Robert G. Sherding, DVM, DACVIM
Esophagitis is characterized by acute or chronic inflammation of the esophagus resulting from mechanical, corrosive, or acid-peptic injury to the mucosa. Mild esophagitis may be self-limiting or resolve with medical treatment.
Esophagitis is characterized by acute or chronic inflammation of the esophagus resulting from mechanical, corrosive, or acid-peptic injury to the mucosa. Mild esophagitis may be self-limiting or resolve with medical treatment. Severe esophagitis can lead to serious complications of esophageal necrosis, perforation, fibrosis, and stricture formation. Esophageal strictures result from deep circumferential injury of the esophagus and healing by intramural fibrosis, which results in a narrow, restrictive lumen.
The potential causes of esophagitis and esophageal stricture include: esophageal foreign bodies, gastroesophageal reflux (secondary to general anesthesia, hiatal hernia, or malpositioned esophageal feeding tubes), acid-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 (Gualtieri 2001; Han 2003; Sellon 2003; Gualtieri 2006; Willard 2009; Jergens 2010). Esophagitis can also occur secondary to putrefaction of ingesta and secretions that accumulate in the esophagus in animals with megaesophagus, vascular ring anomaly, and diverticula. Other rare causes include eosinophilic eosophagitis and esophageal infections (Pythium, Candida, and Spirocerca lupi).
Esophageal foreign bodies are common causes of esophagitis, especially in small dogs (< 10 kg); e.g., bones, chew toys, plastic, rubber, pins, needles, fishhooks, string, and partially vomited trichobezoars (in cats) (Ryan 1975; Houlton 1985; Spielman 1992; Michels 1995; Rousseau 2007; Leib 2008; Gianella 2009). Most esophageal foreign bodies lodge at the thoracic inlet, base of the heart, or GES, which are the least distensible regions of the esophagus. Depending on the type of object, its size and shape, and the length of time it is in contact with the mucosa, foreign bodies can injure the esophageal mucosa during passage or through impaction and pressure necrosis when they become entrapped. Foreign bodies with sharp edges and points, especially bones, can become deeply embedded and lacerate or even perforate the esophagus, and with time tightly wedged objects can cause circumferential pressure necrosis. In cats, large trichobezoars that are expelled from the stomach during vomiting may become lodged in the esophagus causing severe erosive esophagitis and stricture formation, presumably through the effects of pressure and prolonged mucosal contact with gastric acid and pepsin absorbed into the impacted hairball (Sherding 2011). In one report, 5 of 60 dogs (12%) with moderate to severe foreign body-induced esophagitis subsequently developed strictures (Rousseau 2007). Esophageal foreign body obstruction caused by dental chew treats resulted in strictures in 6 of 25 dogs (24%) in another report (Leib 2008).
Causes of reflux esophagitis include general anesthesia, GES dysfunction (e.g., hiatal hernia, tumors involving the GES), and abnormal gastric retention associated with delayed gastric emptying. Acid-peptic esophagitis secondary to persistent vomiting or hypergastrinemia (gastrinoma) has a similar pathogenesis. Reflux esophagitis in hiatal hernia is attributable to displacement of the GES into the thorax. Idiopathic reflux esophagitis in some dogs and cats is presumably the result of GES incompetence and dysmotility. Esophageal damage caused by GE reflux is primarily attributed to prolonged mucosal contact with refluxed gastric acid, digestive enzymes (pepsin, pancreatic proteases), and bile acids. The severity of reflux injury to the esophagus depends on the frequency, composition, and contact time of the reflux. Overall, 65% of esophageal strictures in dogs and cats occur following general anesthesia (Galatos 1994; Harai 1995; Melendez 1998; Leib 2001; Adamama-Moraitou 2002; Wilson 2004; Bissett 2009). This is presumably due to the reflux of gastric contents associated with relaxation of the GES and the delayed clearance of the refluxate from the esophagus in the anesthetized animal.
Corrosive injury to the esophagus can result from several oral medications and ingested chemicals. The severity of the injury depends on chemical concentration, pH, duration of contact with the mucosa, and distribution of the lesion (e.g., focal vs. diffuse injury). Oral tablet and capsule medications with high acidity, especially doxycycline and clindamycin in cats, can cause severe focal esophagitis and strictures (Melendez 2000; McGrotty 2002; German 2005; Trumble 2005; Beatty 2006). The corrosive effects of these medications is worse in cats because of the slower esophageal transit in cats and prolonged esophageal retention and mucosal contact time when tablets or capsules are administered as a “dry swallow” (Graham 2000; Westfall 2001). Ingested chemical irritants are usually concentrates that have highly acidic, alkaline, or oxidant properties. This should be suspected when esophagitis is accompanied by stomatitis and oropharyngeal ulcerations (mucositis). Examples include chlorine granules, button batteries, and undiluted quaternary ammonium disinfectants such as benzalkonium chloride that cats can lick from their paws and haircoat (Bilbrey 1989; Hofmeister 2006).
The clinical signs of esophagitis usually develop within 1 to 3 days following an anesthetic procedure or mucosal injury, and include regurgitation, dysphagia, odynophagia, retching, gagging, repeated swallowing, and salivation (Sellon 2003; Jergens 2010). In mild esophagitis, clinical signs may be subtle or absent. Nonspecific lethargy, anorexia, salivation, and vague discomfort may precede the onset of regurgitation. Dysphagia (difficulty swallowing) is characterized by exaggerated attempts to swallow with the head and neck extended, and is often accompanied by gagging, retching, odynophagia (pain on swallowing), and excessive salivation. Vomiting and regurgitation can occur together when esophagitis is caused by hiatal hernia or persistent vomiting. A finding of oropharyngeal irritation accompanied by signs of acute esophagitis suggests ingestion of a corrosive substance.
An esophageal stricture should be suspected when regurgitation develops within 1 to 4 weeks of a potential inciting esophageal injury, e.g., anesthesia, vomiting, or ingestion of a foreign object or corrosive medication or substance. The clinical signs of stricture, which are attributable to esophageal obstruction and inflammation, include regurgitation, odynophagia, hypersalivation, dysphagia (solids more than liquids), and weight loss (Harai 1995; Melendez 1998; Leib 2001; Adamama-Moraitou 2002; Bissett 2009; Willard 2009). The appetite is often good or even ravenous because of inability to swallow food past the strictured area. Regurgitation often occurs shortly after eating, while liquids are preferentially retained. Regurgitation can be delayed after eating in caudal thoracic strictures because the spacious dilated esophagus cranial to the obstruction acts as a food reservoir. Depression, fever, cough, tachypnea, dyspnea, mucopurulent nasal discharge, and abnormal pulmonary auscultation can indicate complicating aspiration pneumonia.
In esophagitis, survey thoracic radiographs are usually unremarkable except for the occasional presence of small amounts of air in the esophagus. In some cases the underlying cause of esophagitis is identified (e.g., foreign body, hiatal hernia, or caudal esophageal mass with Spirocerca lupi). In hiatal hernia the displaced stomach may be identified as a mass in the dorsocaudal mediastinum cranial to the hiatus. Contrast esophagrams are normal in mild cases, but the mucosal surface may appear irregular with secondary hypomotility in severe cases. Segmental narrowing of the lumen can result from spasticity, intramural edema, and focal indistensibility caused by inflammation, which can be difficult to differentiate from a developing stricture. Contrast videofluoroscopy is helpful for identifying episodic gastroesophageal reflux or intermittent hiatal herniation that can cause esophagitis.
The diagnosis of esophageal stricture can be confirmed by barium contrast radiography of the esophagus or esophagoscopy. Survey radiographs are often normal unless the esophagus is distended with food, fluid, or air cranial to the stricture. Barium contrast radiography usually confirms the site of the stricture and reveals dilation of the esophagus cranial to the stricture site. Radiographs may not be able to differentiate a fibrous stricture from severe focal inflammation or neoplasia.
Esophagitis is an endoscopic diagnosis based on mucosal abnormalities that can include hyperemia, increased friability, ease of bleeding when rubbed by the endoscope tip, granular surface texture, accentuated folding, erosions, ulcers, focal necrosis, pseudomembranes, pale white areas of fibrosis with indistensibility, strictures, and GES abnormalities (Gualtieri 2001; Han 2003; Sellon 2003; Gualtieri 2006; Willard 2009; Sherding 2011). Inflammatory lesions in the caudal thoracic esophagus are indicative of reflux esophagitis, especially linear erythematous streaks and erosions radiating from the GES accompanied by a wide open sphincter and pooling of gastrointestinal contents (food, fluid, or bile) in the distal esophagus. Reflux of gastric contents may be observed during endoscopy. In reflux esophagitis microscopic inflammation and epithelial changes may be evident before abnormalities can be seen with an endoscope, so if chronic reflux injury is suspected, mucosal biopsies should be taken adjacent to the GES to identify hyperplastic, dysplastic, and metaplastic epithelial changes.
Esophagoscopy is the most reliable method for diagnosis of esophageal stricture and for determining the luminal diameter, stricture length, and presence of associated esophagitis. Approximately 80 to 90% of strictures in dogs and cats are located in the intrathoracic esophagus, especially between the heartbase and gastroesophageal junction. The degree of narrowing varies, but the luminal diameter averages 5 mm. The stricture length averages 1 cm, but it can vary from a thin band, web, or ridge of fibrotic tissue to a segmental narrowing up to 10 to 15 cm in length. Single strictures are found in 80% of patients, but diffuse esophagitis can result in 2 or 3 strictured areas in some animals.
A narrowed region of the esophagus that fails to distend with insufflation and impedes passage of the endoscope is usually the first indication of a stricture. Most strictures appear as focal circumferential narrowings formed by smooth, glistening-white, fibrotic rings or ridges (Harai 1995; Melendez 1998; Leib 2001; Adamama-Moraitou 2002; Bissett 2009). Occasionally strictures form a web or imperforate membrane across the lumen. Concurrent esophagitis in 40% of cases causes the adjacent mucosa to be erythematous, hemorrhagic, friable or ulcerated. With chronicity (weeks), contraction of deep fibrotic tissue can distort the tubular axis of the esophagus, causing the lumen to appear angular or spiral shaped rather than tubular. The degree of dilation of the esophagus cranial to the stricture depends on the duration and extent of obstruction. Benign strictures must be differentiated from other causes of esophageal obstruction, such as neoplasia or extraluminal compression caused by a vascular ring anomaly or periesophageal mass. Mucosal biopsy is recommended to determine if an atypical appearing stricture is benign or malignant.
Medical management of esophagitis
Esophageal inflammation decreases gastroesophageal sphincter (GES) tone and esophageal motility. This results in a vicious cycle whereby decreased GES tone promotes GE reflux, and decreased esophageal motility impairs normal peristalsic clearance, which prolongs mucosal contact with refluxate (acid, enzymes, bile salts) and worsens the esophagitis. Therefore once esophagitis occurs from any cause, it may be perpetuated by GE reflux.
To reduce the potential for further damage from reflux of gastric acid, a proton pump inhibitor (e.g., omeprazole; 0.7-1.0 mg/kg q24h PO) is given to control acid secretion, and a prokinetic, e.g., cisapride (0.5 mg/kg q8h PO) or metoclopramide (0.4 mg/kg q8h PO), is given to decrease reflux by promoting gastric emptying and enhancing GES tone. Sucralfate suspension (100 mg/kg q8h PO, up to a maximum of 1 gram) can be added as a mucosal protectant. Some authors recommend a broad-spectrum antibiotic (e.g., amoxicillin clavulanate) to control bacterial colonization of the injured mucosa. The efficacy of systemic corticosteroids for preventing fibrosis and stricture formation is controversial and not well supported with evidence; however, some authors have recommended oral prednisone or prednisolone (1 to 2 mg/kg/day for the first 3 weeks and then tapered over the next 2 to 3 weeks) in the medical management of their stricture patients. If intralesional triamcinolone is given at the time of stricture dilation, then systemic corticosteroids should not be needed. Corticosteroids should not be given to animals with aspiration pneumonia. Percutaneuous endoscopic gastrostomy (PEG) tube feeding is sometimes used to bypass the esophagus in patients with severe mucosal injury and in patients that are unable to tolerate food intake without persistent dysphagia, odynophagia, and regurgitation.
Endoscopic-guided balloon dilation and bougienage of strictures
Diagnostic esophagoscopy is usually followed by endoscopic-guided mechanical dilation of the stricture using either balloon catheter dilation or bougienage. These procedures result in a favorable outcome in 70 to 88% of stricture patients, based on ability to eat softened or solid food and drink water with minimal dysphagia or regurgitation (Harai 1995; Melendez 1998; Leib 2001; Adamama-Moraitou 2002; Bissett 2009). Serious complications of stricture dilation occur in 5 to 10% of patients, including moderate to severe mucosal tearing, hemorrhage, and perforation. The dilation procedure can be performed with either endoscopic or fluoroscopic guidance. Esophagoscopy enables visual assessment of the extent of the stricture, visual guidance of the balloon dilator or bougie into the stricture lumen, and then immediate reassessment of the esophagus following dilation. Esophagoscopy also allows identification of associated esophagitis and underlying predisposing causes of stricture formation (e.g., gastroesophageal reflux, hiatal hernia).
Inflatable balloon catheters dilate strictures by radial stretch forces on the esophageal wall, whereas bougies exert longitudinal shearing forces. Studies comparing these two techniques in human stricture patients have found them to be equally safe and effective. In dogs and cats, an overall favorable outcome of 70% to 88% is reported with balloon catheter dilation (Harai 1995; Melendez 1998; Leib 2001; Adamama-Moraitou 2002) compared with 71% for bougienage (Bissett 2009). In both balloon dilation and bougienage the likelihood of success of dilation is not influenced by the cause, duration, location, or initial luminal diameter of the stricture (Leib 2001; Bissett 2009). The presence or absence of concurrent esophagitis also does not affect overall outcome, but cases with esophagitis might require more dilations. The complication rates are also similar for both dilation techniques.
Endoscopic balloon dilation uses a set of balloon dilators that are either passed through the endoscope channel (through-the-scope type; TTS) or advanced over a guide wire (over-the-wire type; OTW) with endoscopic guidance. Controlled Radial Expansion Balloon Dilators (CRE™; Boston Scientific/Microvasive) are designed to provide pressure-controlled diameters with minimal “waisting” at the point of contact with the stricture. Various balloon sizes (6 to 30 mm) accommodate animals of varying sizes and strictures of varying diameters, and enables incremental increases in dilation diameter. Balloon dilators are intended for a single use in people; however, they are readily reused several times in animal patients. To inflate the balloons to the specified pressure, a balloon inflator with integrated pressure gauge (Alliance II® Integrated Inflation Device; Boston Scientific/Microvasive) is also needed.
A variety of protocols for balloon dilation have been reported, however, definitive guidelines have not been established for (1) the initial balloon size (dilation diameter), (2) the optimal final dilation diameter, (3) the optimal hold-time for each balloon inflation, (4) the number of sequential dilations per session, (5) the total number of dilation sessions, (6) the interval of time between repeated dilation sessions, (7) ancillary procedures during dilation, or (8) postdilation treatment. The number of repeat dilation sessions required and interval between sessions is variable. In most studies the median number of dilation sessions has been from 2 to 4; however, some patients have been successfully treated with 1 dilation session and others have required 10 or more. General guidelines for the final dilation endpoints are 10 to 12 mm for cats and small dogs weighing < 8 kg; 12 to 16 mm for dogs weighing 8 to 20 kg; 16 to 20 mm for dogs weighing 20 to 40 kg; and 20 to 30 mm for dogs over 40 kg. Ancillary procedures that have been used empirically to augment the stricture dilation procedure include intralesional injection of triamcinolone into the stricture site, endoscopic-guided laser or electrosurgical incision of the stricture ring, and application of mitomycin-C to the stricture site as an antifibrotic agent.
Bougienage involves the passage of a lubricated rigid or semi-rigid mechanical dilator or bougie through the stricture. The sequential passage of progressively larger bougies results in stretching and dilation of the stricture. A variety of bougies are available, including metal olive bougies and tapered, wire-guided Savary-Gilliard dilators. Various sized diameters of these devices are needed to incrementally dilate the stricture lumen. Bougies have either rounded tips or tapered ends, and their bases are wider than their tips. The narrow tip is advanced into the stricture lumen, and the widest part of the bougie dilates the stricture as it is advanced. A retrospective analysis of bougienage for treating esophageal strictures in 28 dogs and cats used wire-guided Savary-Gilliard dilators, which are available as sets of bougies sized in 1 mm increments from 5 to 20 mm in diameter (Cook Medical) (Bissett 2009).
In patients undergoing stricture dilation, adjunctive therapy for esophagitis (see Medical Management section) should be instituted during the series of dilations and continue for 2 to 3 weeks after the last procedure.
Stenting of esophageal strictures
Intraluminal stenting is emerging as a potential palliative intervention for esophageal strictures in patients that fail with repeated dilations (>5 to 10) to maintain a luminal diameter sufficient to allow eating and drinking without frequent regurgitation.
Adamama-Moraitou K. K., et al (2002). Can J Vet Res 66: 55-59. Beatty JA, et al (2006). J Feline Med Surg 8: 412-419.
Bilbrey SA, et al (1989). J Am Anim Hosp Assoc 25: 31-34.
Bissett SA, et al (2009). J Am Vet Med Assoc 235: 844-850.
Galatos AD, et al (1994). J Small Anim Pract 35: 638-642.
German AJ, et al (2005). J Feline Med Surg 7: 33-41.
Gianella P, et al (2009). J Small Anim Pract 50: 649-654.
Gibson CJ, et al (2010). Vet Pathol 47: 116-119.
Glanemann B, et al (2008). J Feline Med Surg 10: 505-509.
Graham JP, et al (2000). Am J Vet Res 61: 655-657.
Gualtieri M (2001). Vet Clin North Am 31: 605-630.
Gualtieri M, et al (2006). J Am Anim Hosp Assoc 42: 65-70.
Han E, et al (2003). J Am Anim Hosp Assoc 39: 161-167.
Harai BH, et al (1995). J Vet Intern Med 9: 332-335.
Hofmeister AS, et al (2006). J Am Vet Med Assoc 229: 1266-1269.
Houlton JE, et al (1985). J Small Anim Pract 26: 521.
Jergens AE (2010). Textbook of Veterinary Internal Medicine. SJ Ettinger; Elsevier: 1487-1499.
Leib MS, et al (2001). J Vet Intern Med 15: 547-552.
Leib MS, et al (2008). J Am Vet Med Assoc 232: 1021-1025.
McGrotty YL, et al (2002). J Small Anim Pract 43: 221-223.
Melendez LD, et al (1998). Eur J Comp Gastroenterol 3: 31-36.
Melendez LD, et al (2000). Feline Pract 28: 10.
Michels GM, et al (1995). J Am Vet Med Assoc 207: 1194-1197.
Richter, K (2009). ACVIM Forum, Montreal, Canada.
Rousseau AJ, et al (2007). J of Veterinary Emergency and Critical Care 17: 159-163.
Ryan WW, et al (1975). J Am Anim Hosp Assoc 11: 243-249.
Sellon RK, et al (2003). Vet Clin North Am 33: 945-967.
Sherding RG, et al (2011). Small Animal Endoscopy, 3rd Ed. TR Tams, Elsevier: 41-96. S
pielman BL, et al (1992). J Am Anim Hosp Assoc 28: 570-574.
Trumble C. (2005). J Feline Med Surg 7: 241-242.
Westfall DS, et al (2001). J Vet Intern Med 15: 467-470.
Willard MD, et al (2009). Current Veterinary Therapy XIV. JD Bonagura, Elsevier: 482-486.
Wilson DV, et al (2004). J Am Anim Hosp Assoc 40: 455-460.