Clinical signs suggestive of esophageal disease include regurgitation, dysphagia, odynophagia, salivation, retching, gagging, and repeated swallowing. Other less specific signs can include weight loss, anorexia or ravenous appetite, and depression.
Clinical signs suggestive of esophageal disease include regurgitation, dysphagia, odynophagia, salivation, retching, gagging, and repeated swallowing. Other less specific signs can include weight loss, anorexia or ravenous appetite, and depression. Aspiration pneumonia, a frequent complication of esophageal disease, can cause fever, cough, tachypnea, and dyspnea. Most esophageal diseases in dogs and cats are diagnosed by the signalment, history, physical examination, survey thoracic radiography, barium contrast esophagraphy (“barium swallow”), and esophagoscopy.
Survey and static-image barium radiography are generally adequate for diagnosis of megaesophagus. Other functional motility disorders are best evaluated by a dynamic contrast imaging procedure (3-phase barium videofluoroscopy). Ancillary laboratory tests are useful for identifying underlying causes of esophageal hypomotility and acquired megaesophagus. Esophagoscopy is indicated in patients with regurgitation and dysphagia when radiography is inconclusive, and is most useful for diseases that disrupt the mucosa or obstruct the lumen; for example, foreign bodies, esophagitis, strictures, tumors, and gastroesophageal intussusception. Other specialized procedures for evaluating esophageal function include nuclear scintigraphy, manometry, pH monitoring, and electromyography, but these studies are difficult and not routinely performed in dogs and cats.
Regurgitation is the hallmark of esophageal disease and is defined as the passive evacuation of food or fluid from the esophagus. Regurgitation results primarily from local mechanical events within the esophagus and must be distinguished from vomiting, which is a centrally mediated reflex characterized by the active evacuation of gastroduodenal contents preceded by nausea, hypersalivation, retching, and abdominal contractions. The history should determine the age of onset of regurgitation, the duration of signs, the timing of regurgitation in relation to eating, and a description of the regurgitated material. Observations or videorecordings of eating and drinking behavior are helpful.
The timing of regurgitation in relation to eating is determined by the location of the esophageal abnormality, the degree of luminal obstruction, and the reservoir effect of esophageal dilation. Regurgitation immediately after eating is most likely to occur with esophageal obstruction, especially involving the cranial esophagus. Regurgitation may be delayed for hours with megaesophagus, diverticulum, and caudal obstructions, because the dilated esophagus provides a reservoir for prolonged retention of ingesta. The regurgitated material is usually composed of undigested food (often tubular), water, and frothy saliva. In comparison, vomitus usually consists of partially digested food mixed with yellow bile-stained fluid. Dogs and cats with megaesophagus usually regurgitate both solids and liquids. Tolerance of liquids but not solid foods is more typical of obstructive esophageal diseases. Halitosis can result from putrefaction of ingesta after prolonged retention in a diverticulum or dilated esophagus. Both regurgitation and vomiting can occur together in dysautonomia, hiatal hernia, gastroesophageal intussusception, and vomiting disorders complicated by secondary reflux esophagitis.
Dysphagia, odynophagia, and salivation
Dysphagia, or difficult swallowing, usually suggests the presence of oropharyngeal disease or cricopharyngeal sphincter dysfunction, but also can be seen with cranial esophageal diseases such as foreign body, stricture, or esophagitis. Dysphagia is characterized by repeated attempts to swallow with extension of the head and neck during swallowing, and is often accompanied by gagging, retching, odynophagia (pain on swallowing), and ptyalism (excessive salivation). Anorexia and unexplained salivation may be the only clinical signs in some patients with painful esophageal disease, especially esophagitis. Esophageal dysphagia and salivation must be differentiated from oropharyngeal dysphagia and salivary gland diseases, such as sialoadenitis and sialoadenosis.
Historical findings indicative of esophageal injury
The history is important for identifying potential causes of esophageal injury that could culminate in severe esophagitis or esophageal stricture, including esophageal foreign bodies, gastroesophageal reflux (secondary to general anesthesia, hiatal hernia, or malpositioned esophageal feeding tubes), acid or peptic injury from persistent vomiting, irritating oral medications (e.g., doxycycline, clindamycin), ingestion of corrosive chemicals, radiation injury, thermal injury from overheated (microwaved) food, and prior esophageal surgery. Esophageal foreign bodies are common, especially in small dogs (< 10 kg); for example, bones, chew toys, plastic, rubber, pins, needles, fishhooks, string, and partially vomited trichobezoars (especially in cats). Clinical signs of esophagitis ususally develop within 1 to 3 days following injury or an anesthetic procedure and include regurgitation, dysphagia, salivation, odynophagia, retching, gagging, and repeated swallowing. Mild esophagitis can be self-limiting and clinical signs may be subtle or absent. Severe esophagitis or foreign body impaction can lead to serious complications of esophageal necrosis, perforation, fibrosis, and stricture. Esophageal strictures result from deep circumferential injury of the esophagus that heals by intramural fibrosis, resulting in narrowing of the lumen and reduced distensibility. Regurgitation (solids more than liquids) from strictures usually begins within 1 to 4 weeks after the inciting esophageal injury.
Other clinical signs in esophageal disease
Weight loss and poor body condition can occur secondary to persistent regurgitation and inability to retain ingested food. An otherwise healthy animal with persistent regurgitation may have a ravenous appetite. This is common in animals with megaesophagus, vascular ring anomaly, and some esophageal strictures. In contrast, anorexia can occur in animals that have painful and difficult swallowing associated with severe esophagitis, stricture, esophageal foreign body, or neoplasia. Secondary aspiration pneumonia can result in anorexia, depression, cough, tachypnea, dyspnea, and fever.
Laryngeal paralysis (stridor and voice change) can be associated with acquired megaesophagus in dogs. Severe gastroesophageal reflux can cause signs of chronic laryngitis (stridor, voice change) from exposure of the larynx to gastric refluxate. Disorders of the esophageal hiatus (e.g. hiatal hernia, reflux esophagitis) can be complications of chronic obstructive airway conditions such as laryngeal paralysis and brachycephalic syndrome, presumably from enlargement of the esophageal hiatus and laxity of the surrounding support structures caused by abnormally negative intrathoracic pressure. Increased intraabdominal pressure associated with vomiting or blunt abdominal trauma can also cause hiatal hernia.
Age and breed associations
Young puppies and kittens that persistently regurgitate undigested food beginning shortly after weaning should be evaluated for vascular ring anomaly, congenital idiopathic megaesophagus, and congenital esophageal stenosis. The congenital form of megaesophagus is heritable in wire-haired Fox Terriers, Miniature Schnauzers and probably many other breeds. Increased prevalence of megaesophagus is reported in Irish Setters, Great Danes, German Shepherds, Labrador Retrievers, Newfoundlands, Chinese Shar-Peis, and Siamese cats. Acquired megaesophagus and oropharyngeal dysphagia can be associated with various types of myopathy (e.g., myasthenia gravis, muscular dystrophies, and polymyositis). Vascular ring anomalies have been reported in many breeds of dogs and cats, but German Shepherds, Irish Setters, and Labrador Retrievers appear to be at increased risk. Young Chinese Shar-Pei dogs are predisposed to congenital hiatal hernia. Bulldogs and other brachycephalic breeds with upper airway obstruction have a high prevalence of concurrent hiatal abnormalities, reflux esophagitis, esophageal deviation, gastroduodenal disease.
Megaesophagus and esophageal hypomotility
Megaesophagus is characterized by severe diffuse esophageal hypomotility and flaccid dilation of the esophagus. Primary megaesophagus is usually idiopathic and can be either congenital or acquired. Secondary megaesophagus results from an underlying neuromuscular disorder that causes esophageal hypomotility, and may be accompanied by weakness and atrophy of skeletal muscles or the presence of neurologic deficits (especially of cranial nerves. Dysautonomia, which is a generalized autonomic neuropathy that can cause of megaesophagus, is suggested by mydriasis and loss of pupillary reflexes, decreased tear production, dry mucous membranes, bradycardia, dysuria, decreased anal tone, and diarrhea or constipation. The signs of megaesophagus are persistent regurgitation, weight loss, and poor body condition. Young dogs and cats with congenital megaesophagus may have stunted growth. Palpation of the ventral cervical region near the thoracic inlet may identify esophageal distention. Depression, fever, cough, tachypnea, dyspnea, mucopurulent nasal discharge, and abnormal pulmonary auscultation can indicate complicating aspiration pneumonia.
In megasophagus, survey thoracic and cervical radiographs are usually diagnostic of a severely enlarged esophagus distended with air, fluid, or food. Alveolar lung opacity may indicate complicating aspiration pneumonia. If survey radiographs are inconclusive, a static-image barium contrast esophagram can confirm the esophageal dilation. Radiography also helps rule out other causes of regurgitation, such as foreign bodies, diverticula, and obstructive diseases (e.g., vascular ring anomalies, strictures, tumors, periesophageal masses). Megaesophagus in young animals must be differentiated from vascular ring anomaly; i.e., persistent right aortic arch (PRAA). In PRAA the esophagus becomes entrapped and constricted circumferentially by the ligamentum, aorta, and base of the heart. Survey and barium radiographs usually show a focal dilation of the esophagus cranial to the heart as compared to the diffuse dilation seen in megaesophagus. Extreme distension of the cranial thoracic esophagus may form a diverticulm in some cases. A characteristic leftward deviation of the trachea near the cranial border of the heart is a consistent finding in PRAA on VD or DV radiographs. Extralumenal compression of the esophagus in PRAA can also be seen endoscopically.
The diagnosis of esophageal motility dysfunction in animals without overt megaesophagus requires barium swallow videofluoroscopy to assess the intensity and coordination of peristalsis and the coordinated functioning of the sphincters. Continuous videofluoroscopic recording of swallowing provides a dynamic evaluation of the oropharyngeal, esophageal (both primary and secondary peristalsis), and gastroesophageal phases of swallowing. Sequential 3-phase contrast videofluoroscopy can be performed in the unsedated animal using barium liquid, barium paste, and barium-soaked food (kibble, canned, or both). Sternal positioning may be preferable to lateral positioning for videofluoroscopic evaluations of swallowing and esophageal transit. Abnormal findings can include cricopharyngeal sphincter dysfunction, abnormal propulsion (absence or lack of intensity of peristalsis), gastroesophageal sphincter (GES) dysfunction (including reflux), and lack of coordination between the motor phases of swallowing. Diffuse or segmental esophageal hypomotility can also occur secondary to esophagitis, hiatal hernia, and obstructive esophageal lesions, such as strictures, vascular ring anomalies, and leiomyomas.
Esophagoscopy is less reliable than radiography for confirming megaesophagus, but it can help rule out obstructive causes of esophageal dilation (e.g., vascular ring anomalies, strictures, tumors) and evaluate for secondary esophagitis. Esophageal motility and lumen size are difficult to assess with endoscopy because the normal esophagus becomes flaccid and dilated with general anesthesia and insufflation of air. The typical endoscopic appearance of megaesophagus is a markedly dilated, flaccid esophagus throughout its entire length, with variable amounts of saliva, fluid, and food residue in the lumen. On initial insertion of the endoscope the normal esophagus in a fasted animal is usually empty, so a motility, hiatal, or obstructive disorder should be suspected when the esophagus contains a pool of fluid and ingesta. Megaesophagus must be differentiated from segmental dilations or sacculations that develop cranial to obstructions caused by vascular ring anomalies, strictures, tumors, or periesophageal masses. A diverticulum of the cranial thoracic esophagus sometimes develops as a complication of chronic megaesophagus. The esophageal mucosa in megaesophagus is usually normal in appearance, except when putrefaction of retained ingesta results in erosive esophagitis.
Megaesophagus is often idiopathic, but this is a diagnosis of exclusion. Megaesophagus can also occur secondary to various underlying neuromuscular disorders that impair esophageal motility, such as myasthenia gravis, polymyositis, muscular dystrophy, other polymyopathies, peripheral neuropathies, central nervous system disease, dysautonomia, botulism, tick paralysis, tetanus, anticholinesterase toxicity, lead toxicity, hypoadrenocorticism, and possibly hypothyroidism. Appropriate diagnostic testing may be needed to rule these out. In addition to a neurologic exam, a minimum database should include serum electrolytes, creatine kinase (CK), thyroid panel, and baseline cortisol (followed by ACTH stimulation if indicated). Evaluation of a serum acetylcholine receptor antibody titer for acquired myasthenia gravis is especially important, even in the absence of generalized muscle weakness, because focal myasthenia can account for 25% of acquired canine megaesophagus cases. Other tests can include EMG, skeletal muscle biopsy with immunohistochemistry, nerve conduction, nerve biopsy, and toxin assays.
Esophageal diverticula are large pouch-like sacculations of the esophageal wall that interfere with the orderly movement of ingesta through the esophagus. Diverticula can be identified by radiography or endoscopy. Survey thoracic radiographs show the air-, fluid-, or food-filled esophageal sacculation or pouch, and contrast radiography demonstrates pooling of barium in the diverticulum. Diverticula are usually seen in the cranial mediastinal and epiphrenic regions of the esophagus. Most diverticula are acquired pulsion diverticula that result from increased intraluminal pressure and food impaction associated with esophageal injury (esophagitis), hypomotility (megaesophagus), or obstruction (e.g., vascular ring anomaly, foreign body, stricture, and tumor). When an acquired diverticulum is identified radiographs should be evaluated carefully for an underlying cause. Traction diverticula from external traction and distortion of the esophagus caused by periesophageal inflammatory adhesions are rare. Congenital diverticula also are rare. On contrast radiographs a redundant flexure or deviation of the esophagus at the thoracic inlet is a common incidental finding in clinically normal brachycephalic and Chinese shar-pei dogs and should not be mistaken for a diverticulum. These false diverticula lack pooling of food and fluid and they decrease or disappear with extension of the neck.
In esophageal diverticulum, esophagoscopy reveals a saclike outpouching of the esophageal lumen, often with erosive esophagitis of the mucosa that lines the diverticulum. Food, fluid, or hair may have to be removed from the diverticulum before it can be adequately visualized. If a diverticulum is small, the only obvious finding may be a focal pooling of fluid. Because of the thin, weakened wall of the diverticular sac, caution must be used to avoid perforation.
Hiatal hernia and dysmotility of the gastroesophageal sphincter (ges)
Hiatal hernia is a congenital or acquired protrusion of a portion of the stomach through the esophageal hiatus of the diaphragm, which can be the result of congenital or acquired laxity in the hiatal opening. Clinical signs are often intermittent and attributable to secondary reflux esophagitis caused by displacement of the GES into the thorax. A sliding hiatal hernia, which is most common, is a cranial displacement of the abdominal segment of the esophagus, gastroesophageal junction, and cardia region of the stomach through the esophageal hiatus of the diaphragm into the thorax. Paraesophageal hiatal hernia is rare and occurs when a portion of the stomach (usually the fundus) herniates through the hiatus into the caudal mediastinum alongside the caudal thoracic esophagus. Idiopathic reflux esophagitis also can occur independent of hiatal hernia, presumably from dysmotility and incompetence of the GES.
Hiatal hernia and gastroesophageal intussusception are usually identified on survey thoracic radiographs as a fluid- or gas-filled soft tissue mass (the stomach) in the dorsocaudal mediastinum cranial to the hiatus, but only if the stomach is displaced at the time of the radiograph. The normal gastric gas bubble seen in the cranial abdomen may be smaller and displaced. A contrast esophagram usually confirms the presence of hiatal hernia. The gastroesophageal junction and gastric rugae are visible cranial to the diaphragm. Gastroesophageal reflux of barium is sometimes identified. Hiatal hernias that are small and reduce spontaneously are a diagnostic challenge because of their intermittent nature and unknown clinical significance. Applying pressure on the abdomen at the time of exposure may induce herniation at the hiatus. Fluoroscopy improves the chances of identifying an intermittent hernia and episodic reflux.
Endoscopic findings indicative of hiatal hernia include: pooling of fluid or ingesta in the caudal esophagus; enlargement of the esophageal hiatal opening; dilation and cranial displacement of the GES into the thorax; rugal folds of the stomach protruding through the hiatus into the caudal thorax as viewed from the esophageal and gastric retroflex positions; and, evidence of reflux esophagitis in the caudal esophagus (erythematous or erosive streaks radiating from the GES accompanied by a wide open sphincter). A pseudo-pouch can be seen if the stomach is herniated at the time of insertion of the endoscope. This effect is created by narrowing of the lumen as the scope advances through the cranially displaced gastroesophageal junction followed by a dilated region of the lumen lined by rugal folds, representing the intrathoracic portion of the stomach lumen.
Gastroesophageal intussusception is an invagination of the stomach into the lumen of the caudal esophagus. Like hiatal hernia, it can be a consequence of laxity of the esophageal hiatus and may occur intermittently. It is often a complication of esophageal hypomotility or megaesophagus. Barium esophagram and endoscopy can confirm rugal folds of the invaginated stomach forming an obstructing intralumenal mass that fills the caudal thoracic esophagus.