Esophagitis is much more common than many clinicians are aware. The difficulty partly arises from the fact that esophagitis can present with clinical signs that lead one to believe the dog is vomiting instead of regurgitating. Furthermore, mild esophagitis may only cause minor signs (mild regurgitation of mucus and phlegm) while severe esophagitis can cause so much pain that patients refuse to swallow water or even saliva. Because there can be so wide a range of clinical signs, it is easy to forget that esophagitis is a differential for a patient. It is critical to identify when severe esophagitis is present because delayed diagnosis can have serious clinical repercussions. Substantial inflammation of the esophageal mucosa causes muscular weakness by interrupting the reflex arcs within the esophagus and/or between the esophagus and the brain. However, this weakness is not always reflected by finding megaesophagus. Most patients have very minor esophageal distention and yet can have major signs. Likewise, barium esophagrams can have relatively minor changes and not reflect the severity of the esophagitis. Esophagoscopy typically shows an edematous, reddened, bleeding esophageal mucosa, ± structure formation, making it the diagnostic method of choice to find esophagitis. However, in rare cases, there may be more subtle changes with thickening and discoloration (especially at the lower esophageal sphincter of cats).
Adding to this problem is the fact that there is such a wide range of causes of esophagitis. Severe esophagitis may be caused by anesthetic procedures in which animals are placed in dorsal recumbency and then have gastric acid pool in their esophagus for relatively long periods of time. However, gastroesophageal reflux from any cause can be responsible. Hiatal hernias occasionally are responsible for such reflux. Rare animals ingest caustic substances (e.g., lye), and some cats will lick caustic disinfectants off their fur. However, a surprisingly large number of animals are administered caustic substances by veterinarians. In particular, tetracyclines, NSAIDs, ciprofloxacin, and clindamycin are recognized as having substantial potential to cause esophagitis. Pills and capsules are notorious for lodging in the esophagus of cats, and it is therefore not surprising that doxycycline is a recognized cause of esophageal stricture in cats. Esophagitis may also be secondary to any cause of protracted vomiting. In particular, parvovirus enteritis may cause such intense vomiting that esophagitis results. If a vomiting animal has the character of its vomitus change, which seems to suggest regurgitation, consider the possibility that esophagitis has occurred secondary to the persistent vomiting. Gastrinoma (a tumor which secretes gastrin and results in massive gastric acid secretion) also causes esophagitis because of the vast and unending amounts of acid the esophagus is exposed to as the dog continually vomits. Gastroesophageal reflux may be potentiated by or even caused by esophagitis (which may be caused by reflux in the first place). Thus, there may be a positive feedback loop which can be hard to break (i.e., esophagitis causes more reflux which causes more esophagitis which causes more reflux which causes...). Rarely there can be spontaneous inflammation, as seen with eosinophilic esophagitis in dogs. Brachycephalic dogs seem to have an increased incidence of gastroesophageal reflux, esophagitis, and perhaps hiatal hernia. Finally, esophageal foreign bodies typically cause varying degrees of esophagitis. The esophagus is far more susceptible to pressure necrosis from a foreign body than are the stomach or intestines.
You should seek to prevent further gastroesophageal reflux by keeping the stomach as empty as possible by using prokinetics such as metoclopramide or, preferably, cisapride. Studies in people show that cisapride is clearly more effective than metoclopramide. The only real advantage of metoclopramide is that it can be given by injection; a useful fact in animals that are regurgitating profusely. In addition, gastric acid secretion should be minimized and preferably abolished. H2 receptor antagonists (e.g., cimetidine, ranitidine, famotidine) suppress gastric acid secretion, but they do not eliminate it. This is because they are competitive inhibitors. That means that there is constantly some degree of competition between the H2 receptor antagonists and the stimuli for acid secretion. Omeprazole, lansoprazole, pantoprazole and esomeprazole are non-competitive inhibitors of gastric acid secretion. Therefore, these drugs can be noticeably more effective and for much longer than the H2 blockers.
Sucralfate is of uncertain value in patients with esophagitis. Unless there is some gastric acid reflux into the esophagus (which you are desperately trying to stop in the first place), it is doubtful that the sucralfate is of much use. If you use it, it should be administered as a slurry.
A combination of omeprazole and cisapride seems to be the most effective medical treatment regime. Antibiotics are used to treat secondary infections, but nobody really knows if they do anything in this regard. Glucocorticoids have been thought to help retard fibrous connective tissue proliferation and cicatrix, but their effectiveness is uncertain (and they might predispose to infection). Placing a PEG tube seems to have some real advantages in patients with very severe disease. First, we will then know that the cisapride and omeprazole tablets will reach the stomach. Second, we will also know that the animal will receive its caloric and protein needs, and hopefully with less irritation to the esophagus than would have occurred otherwise.
If there is severe esophagitis, cicatrix may form and obstruction develop subsequently. Diagnosis of stricture is best accomplished by esophagoscopy if the operator is familiar with such obstructions. It is surprisingly easy to pass a slender endoscope through a stricture and never recognize the stricture. It is also surprisingly easy to miss a partial obstruction due to a stricture with a barium esophagram. If you suspect a stricture and must use a barium esophagram to make the diagnosis, use barium mixed with solid food. Balloon dilatation or bouginage is recommended if a stricture has occurred. Many animals need to have 2–6 dilatation procedures (all the while being treated for esophagitis), although some only need one procedure and some need more than 15. Do not try to resect the stricture unless you have had prior dilatation procedures fail.
Cicatrix (i.e., scarring) may occur after an episode of severe esophagitis from any cause (including foreign objects). It is particularly easy to miss this problem on a barium swallow if only liquid barium is used. If radiographs using liquid barium are nonrevealing, repeat the study using barium mixed with food, which is more likely to stop at a partial obstruction. Endoscopy is very good at finding these lesions; however, you must keep in mind the size of the patient as you evaluate the esophageal lumen. A partial stricture will be very obvious in a 10-lb dog or cat but may not be apparent in an 85-lb animal. Balloon-dilatation or bouginage is usually effective; it is also more likely to be successful than surgery and resection of the affected area. In general, surgical resection should be a last ditch resort and only used if esophageal ballooning or bouginage has failed despite repeated dilatations. However, you must use proper esophageal balloons because Foley catheters and endotracheal tubes with inflatable cuffs will often not allow you to dilate a dense or mature stricture. More difficult cases (i.e., those with extensive strictures or with concurrent severe esophagitis) may benefit from a couple of techniques. Endoscopic administration of intralesional steroids may help minimize reformation of the stricture. Typically we put 1–2 ml of Vetalog® at the site of the stricture either before or after ballooning. Another technique is to make 3–4 equidistant cuts into the stricture using an electrocautery device (i.e., either a snare or a knife) prior to ballooning. This helps the stricture to "break" open at multiple spots with the idea that there will be 3 or 4 smaller, less deep lacerations at the stricture site instead of one major, deep laceration which is more likely to restricture. However, you should not attempt to use cautery through an endoscope unless you have some training less you cause too much trauma to the tissues or destroy your endoscopic equipment.
Another technique is to "paint" the site where the stricture was broken down with mitomycin C (not mithromycin C, there is a difference). A 5-mg bottle is reconstituted and soaked up into a gauze sponge. Then this sponge is endoscopically placed on the site where the stricture was broken up for 5 min. Then it is flushed off with 60 ml of water.
Finally, for particularly difficult cases, stents may be placed in the esophagus. These must be sutured in place. The major point to remember is that if an animal starts to have problems days to weeks after anesthesia, consider strongly the possibility that an esophageal stricture has developed secondary to esophagitis. If you are treating an esophageal stricture, remember that you may need to do 1–15 dilatations. If esophagitis is diagnosed, you need to treat it aggressively in order to help prevent the stricture from recurring quickly.
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