Esophageal disorders: Before you can stomach GI disease (Proceedings)

Disorders of the esophagus include inflammation (esophagitis), neuromuscular dysfunction (megaesophagus, dysautonomia), anatomical abnormalities (stricture, herniation), obstruction (foreign bodies, vascular ring anomalies, extraluminal masses), and neoplasia.

Regurgitation is the most common clinical sign of esophageal disease and discriminating between regurgitation and vomiting is an important initial step in the diagnostic process. Owners frequently assume that anytime something that had previously gone into their pet's mouth and now appears on their floor got there because their pet vomited. As long as the owner has actually witnessed the event, an accurate (and/or graphic!) description of the difference between the two processes should verify the form of expulsion in most cases, but not always. In lieu of an eye witness account, a description of a "tube-like" undigested mass of kibble appearing shortly after mealtime is considered highly suggestive of regurgitation. Unfortunately, although this is a classic description, it is also a rather rare one. At a referral hospital such as Colorado State University (CSU) we will occasionally be presented with a pet for a "GI work-up" that has already had several sets of abdominal radiographs, all reported as "normal abdomen". It is not until a particularly enthusiastic (and theatrical) veterinary student physically demonstrates the difference between vomiting and regurgitation to the owner (or when the critique of the previous radiographs begins, as it should, with an evaluation of those structures that are "not of interest", such as the caudal thoracic cavity), that the mystery is solved and the diagnostic efforts are modified appropriately. Other clinical signs that maybe associated with an esophageal disorder include ptyalism and dyspnea or cough, although these are obviously not specific. Physical examination rarely reveals esophageal dilation, but signs of systemic disease (weakness, neuromuscular abnormalities) maybe present.

It should also be kept in mind that not only can esophageal disorders go unrecognized by looking to far too soon (to the stomach and beyond), but dysphagia (difficulty swallowing), odynophagia (painful swallowing), repeated attempts at swallowing, or as one owner presented their pet's problem, "water coming out the nose", can be indicative of problems occuring before or because of an inability to effectively move either food or liquid from the oral cavity into the esophagus. Cricopharyngeal dysphagia is the most frequent swallowing disorder seen at CSU, and best appreciated with fluoroscopy. It is imperative that the distinction between Asynchrony and Achalsia be carefully considered as the therapeutic approach and prognosis can be quite different between the two forms.

Regurgitation is the most common clinical sign of esophageal disease and megaesophagus is the most common cause of regurgitation (Figure 1), so THORACIC, not abdominal radiographs are an essential initial diagnostic step in a regurgitating patient. Note; recent reports reveal that it is possible to have esophageal dysfunction, even an esophageal motility disorder, without radiographic evidence of a megaesophagus. In this case, fluoroscopy is an excellent tool for real-time evaluation of the movement (or lack thereof) of both liquid and solids from the oral cavity into the stomach. Gastroesophageal reflux disease (GERD) is a well established condition in humans but rarely diagnosed in our pet population; fluoroscopy is an excellent way to visualize abnormal movement of material from the stomach into the distal esophagus.

Figure 1

Idiopathic megaesophagus is the most common cause of regurgitation in the dog, with the condition being characterized as either congenital or acquired, and if acquired, either secondary or idiopathic. The congenital form is present at birth and often becomes clinically apparent shortly after weaning. It is an autosomal dominant trait in Miniature Schnauzers and Fox terriers, but otherwise appears most often in large breed dogs. It is rarely seen in cats.

Table 1

The most commonly diagnosed cause of acquired secondary megaesophagus is myasthenia gravis (Table 1), where megaesophagus maybe the only sign in the focal form of the disease. Other rule-outs include hypoadrenocorticism, lead poisoning, lupus myositis, and severe forms of esophagitis. Whether or not hypothyroidism is actually a cause of megaesophagus or simply present as a concurrent condition remains controversial, with several reports claiming resolution of megaesophagus following thyroid hormone supplementation, especially in Boxers.

Most cases of acquired megaesophagus in adult dogs are considered idiopathic, with no identifiable etiology. It is still extremely important to pursue a diagnostic work-up, including a minimum data base and, where indicated, specific tests for hypoadrenocorticism, myasthenia gravis, lupus, abnormal nerve conduction or muscle contraction, and again where indicated, thyroid evaluation. The importance of plain thoracic radiographs has already been established, as well as the utility of fluoroscopy. Barium studies can also be used to assess esophageal motility if fluoroscopy is unavailable. Endoscopy is the diagnostic tool of choice for visualizing inflammation of the esophagus, although it can be difficult to determine whether esophagitis is the cause, or the consequence of esophageal dysfunction.

Obviously, if an underlying cause is identified that cause should be specifically treated. In the absence of a treatable cause the challenge becomes effective management of the condition (providing nutrition) and its consequences (aspiration pneumonia). Dogs should be fed small frequent meals of a high-calorie diet from an elevated position. The consistency of the diet can be altered for each individual patient; some dogs appear to handle gruel while others seem to do better with small meatballs. In cases where it is impossible to provide adequate caloric intake orally, or where there have been repeated bouts of aspiration pneumonia, a low-profile gastrostomy feeding tube can be placed for use indefinitely. Prokinetic agents are unlikely to be of much benefit in these dogs, but an oral sucralfate suspension should be used in cases of active esophageal erosions or ulceration, and an antacid (proton pump inhibitor or H2-blocker) considered prophylactically to help lessen the damage done by stomach contents when they come into contact with esophageal tissue.

The prognosis for adult-onset acquired idiopathic megaesophagus is generally poor, with continued weight-loss and/or repeated bouts of aspiration pneumonia often leading to the euthanasia of these animals. In cases where an underlying cause is identified and treated, the prognosis is much better.

Esophagitis often manifests clinically as ptyalism, halitosis, reluctance to eat, or odynophagia. Esophageal tissue has much less ability to protect or repair itself than gastric mucosa, making early and accurate diagnosis especially important. Post-anesthetic esophagitis is more common than clinically appreciated, with patient age, preparation, and type of surgery (intra-abdominal) being important contributing factors. Unlike megaesophagus, plain thoracic films or barium studies are insensitive diagnostic tools for detecting esophagitis. As mentioned, endoscopy allows direct visualization and biopsy of inflamed esophageal tissue (although it can be difficult to obtain quality biopsy samples from the esophagus).

Esophageal rest, oral sucralfate suspensions, and antacids (omeprazole is preferred over H2-blockers in most cases of esophagitis) form the foundation of treatment for esophagitis.

Chronic or severe esophagitis is one cause of esophageal stricture formation. Other causes include administration of oral medications (doxycycline in cats for example), ingestion of caustic substances, esophageal foreign bodies or surgery, neoplasia, and gastroesophageal reflux (as described above in post-anesthetic patients). Regurgitation and dysphagia, along with many of the clinical signs discussed already maybe present, and a thorough history may reveal a likely inciting event (cats treated with "a pill" for upper respiratory disease, for example). Plain thoracic films may reveal dilation of the esophagus proximal to the stricture or a soft-tissue mass, and a barium study would provide a definitive diagnosis. At CSU we invariably perform plain thoracic films (also allows assessment for aspiration pneumonia) but often bypass a barium study in favor of direct visualization and evaluation with the endoscope if the history and clinical signs are consistent with an esophageal stricture. At CSU we treat esophageal strictures with balloon dilation and intra-lesional injections of triamcinolone, often accompanied by oral sucralfate and a short course of oral prednisone at an anti-inflammatory dose. Clinical resolution often requires multiple procedures as re-stricturing is a common complication, so consideration is given to early placement of a gastrostomy feeding tube to provide esophageal rest and adequate nutrition between endoscopic examinations/procedures. Esophageal perforation is a rare but life-threatening complication of esophageal stricture dilation and usually occurs at the time of the initial procedure or during one of the follow-up dilations.

Megaesophagus associated with dysautonomia will be covered in a separate presentation. Hiatal hernias and vascular ring anomalies are usually surgical conditions, and will not be described here. The endoscopic removal of esophageal foreign bodies is beyond the scope of this presentation, but these cases should be dealt with as an emergent condition. Esophageal neoplasia is extremely rare in cats and dogs, although interestingly it is frequently associated with Spirocerca lupi.

Drug dosages for megaesophagus