchrony, the time interval between onset of swallowing (closure of the epiglottis) and maximum pharyngeal contraction is normal, but the time to opening of the cranial esophageal sphincter is significantly prolonged [5]. Cricopharyngeal achalasia is a lack of relaxation of the cranial esophageal sphincter during the cricopharyngeal stage of swallowing. It is observed less commonly than asynchrony [6] With both conditions, movement of the bolus into the caudal pharynx by movement of the tongue and pharyngeal constriction is normal. A thin stream of contrast medium may pass through the cranial esophageal sphincter. When the bolus of food in the cranial cervical esophagus is sufficient, primary esophageal peristalsis is initiated, and the food passes normally into the stomach. The food that does not pass through the cranial esophageal sphincter is expelled through the mouth, sometimes accompanied by nasal reflux and laryngotracheal aspiration.

Surgical management of cricopharyngeal dysphagia may be indicated. Surgery consists of a cricopharyngeal myotomy (incision of the cricopharyngeus muscle on dorsal midline of the larynx, sometimes accompanied by a partial or complete incision of the thyropharyngeus muscle) or myectomy. It is crucial to differentiate between pharyngeal and cricopharyngeal dysphagia as surgery can exacerbate signs of pharyngeal dysphagia [2]. Although it has been reported that surgery results in an immediate and continued resolution of all signs of dysphagia and nasal regurgitation in dogs with cricopharyngeal dysphagia [7], one study reported poor long-term results [8]. In the latter study, complete, long-term resolution of signs occurred in one dog, transient complete resolution (with recurrence of dysphagia at 2 to 36 weeks after surgery) occurred in 3 dogs, a permanent, partial resolution occurred in 3 dogs, and no improvement was noted after surgery in 6 dogs. The reason for this disparity may reflect a lack of long-term follow-up in some earlier reports. In individual cases, there may be a failure to transect all the bands of the cricopharyngeus muscle, an incorrect initial diagnosis, or concurrent pharyngeal or esophageal dysfunction [9]. A poor outcome may be seen in older dogs, dogs with concurrent aspiration pneumonia or malnutrition that is not addressed prior to surgery, or where cricopharyngeal dysphagia is complicated by other anatomic or functional conditions, such as myasthenia gravis, laryngeal paralysis, or esophageal stricture [8].

Esophageal Phase

Esophageal disorders are relatively common in the dog and cat. The entire length of the canine esophagus is composed of striated muscle, whereas the caudal one third to half of the feline esophagus is composed of smooth muscle. During normal swallowing, a food bolus is delivered to the cranial cervical esophagus through the relaxed cricopharynx. The bolus initiates a primary peristaltic wave in the esophagus, which propels the bolus aborally to the gastroesophageal junction. The transit time for the bolus from the cervical esophagus to the stomach is approximately 3 to 4 seconds [3]. Initiation of a primary peristaltic wave depends on the presence of a sufficiently large bolus distending the cervical esophagus; several swallows may be needed to produce a bolus that initiates a primary peristaltic wave. If the primary peristaltic wave fails to propel the bolus through the gastroesophageal junction, esophageal distention results in the generation of a secondary peristaltic wave. In normal animals, no significant amount of food should be retained in the esophagus at the end of eating.

The hallmark clinical sign of esophageal-phase dysfunction is regurgitation [3]. Regurgitation is the passive, retrograde expulsion of esophageal or gastric contents. Regurgitation, as distinct from vomiting, is characterized by minimal retching, minimal abdominal or thoracic muscle contraction, and the expulsion of a mucus-covered, sausage-shaped mass of food with a neutral or alkaline pH. Regurgitation may occur minutes to hours after eating. Other clinical signs may include weight loss accompanied by an increased appetite and signs of aspiration pneumonia.

Definitive diagnosis of esophageal-phase dysfunction is usually made by radiographic examination. Most esophageal-phase problems can be diagnosed by plain radiography or radiography following administration of a barium meal or liquid contrast medium.

The causes of esophageal-phase dysfunction can be broadly divided into mechanical or anatomic lesions, functional or neurologic disorders, and inflammatory conditions. Mechanical obstruction of the esophagus can result from the presence of a luminal or mural lesion or from compression from adjacent structures. Causes of mechanical obstruction include esophageal foreign bodies, strictures, neoplasms, vascular ring anomalies, hiatal hernias, and gastroesophageal intussusceptions. The presence of a mechanical obstruction results in a variable degree of obstruction of the esophagus. Esophageal obstruction results in the accumulation of food and secretions proximal to the obstruction and distention of the esophagus. Esophageal distention disrupts normal neuromuscular function and decreases peristalsis. The extent of distention of the esophagus proximal to the obstruction is the major determinant of long-term prognosis after successful relief of the obstruction.

Esophageal foreign bodies are a common problem in dogs and are occasionally diagnosed in cats. The most common foreign bodies in dogs are ingested bones. Esophageal foreign bodies most commonly lodge at the thoracic inlet, heart base, and caudal esophagus where extraesophageal structures restrict esophageal dilation [9]. Esophageal foreign bodies cause mechanical obstruction of the esophagus and can result in pressure necrosis and perforation of the esophageal wall.

Esophageal strictures are uncommon in dogs and cats. Acquired esophageal strictures are more common than congenital strictures. Acquired strictures result from severe, circumferential esophageal injury extending into the muscular layer of the esophageal wall. The damaged esophagus heals by fibrosis and wound contracture, resulting in a narrowed esophageal lumen and obstruction. The most common cause of acquired esophageal strictures in dogs and cats is esophageal reflux during anesthesia; other causes include chronic vomiting, ingestion of corrosive substances, thermal burns, radiation injury, foreign body ingestion, and surgery. The reader is referred to Vascular Ring Anomalies for more information on vascular ring anomalies and to Hiatal Hernia for more information on hiatal hernias.

Causes of functional or neurologic disorders of the esophagus include congenital megaesophagus, acquired megaesophagus, and dysautonomia.

Esophagitis can be acute or chronic. Causes of esophagitis in dogs and cats include swallowing caustic substances, esophageal foreign bodies, and gastroesophageal reflux.

Gastroesophageal Phase

Dogs have an increase in thickness of the circumferential striated muscle layer at the gastroesophageal junction, which correlates with the accepted location of the high-pressure zone at the gastroesophageal junction and may represent the anatomically ill-defined caudal (or lower or cardiac) esophageal sphincter [10]. Other proposed anatomic contributors to the lower esophageal high-pressure zone include the diaphragmatic crural muscles, the angle at which the esophagus and stomach meet and the folds of the gastroesophageal mucosa. It has also been suggested that the intra-abdominal portion of the esophagus is subjected to higher pressure than the intrathoracic portion, although one anatomic study found that the intraabdominal portion of the esophagus in dogs could not be consistently demonstrated [10].

The gastroesophageal phase is the final component of normal swallowing. As the peristaltic wave carries the bolus along the esophagus, the myenteric plexus mediates relaxation of the esophagus ahead of the bolus, permitting the passage of the bolus down the esophagus and through the gastroesophageal junction into the stomach. On fluoroscopic contrast examinations in normal dogs, the bolus of food will occasionally stop in front of the gastroesophageal junction and then enter the stomach with the following bolus. Reflux of food from the stomach into the distal esophagus also occurs occasionally; refluxed food is then carried by a secondary peristaltic wave through the gastroesophageal junction into the stomach [3]. In normal dogs, no food remains in the esophagus after completion of a meal.

Esophageal achalasia is a disease described in humans in whom a failure occurs of reflex relaxation of the gastroesophageal sphincter during swallowing. On thoracic radiographs in dogs with megaesophagus, the caudal thoracic esophagus narrows as it approaches the diaphragm and this "stenotic" appearance should not be misinterpreted as esophageal achalasia. Myotomy of the gastroesophageal sphincter is not recommended in cases of megaesophagus. In a single case report of a dog with apparent esophageal achalasia that responded to myotomy, the diagnosis was established by fluoroscopic contrast studies and was not confirmed by manometry [11].

Gastroesophageal reflux is a disorder involving reflux of gastrointestinal contents into the esophagus. The severity of the resulting esophagitis depends on the frequency and composition of the refluxed material. The combination of gastric acid, pepsin, trypsin, and bile acids can produce severe esophagitis. Gastroesophageal reflux is poorly documented in dogs and cats, and is probably under-diagnosed [12]. It is associated with chronic vomiting, disorders of gastric emptying, hiatal hernia, and anesthesia-induced decreases in the pressure of the lower esophageal high-pressure zone [12]. The reader is referred to Chapter 27 for more information on hiatal hernias.