Gastrointestinal motility disorders caused by esophageal disease

dvm360dvm360 December 2020
Volume 51
Issue 12

Esophageal diseases are an important cause of dysmotility and regurgitation in dogs and cats. Here’s what you should know about these disorders.

Gastrointestinal (GI) motility disorders are challenging for many veterinary practitioners, in part because they are caused by a range of conditions affecting the esophagus to the colon. This article focuses on esophageal diseases implicated in motility disturbances.

Check out the July 2020 issue of Vetted®, where Jergens outlined appropriate diagnostic evaluation and treatment options for disturbances throughout the GI tract.

Overview of esophageal disease

Numerous diseases influence esophageal structure and function, and can cause clinical signs in dogs and cats, especially regurgitation. Broadly speaking, esophageal disorders can be grouped into motility disturbances (eg, megaesophagus [ME], hiatal hernia, diverticula), obstruction (eg, esophageal foreign body, stricture, neoplasia), and esophageal inflammation (eg, esophagitis, fistula). Primary structural/inflammatory disorders of the esophagus, including esophagitis, stricture, and gastroesophageal (GE) reflux, can result in diffuse or segmental dysmotility and clinical signs of esophageal disease, including regurgitation, dysphagia, odynophagia, and vomiting.

Is it vomiting or regurgitating?

Classically, patients that regurgitate do not retch and do not have premonitory signs (eg, salivation, repeated swallowing, anxiety). Regurgitation is a passive process in which the patient lowers the head and food, fluid, and/or saliva exits by means of gravity alone. The food, saliva, or white froth may be undigested, cylindric in appearance, and will not contain bile. Importantly, regurgitation may occur before, during, or several hours after meal ingestion.

Vomiting is an active neural reflex involving response to 4 major inputs:

  • Higher central nervous system (CNS) center: increased CNS pressure or intracranial disease
  • Vestibular input: idiopathic or in response to motion
  • Chemoreceptor trigger zone: common with bloodborne toxins or metabolites
  • Visceral afferents that are stimulated by abdominal irritation, inflammation, or distension: common

Animals often have premonitory signs before they vomit, and the vomitus may or may not contain bile, blood, or digested food.

History and signalment

A careful patient history is crucial in cases of suspected esophageal disease to determine whether the patient is vomiting or regurgitating (see Is it vomiting or regurgitation?). Once it has been established that a patient is regurgitating, then the focus of the diagnostic workup is on establishing the cause of esophageal disease.

Signalment can provide some clues about the underlying problem. In young dogs that regurgitate, persistent right aortic arch and congenital ME should be high on the list of rule-outs. If the onset of regurgitation and dysphagia is acute, foreign body should be considered in the differential diagnosis. For clinical signs lasting several weeks, esophagitis and esophageal stricture would be potential causes of regurgitation. Chronic regurgitation would be more indicative of ME, chronic esophagitis, or stricture formation. It is also important to remember to ask clients about any oral medications the patient might be taking. Cats are exquisitely sensitive to drug-induced (eg, doxycycline, clindamycin) esophagitis.

Other disorders, including hiatal hernia, esophageal diverticula, and chronic esophagitis, may be associated with esophageal dysmotility, so it is important to diagnose and treat these conditions specifically. Cats with dysautonomia commonly present with a history of progressive anorexia, weight loss, constipation, regurgitation, and/or vomiting. Abnormalities observed on physical examination in these cats are unique and include dilated and unresponsive pupils, prolapsed nictitating membranes, distended urinary bladder, dry mucous membranes, absent anal tone, bradycardia, and reduced lacrimation.

Diagnostic evaluation

The diagnostic workup for esophageal disease relies heavily on radiology and endoscopy (ie, esophagoscopy), which provide complementary information in many cases. Routine lab work (complete blood cell count, biochemical profile, and urinalysis) should also be performed to assess overall health status and rule out metabolic/systemic diseases as a cause of clinical signs. In many cases, routine lab results will be normal. The cause may be acquired, particularly in ME cases, and specialized testing (eg, thyroid panel/corticotropin stimulation test, toxin screen, acetylcholine receptor antibody titer) can be helpful. Urinalysis can assess for pathologic proteinuria seen with immune-mediated diseases. Chemistry panels can help to evaluate skeletal muscle inflammation where serum creatine kinase may be elevated. Because the canine esophagus is composed entirely of skeletal muscle, it may be affected by several immune-mediated disorders, including acquired myasthenia gravis (MG), muscular injury, and inflammatory myositis.

Diagnostic imaging is a very important tool, and 2 radiographic views (lateral and ventrodorsal) should always be taken to fvisualize the entire length of the esophagus. When survey films are inconclusive, barium contrast procedures (esophagram) aid in identifying structural/functional disturbances to the esophagus.

Esophageal obstruction

Vascular ring anomaly, such as persistent right aortic arch, can cause extraluminal esophageal obstruction. A diagnosis of vascular ring anomaly is suspected based on supportive history (intolerance to solid foods at weaning) and thoracic radiography. When performing a barium contrast esophagram, a persistent right aortic arch will appear as a constriction over the base of the heart with dilation of the esophagus observed cranial to the extraluminal compression. Surgery is the preferred therapy; however, residual defects in esophageal motility may persist despite corrective surgery. In these instances, the prognosis is guarded due to continued esophageal dysfunction.

Foreign bodies in the esophagus are also problematic because they cause mechanical obstruction and mucosal trauma that may result in serious consequences, including esophagitis, localized dysmotility, and perforation. The incidence of esophageal foreign bodies is considerably lower in cats than in dogs. Diagnosis in both species is based on the combination of esophageal signs and a history of foreign body ingestion. Thoracic radiography with or without contrast will detect the presence of esophageal foreign body. Esophagoscopy confirms the diagnosis and permits endoscopic removal of the foreign body in most instances (Figure 1).

Figure 1. Large bone foreign bodies obstructing the mid-esophageal lumen in a 1-year-old mixed-breed dog. The bones were removed successfully by esophagoscopy.

Esophageal stricture

Esophageal stricture is a pathologic narrowing of the esophageal lumen (Figure 2). Strictures may be congenital (rare) or acquired secondary to severe mucosal injury. Most strictures are acquired through chemical injury from swallowed substances, thermal injury from ingestion of hot foods, intraluminal trauma (eg, esophageal foreign body), GE reflux causing severe esophagitis, complications of esophageal surgery, and intraluminal (neoplasia) or extraluminal (abscess, granuloma) mass lesions.

Figure 2. Mid-esophageal stricture in a 2-year-old cat. The cat had undergone elective surgery 3 weeks prior to presentation and likely refluxed under general anesthesia, causing severe esophagitis and eventual stricture formation.

Clinical signs of progressive regurgitation and dysphagia are related to the rapidity and severity of the luminal narrowing. Survey thoracic radiographs fail to identify esophageal strictures. Contrast radiography is required to delineate the number and location of strictures within the esophagus. Mild benign strictures may be managed medically by feeding a semi-liquid diet to provide adequate nutrition. In animals with severe stricture, a gastrostomy tube may be placed at the time of esophageal dilation to provide continuous enteral nutritional support. Esophageal strictures are best managed by mechanical dilation using balloon catheters (Figure 3).

Figure 3. Balloon dilation of an esophageal stricture in a cat. A fixed balloon catheter is correctly positioned to apply radial dilation pressure to the strictured site.

Gastroesophageal reflux

GE reflux is likely more common than clinically recognized.1 It is composed of various gastric fluids, including pepsin, pancreatic enzymes, and bile salts, all of which irritate the esophageal mucosa and may cause injury. Clinical signs of GE reflux can include regurgitation, salivation, neck extension, and odynophagia. Repeated reflux episodes, either secondary to vomiting or caused by defects (reduced tone) in the lower esophageal sphincter (LES), contribute to esophageal mucosal injury but are difficult to detect radiographically. Esophagitis resulting from GE reflux is an endoscopic diagnosis made by visualizing erythema, mucosal erosions, GE reflux, and/or increased friability with acute injury to the esophagus (Figure 4), whereas chronic esophagitis is characterized by granular surface texture, white areas of fibrosis, and strictures.

Figure 4. Severe esophagitis due to foreign body ingestion and persistent gastroesophageal reflux in a 9-year-old dog. Note the severe erythema and erosive lesions present in the distal esophagus.

Esophagitis is often a presumptive diagnosis with initial treatment aimed at removing the underlying cause (ie, GE reflux), if possible. There is clear evidence that treatment with proton pump inhibitors (PPIs), such as omeprazole, provides superior gastric acid suppression compared with histamine-2 (H2) receptor antagonists (eg, ranitidine, famotidine) for acid-related esophagitis. One strategy to reduce the severity of anesthetic-associated GE reflux is to administer 2 oral doses of omeprazole 18 to 24 hours and again 4 hours before anesthetic induction. Pretreatment with cisapride (if available) also may reduce GE reflux by promoting gastric emptying and increased LES pressure. Sucralfate is a mucosal protectant that binds to damaged mucosa and provides physical protection from acid-peptic disease. There is no evidence that combining sucralfate with either a PPI or an H2 receptor antagonist for treatment of esophagitis is superior to use of PPIs alone.

Hiatal hernia

Hiatal hernia is a protrusion of the abdominal viscera, most often the cardia and fundus of the stomach, through the esophageal hiatus into the caudal mediastinum. Dogs and cats with hiatal hernia present with regurgitation, hypersalivation, vomiting, and odynophagia. The diagnosis is based on findings from survey thoracic radiography and contrast radiography, including fluoroscopy. Imaging shows the presence of an air- or fluid-filled, often oval-shaped, soft tissue opacity within the caudodorsal thoracic cavity (Figure 5).Esophagoscopy confirms the presence of esophagitis with cranial displacement of the LES and an enlarged esophageal hiatus. Among dogs, Shar-Peis are congenitally predisposed to this problem.2

Figure 5. Esophagram, lateral thoracic radiograph. Classic hiatal hernia in a 3-year-old dog showing cranial displacement of the stomach through the esophageal hiatus.

Medical and surgical therapies are available for hiatal hernia. Medical treatment is generally pursued first and includes a combination of acid suppressants (eg, twice-daily oral omeprazole), prokinetics (eg, metoclopramide or cisapride to increase LES tone and stimulate gastric empting), and cytoprotective agents (eg, sucralfate as a diffusion barrier agent).


Key points

Esophageal dysmotility has a variety of causes, some of which are idiopathic.

  • In dogs and cats, esophageal dysmotility may occur secondary to esophagitis.
  • Thoracic radiography and endoscopy are complementary diagnostic tools. Endoscopy also provides therapeutic options, including removal of esophageal foreign bodies, balloon dilation of strictures, and placement of enteral feeding tubes.
  • The severity of esophageal dilation with ME does not relate to the severity of GI signs.
  • Aspiration pneumonia is a common sequela of esophageal diseases. Dorsoventral thoracic radiographs are the most sensitive in detecting abnormal lung patterns.
  • A creatine kinase test should be performed to evaluate for esophageal muscular injury seen with myositis or neuromuscular injury.
  • An acetylcholine receptor antibody titer should be performed to rule out acquired myasthenia gravis as a cause of megaesophagus.
  • Patients with megaesophagus carry a guarded to poor prognosis.
  • Often, clinicians can treat animals through an ME medical crisis, but clients become frustrated with recurring regurgitation, aspiration pneumonia, and the poor quality of life of their pets.

ME is generalized esophageal dilation with hypomotility (lack of primary peristaltic waves).3 It is common in dogs but rare in cats. ME can be idiopathic or acquired, and due to primary or secondary causes. History and physical examination findings can be variable. ME is characterized by severe diffuse esophageal dilation with hypomotility. Weight loss, anorexia, lethargy, pulmonary crackles, and secondary aspiration pneumonia may be identified in some patients. Other animals may have a ravenous appetite because they cannot hold down their food.

Clinical signs of cough, wheezing, and dyspnea may also be observed secondary to aspiration pneumonia. Often, the initial discovery of a dilated esophagus occurs when screening the thorax for respiratory disease. Other associated disorders seen with ME include neuromuscular diseases and acquired MG in dogs, and acquired MG and dysautonomia in cats.3

Congenital ME, which is rare, is thought to cause hypomotility due to delayed maturation of esophageal function. Congenital idiopathic ME has been reported in cats with pyloric dysfunction. Acquired MG may cause localized clinical signs of ME and regurgitation with or without generalized weakness. Esophageal dysmotility can also occur in association with other disorders, including dysautonomia, GE reflux, hiatal hernia, esophageal stricture, acquired MG, and mediastinal masses (eg, thymoma, lymphoma).3

Regurgitation is the most common clinical sign associated with ME in dogs, with frequency varying from intermittent to several episodes per day.3 In cats, ME is associated primarily with MG, causing generalized weakness as the predominant clinical sign. Physical examination in animals with MG may reveal excessive salivation, regurgitation or dysphagia, weight loss, and generalized muscle weakness.

Radiographically, the esophagus may be dilated with air, ingesta, fluid, or all of these (Figure 6). Two views should always be obtained to identify any areas of localized aspiration pneumonia. Motility patterns can be investigated with fluoroscopy, where the presence of primary and secondary peristalsis is assessed using barium contrast alone and mixed with food.

Figure 6. Lateral thoracic radiograph demonstrating idiopathic adult-onset megaesophagus in an 8-year-old dog. The whole esophageal body is uniformly and grossly distended with air.

Treatment of idiopathic ME is largely supportive and focuses on meeting the nutritional needs of the patient while managing secondary complications such as aspiration pneumonia.3 For pets that are willing to eat, clients should choose the dietary consistency (ie, kibble vs gruel vs wet food) that best minimizes regurgitation episodes. In debilitated animals, placement of a percutaneous endoscopic gastrostomy tube ensures access for enteral nutrition. Empiric antimicrobial therapy is indicated for patients with aspiration pneumonia. Cisapride therapy may be beneficial in stimulating distal esophageal motility in cats but has no effect on esophageal muscle stimulation in dogs. Medical therapy for acquired MG involves use of pyridostigmine and/or glucocorticoids depending on the clinical response and serial measures of acetylcholine receptor antibody titers.

Albert E. Jergens, DVM, PhD, DACVIM, AGAF, is an internist and holds the Donn E. and Beth M. Bacon Professorship in Small Animal Medicine and Surgery, and serves as associate chair for research and graduate studies, in the Department of Veterinary Clinical Sciences at Iowa State University College of Veterinary Medicine.


  1. Marks SL, Kook PH, Papich MG, Tolbert MK, Willard MD. ACVIM consensus statement: Support for rational administration of gastrointestinal protectants to dogs and cats. J Vet Intern Med. 201;32(6):1823-1840. doi:10.1111/jvim.15337
  2. Callan MB, Washabau RJ, Saunders HM, Kerr L, Prymak C, Holt D. Congenital esophageal hiatal hernia in the Chinese shar-pei dog. J Vet Intern Med. 1993;7(4):210-215. doi:10.1111/j.1939-1676.1993.tb01009.x
  3. Washabau RJ, Day MJ, eds. Canine and Feline Gastroenterology. Elsevier; 2013.
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