Esophageal strictures

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Luminal esophageal obstruction is the most commonly diagnosed esophageal disorder in horses and is often caused by impaction with feed or bedding material[1].

Esophageal diverticula are a similar but unrelated eosophageal disease of horses.

Although resolution of esophageal impaction is most often achieved conservatively, internal esophageal trauma can cause considerable damage and ulceration of the mucosa[2]. Spontaneous healing of mucosal defects with conservative management consisting of administration of antibiotics and NSAIDs as well as feeding of soft feed has been reported[3]. However, because the healing process is thought to occur mainly by contraction fibrosis[4], stricture formation and significant reduction of the esophageal lumen may result, predisposing the horse to recurrent episodes of obstruction. Esophageal strictures can also be congenital or may occur after external neck trauma, as a sequela of previous esophageal surgery, or after esophageal rupture.

Based on the involvement of the different layers of the esophageal wall and the resultant location of fibrosis, esophageal strictures are categorized as follows:

  • Type I — Lesions involving the adventitia and tunica muscularis
  • Type II — Lesions involving only the mucosa and submucosa
  • Type III — Strictures involving all layers of the esophageal wall

Determination of the type of esophageal stricture is important because, to a certain extent, it dictates the type of surgical treatment and the prognosis. The proportion of the luminal circumference involved in the stricture is also an important prognostic factor because horses with mural strictures involving only a sector of the luminal circumference appear to have a more favorable prognosis with surgical treatment than horses with annular lesions that involve the entire circumference.

A diverticulum is a pocket- or balloon-like projection from the wall of a tubular structure. Esophageal diverticula in horses are acquired and represent local extensions of the esophageal lumen. Two types of diverticula can be differentiated. Traction (true) diverticula result from external traction on the esophageal wall due to periesophageal scarring. Periesophageal fibrosis may occur during healing of wounds external to the neck or after previous esophageal surgery, such as esophagostomy. Contraction associated with healing after esophageal perforation may also result in formation of a traction diverticulum. Traction diverticula are usually clinically asymptomatic and may represent incidental findings on contrast radiographs or during endoscopic examination. Pulsion (false) diverticula are caused by protrusion of esophageal mucosa and submucosa through a defect in the esophageal musculature. It has been hypothesized that damage to the muscle layers of the esophagus occurs because of external trauma[5] or pressure fluctuations in the esophagus, resulting in damage to the esophageal muscle fibers. High fluctuations in esophageal pressure can also occur as a result of obstruction of the esophagus with feed material1 or the use of excessive pressure to resolve a feed obstruction. However, external trauma to the cervical area can also result in formation of pulsion diverticula[6]. Pulsion diverticula most often require surgical treatment because they progressively enlarge, which, in turn, can result in recurrent esophageal obstruction due to extraluminal compression or in rupture and subsequent periesophageal inflammation and infection.


Horses with esophageal strictures usually present with a history of one or multiple episodes of esophageal obstruction. Alternatively, external trauma to the neck (e.g., a kick by another horse), previous esophageal surgery (e.g., esophagostomy), or esophageal rupture may have occurred. If obstruction is caused by an esophageal diverticulum, progressive swelling over the ventrolateral cervical area may be observed. Obstructive esophageal disease is manifested by distress; ptyalism; dysphagia; anorexia; repeated extension of the neck; coughing; and regurgitation of feed, water, and saliva from the mouth and nostrils.

Odynophagia (painful swallowing) may be observed after resolution of esophageal obstruction. The laryngeal and cervical area should be thoroughly palpated. Distention cranial to an esophageal obstruction may be visible or palpable, or if there is no obstruction at the time of presentation, previous esophageal trauma may be evidenced by local scarring or a depression in the contour of the ventral neck originating from fibrous constriction. Crepitus or cellulitis over the area may indicate the loss of esophageal integrity and necessitates thorough esophagoscopic and/or radio­graphic evaluation. A complete oral examination should always be performed because ptyalism, dysphagia, and anorexia are also consistent with oropharyngeal disease (e.g., dental disease, oral neoplasia), a foreign body, or a cleft palate. Careful passage of a nasogastric tube may confirm ongoing obstructive disease or a significant decrease in luminal diameter and may aid in identifying the site of involvement. Prolonged esophageal disease and recurrent episodes of obstruction associated with dysphagia are likely to result in secondary aspiration pneumonia. Therefore, a thorough workup of the lower respiratory tract, including thoracic auscultation, culture and cytology of a transtracheal lavage sample, and diagnostic imaging (e.g., thoracic radiography and ultrasonography), is indicated. Particular attention should be paid to this matter when planning esophageal surgery using general anesthesia.

Idiopathic esophageal strictures are seen in foals. Initial diagnosis based on clinical signs may be difficult in that horses may be presented because they are thought to have either cleft palates or pharyngeal cysts. The diagnosis is confirmed by endoscopic evaluation of the esophagus. Treatment is based on either dilation (bougienage) or surgical relief of the lesion. Critical cases should be referred to advanced surgical centers, and esophagomyotomy or esophageal resection and anastomosis may be attempted.


Esophagoscopy is a safe and rapid method to evaluate mucosal disease and changes in luminal size in standing horses and should be a component of the complete assessment of esophageal disease. A flexible fiber endoscope that is 2 to 3 m long allows evaluation of the entire length of the esophagus. Sedation of the horse for the examination using a2-agonists (e.g., xylazine hydrochlomride, detomidine hydrochloride) results in decreased esophageal motility and increased safety for the patient and handlers. The risk of damage to expensive endoscopic equipment can be further minimized by passing a shortened nasogastric tube into the cranial esophagus and then passing the endoscope through the lumen of the tube[7].

If possible, the endoscope should first be passed through the cardia, and the entire esophagus should be visualized in a caudal to cranial direction by slowly withdrawing the scope under continuous insufflation and irrigation, if necessary. However, substantial reduction of the luminal diameter due to an intraluminal obstruction, a stricture, or a diverticulum at the time of examination may prevent the examiner from passing the fiber endoscope into the stomach. Suspicious segments of the esophagus should be examined several times by repeated passes over the area. The mucosa at the level of the cranial esophageal sphincter may be difficult to evaluate due to repeated stimulation of the swallow reflex. When the endoscope is withdrawn in a caudal to cranial direction, normal longitudinal folding appears in the esophageal mucosa. Transverse folds can be produced by advancing the endoscope toward the stomach, which may give a false appearance of a stricture. Normal swallowing causes temporary obstruction of the view through the endoscope and results in changes in the luminal diameter that could falsely be interpreted as stenotic rings or diverticula. True lesions can be differentiated from these artifacts based on their persistence through several swallowing episodes. Immediately after resolution of an obstructive episode, full-thickness mucosal ulceration of a sector or the entire circumference of the esophagus may be detected. These areas should be reevaluated by endoscopy after 2 months because they are very likely to result in stricture formation. After 60 days, the lumen at the stricture site is at maximal diameter and mucosal healing is complete. During this time, treatment involving administration of broad-spectrum antibiotics and NSAIDs as well as feeding a soft, pasty, roughage-free diet is recommended to facilitate mucosal healing.

During endoscopic examination, esophageal strictures appear as a persistent narrowing of the lumen. Traction diverticula appear as segmental dilations of the esophageal lumen. Differentiation from normal variation and fluctuation of the luminal diameter is based on the persistence of the dilation throughout several swallowing events. In pulsion diverticula, the opening of the diverticulum appears as a defect or hole in the esophageal mucosa rather than dilation.

Because of an increased risk for perforation, esopha­goscopy is contraindicated in cases of corrosive and necrotizing esophagitis after ingestion of caustic substances.


Radiographic evaluation of the esophagus is an important component of the diagnostic workup of esophageal disorders other than acute simple obstructions. However, radiographic evaluation of the thoracic part of the esophagus is often difficult due to the size of the equine thorax and the limited capability of radio­graphic equipment. Esophagoscopy and esophageal contrast studies are necessary before surgery to precisely localize and determine the extent of conditions requiring surgical treatment.

Complete radiographic examination of the esophagus should be initiated with a survey film to establish radio­graphic technique. The normal cervical esophagus is usually not visible on plain films. Several conditions, such as obvious radiopaque obstructions, perforation of the esophagus with gas lucencies in the surrounding soft tissue, or both, may be recognized on survey films and may not require contrast studies. Negative-contrast radiography can be performed by air insufflation via a cuffed nasogastric tube. This may help visualize foreign bodies and identify diverticula or fistulas. Positive-contrast studies are conducted using barium sulfate in liquid or paste form or water-soluble iodinated solutions. Barium sulfate paste coats the esophageal mucosa for several minutes, making the timing of radiographic exposure less critical. Sixty to 100 ml of contrast material is administered via a cuffed nasogastric tube, or by squirting it to the back of the mouth. Caution is indicated when using the latter technique with iodinated solutions. Iodinated contrast materials are hypertonic and can cause severe pulmonary edema if they are accidentally aspirated. If the horse can safely tolerate the procedure, sedation should be avoided for esophagography because it suppresses the swallowing reflex, possibly resulting in aspiration of contrast material.

Esophageal strictures and diverticula are best evaluated by obtaining a double-contrast distention esophagogram. A cuffed nasogastric tube is placed in the proximal esophagus, followed by injection of up to 500 ml of liquid barium sulfate suspension. After most of the barium sulfate solution has cleared, a similar amount of air is injected under pressure into the esophagus, followed by immediate, airtight occlusion of the nasogastric tube. This technique provides optimal visualization of the esophageal mucosal surface.


Without strict adherence to dietary alteration requirements, horses managed medically are prone to recurrence of acute complete obstruction and have poor long-term survival. Conservative management of a stricture is aimed at dilation of the stenotic segment. Bougienage or pneumatic or hydrostatic dilators have minimal practical value in horses because of the limited availability of special equipment and chronicity of the problem. Chronic strictures usually have progressed too far, and the cicatrix is too firm to yield to dilation. For most veterinary surgeons, surgical management of esophageal strictures is reserved as a last option, and the potential pitfalls should be thoroughly discussed with the client. With the clinician mindful of this, surgical management of chronic esophageal strictures is considered superior to medical management.

Esophageal surgery is technically demanding, and complications requiring further surgical intervention are common. Reported surgical techniques for correction of chronic strictures of the equine esophagus include esophagomyotomy, esophagopexy, partial or segmental esophageal resection, esophagoplasty, muscular patch grafting, and mucosal fenestration[8]. Muscle grafting and esophageal replacement techniques are usually used to treat leakage or when tissue deficits exist. Selection of surgical technique is generally based on the type of stricture.

During surgical incision, the esophageal wall separates easily into two distinct sections. The elastic inner section, composed of the mucosa and submucosa, is freely movable within the relatively inelastic outer muscular layer and adventitia. The mucosa, which provides the greatest tensile strength after closure of an esophageal incision, is covered with stratified squamous epithelium and lies in longitudinal folds that obliterate the lumen, except during deglutition.

Esophagomyotomy and Esophagopexy

Strictures that are mural in origin (involving only the outer surgical section) respond to myotomy. For this surgery, the patient should be under general anesthesia, and a nasogastric tube is passed to the level of the stricture to permit easy identification of the involved area. The esophagus is incised longitudinally to the level of the mucosa, through the stricture, and 1 cm distal and proximal to it. The nasogastric tube may be passed through the stenotic area at this point. From this incision, the muscularis is separated by sharp dissection from the mucosa around the entire circumference of the esophagus, or if esophagopexy is performed in conjunction with esophagomyotomy, the mucosa is dissected from the muscularis only 180Ëš around the circumference of the stricture site[9]. When the mucosa is freed using these techniques, removal of a portion of the muscularis or multiple myotomy incisions are seldom necessary. Either the myotomy incision is not sutured or, if esophagopexy has been performed, the incised portions of the ipsilateral muscularis are sutured to the sternocephalic muscle ventrally and the periesophageal fascia dorsally. This results in an increased circumference of the tunica muscularis and creation of a diverticulum.

Following esophagomyotomy, feeding small, frequent quantities of soft feed may be necessary if prestenotic dilation was present before surgery. When this dilation is no longer recognized on radiographs, normal feeding may be resumed. When esophagopexy is performed in conjunction with esophagomyotomy, it is recommended to restrict patient access to dry hay for a minimum of 60 days. Recurrence of postsurgical cicatricial stricture is slow to develop, with clinical signs occurring weeks or months after the operation. Conservative treatment (diet change to a complete pelleted ration) may be all that is necessary to resolve recurrent obstructions. A postsurgical stricture that occurs long after the original operation is usually due to mature nonresilient cicatrix and may not respond to dilation. If this postsurgical stricture is clinically debilitating, it is preferred to allow resolution of the acute inflammation before surgical revision. Surgical reintervention in a stenotic area of the esophagus before allowing acute inflammation from the previous surgery to subside greatly increases the propensity for restricture. If early intervention is necessary, a more hazardous procedure may have to be selected to correct the problem.

Partial Esophageal Resection

Longitudinal esophagomyotomy combined with mucosal resection can relieve strictures caused by esophageal rings or webs and annular stenosis of all muscle layers. Performed with the patient under general anesthesia, this procedure is indicated when the cicatrix involves the mucosa and prevents nasogastric passage. Following my­ot­omy, a longitudinal incision long enough to permit identification of the diseased segment is made through the mucosa. Circumferential incisions are made at the proximal and distal edges of the mucosal cicatrix, which is removed, leaving the muscular tube intact for closure. When mucosal rings or webs are the cause of stenosis, the normal esophageal muscle should be apposed over the mucosal anastomosis, but in the case of annular stenosis that involves the entire esophageal wall, the muscularis should not be sutured. If possible, the horse should be fed through an esophagostomy tube placed through a separate incision distal to the stricture. When this is impossible, frequent feeding of small quantities of soft food may begin 48 hours after surgery and should be continued for a minimum of 10 days.

If the stricture is extensive and the mucosa cannot be sutured, regeneration within the muscle tube can readily occur. The muscularis may be sutured if it is healthy or may be left open if only scar tissue remains. Spontaneous healing can be aided by esophagostomy tube feeding. When the stricture is located too close to the thoracic inlet to permit placement of a separate esophagostomy incision, the tube may be inserted directly through the stricture site. Recurrence of stricture following this procedure may be an indication for complete resection or patch grafting.

Complete Esophageal Resection

Esophageal resection and anastomosis have been recommended if the muscularis is damaged extensively and is useless as a scaffold for mucosal regeneration. Minimizing tension on the anastomosis is essential for a favorable result. Before surgery, it may be advantageous to train the horse to tolerate a standing martingale to prevent elevation of the head. A routine approach to the esophagus is used. A two-layer anastomosis is performed by closing the submucosa and mucosa in a simple continuous or interrupted pattern, followed by closure of the muscular layer in a simple interrupted pattern. The muscularis is the limiting layer of esophageal elasticity, and tension can be eased by making relief incisions adjacent to the anastomosis. After surgery, extraoral alimentation or feeding by esophagostomy is required. If extraoral alimentation is not used, a pelleted slurry should be fed, starting 48 hours after surgery. A diet of roughage should not be offered until evidence of esophageal healing has been confirmed by radiography or esophagoscopy.

Esophagoplasty and Muscular Patch Grafting

Esophagoplasty may not be a viable surgical option for horses. A longitudinal incision in the esophagus with circumferential or transverse closure is of limited use in horses. It is only recommended for lesions less than 2 cm long because of excessive tension on the suture line with longer defects. Most lesions in horses are longer than 2 cm, and the abnormal tissue has poor suture-holding capacity.

No studies define the limits of esophageal resection in horses, but a 3-cm segment is the longest type mentioned in the literature[10]. If the size or nature of the lesion precludes resection and anastomosis, the use of a patch graft should be considered. The sternocephalicus17 and brachiocephalicus muscles appear to be the best for patch grafting[11].

Mucosal Fenestration

A final option for surgical repair of an esophageal stricture involves esophagostomy followed by fenestration of the mucosal and submucosal cicatrix. Extraoral alimentation of the patient is achieved through the esophagostomy, resulting in a traction diverticulum, thereby increasing the lumen size. In one report, several fenestrations were necessary and several longitudinal incisions of the fibrous mucosal cicatrix allowed complete resolution of the obstruction and return of the horse to a normal diet[12].


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  2. Fubini SL, Starrak GS, Freeman DE (1999) Esophagus, in Auer JA, Stick JA (eds): Equine Surgery, ed 2. Philadelphia, WB Saunders, pp:199-209
  3. Craig DR, Shivy DR, Pankowski RL, et al (1989) Esophageal disorders in 61 horses: Results of nonsurgical and surgical management. Vet Surg 18:432-438
  4. Eastwood GL (1983) Esophagitis and its consequences, in Castell DO, Johnson LF (eds): Esophageal Function in Health and Disease. New York, Elsevier Science Publishing, pp:175-186
  5. Craig D, Todhunter R (1987) Surgical repair of an esophageal stricture in a horse. Vet Surg 16:251-254
  6. Ford TS, Schumacher J, Chaffin MK, et al (1991) Surgical repair of an intrathoracic esophageal pulsion diverticulum in a horse. Vet Surg 20:316-319
  7. Wooldridge AA, Eades SC, Hosgood GL, et al (2002) Effects of treatment with oxytocin, xylazine butorphanol, guaifenesin, acepromazine, and detomidine on esophageal manometric pressure in conscious horses. Am J Vet Res 63:1738-1744
  8. Nixon AJ, Aanes WA, Nelson AW, et al (1983) Esophagomyotomy for relief of an intrathoracic esophageal stricture in a horse. JAVMA 183:794-796
  9. Lillich JD, Frees KE, Warrington K, et al (2001) Esophagomyotomy and esophagopexy to create a diverticulum for treatment of chronic esophageal stricture in 2 horses. Vet Surg 30:449-453
  10. McIlwraith CW (1984) Equine digestive surgery, in Jennings PB (ed): The Practice of Large Animal Surgery. Philadelphia, WB Saunders, pp:580-589
  11. Vaughn JT, Hoffer RE (1963) An approach to correction of cervical esophageal stricture in the equine. Auburn Vet:63
  12. Craig D, Todhunter R (1987) Surgical repair of an esophageal stricture in a horse. Vet Surg 16:251-254