Update on Feline Esophageal Diseases: Not That Rare After All
World Small Animal Veterinary Association Congress Proceedings, 2018
E. Robertson
American Board Certified Diplomate Feline Practice, Feline Vet and Endoscopy Vet Referrals, Brighton, East Sussex, UK

Clinical manifestations of oesophageal disease can include regurgitation, dysphagia, odynophagia (pain on swallowing), ptyalism, and exaggerated swallowing. Regurgitation has been defined as the passive expulsion of ingested material (food/liquid) from the oesophagus and stimulated by local events affecting oesophageal structure/function. Attempts should be made to distinguish regurgitation from vomiting. In contrast to regurgitation, vomiting is often preceded by prodromal events such as vocalising, hypersalivation, retching, and abdominal contractions. In theory, this sounds simple; however, this can pose as a true clinical challenge for many practitioners due to their secretive lifestyles and also for the tendency of these patients to not uncommonly experience overlapping comorbidities (e.g., ‘IBD’→vomited trichobezoar→oesophageal foreign body→oesophagitis→regurgitation and vomiting). To add even more complexity, anorexia, coughing, dyspnoea, and pyrexia may also be noted as a possible sequela to oesophageal disease due to aspiration of contents or even oesophageal perforation.

It’s paramount for the practitioner to consider both the patient’s signalment and detailed clinical history/examination to assist with decision making. In 2018, astute owners have beautifully utilised digital information (i.e., smart phone videos) to assist the clinician in making a preliminary diagnosis of oesophageal disease and guide diagnostic decisions.

Oesophageal Disease You’ll Likely Diagnose 2–3x/Year in Your Feline Career!

1. Oesophagitis

Clinical signs of oesophagitis usually develop within 1 to 3 days following an insult (e.g., reflux from previous sedation/GA, access to caustic medications [e.g., doxycycline, clindamycin],1-3 previous local trauma [vomition of trichobezoar], or from thermal injury). Nonspecific lethargy, anorexia, salivation, and vague oral discomfort may precede the onset of regurgitation. In cats, exaggerated attempts to swallow with the head and neck extended, are often accompanied by gagging, retching, odynophagia (pain on swallowing), are often clues of oesophageal pathology.

Two published studies had evaluated the dynamics of tablet/capsule swallowing in cats and highlighted how this phenomenon occurs.4-6 In one study, tablet transit times showed that tablets and capsules made it to the stomach within 5 minutes post-administration 37% and 17% of the time, respectively. In the other study, capsules remained in the oesophagus for more than 4 minutes on 53% of occasions. It’s clear that oesophageal entrapment occurs commonly after tablet and capsule administration in cats, and if the tablet/capsules (or their contents) are potentially irritating to tissues, it’s easy to understand how oesophagitis occurs after these events. Interestingly, both of these studies demonstrated that the administration of a small amount of food or a small bolus of water after tablet/capsule administration was highly successful in promoting prompt and complete passage of tablet/capsules into the stomach.

In oesophagitis, survey thoracic radiographs are usually unremarkable, except for the occasional presence of small amounts of air in the oesophagus. In some cases, the underlying cause of oesophagitis is identified (e.g., foreign body, hiatal hernia, or oesophageal mass). In cases of hiatal hernia, the displaced stomach may be identified as a mass in the dorsocaudal mediastinum cranial to the hiatus. Contrast oesophagrams are normal in mild cases; however, the mucosal surface may appear irregular with secondary hypomotility in severe cases. Segmental narrowing of the lumen can result from spasticity, intramural oedema, and focal indistensibility caused by inflammation, which can be difficult to differentiate from a developing stricture.

Oesophagitis is usually an endoscopic diagnosis based on mucosal abnormalities. If gastrooesophageal reflux is the underlying cause of oesophagitis, lesions are most severe in the distal esophagus and the gastroesophageal junction may appear wide open.

Treatment of Oesophagitis


Soft, low-fat/high-protein diet should as it may improve the lower oesophageal tone and minimise delays in gastric emptying. Elevated feeding may reduce episodes. For severe cases PEG tube may be required.

Mucosal protectants

  • Sucralfate suspension given PO: 100–200 mg/kg BID/TID

Gastric antacids

To reduce gastric acidity and thereby help prevent further esophageal damage during reflux

  • Omeprazole: 1 mg/kg PO BID (this is preferable to less potent H2 blockers)
  • Ranitidine: 1–2 mg/kg PO BID/TID
  • Famotidine: 0.5 mg/kg SID/BID

Other drugs

  • Analgesia (e.g., buprenorphine)
  • Motility-modifying agents (e.g., cisapride) can be of value to increase lower oesophageal sphincter tone and enhance gastric emptying, thereby reducing gastric reflux

2. Oesophageal Stricture

An oesophageal stricture should be suspected when regurgitation develops 1–4 weeks post potential suspect oesophageal injury. Clinical signs are similar to, and often impossible to differentiate from, oesophagitis. The appetite is often good, or even considered ravenous.

Strictures may be single or multiple. Oesophagoscopy +/- fluoroscopy are the most reliable method(s) for diagnosing oesophageal stricture(s) and also for determining the lumenal diameter, stricture length, and presence of associated oesophagitis. Single strictures are found in 80% of patients, but diffuse oesophagitis can result in 2 or 3 strictured areas in some cases.

Management can include endoscopically guided balloon dilatation,7 or rarely, a stent8. The balloon catheter can be passed through the lubricated operating channel of many endoscopes or guided alongside the endoscope to visualize the breaking down of fibrous tissue in a controlled manner. The procedure is repeated at 3- to 5-day intervals for a minimum of three treatments. The total number of dilatations is variable (averaging four times, ranging three to 10) and is determined by the severity of the stricture and the clinical response.

Prognosis of Oesophageal Stricture

Although some severe cases require prolonged therapy, a majority of cases seem to achieve good and acceptable clinical response to balloon dilatation. Some cats will experience complete clinical whilst others may be plagued with only partial response.

3. Oesophageal Foreign Body

Oesophageal foreign bodies (FB) are an occasional problem caused by trichobezoars, string, needles, fishhooks, pins, hairballs, and very occasionally, bones (especially V-shaped avian bones). Oesophageal FBs usually lodge at the thoracic inlet, the base of the heart, or the hiatus of the diaphragm because of the constricting effect of surrounding soft tissue structures in these areas. The extent of secondary oesophageal damage depends on the type of object, its size and shape, and the duration of time in contact with the mucosa.

4. Oesophageal Hypomotility (Megaoesophagus)9

Oesophageal hypomotility refers to a decrease in oesophageal peristalsis. Megaoesophagus is a flaccid dilated oesophagus resulting from a severe diffuse motility disorder.

Both congenital and acquired forms of megaoesophagus occur in cats. A hereditary form of megaoesophagus has been suspected in young cats, especially Siamese. Siamese cats with megaoesophagus frequently have a concurrent gastric emptying disorder with the underlying cause of acquired megaoesophagus being unknown. Occasionally, systemic neuromuscular disease is recognised as a cause of megaoesophagus, for example, myasthenia gravis (secondary to thymoma), tick paralysis, or even dysautonomia/Key-Gaskell.

Symptomatic Treatment for Megaesophagus:

  • Elevated feeding with small frequent meals of varying consistencies to see which is best tolerated
  • Feeding high-quality, calorie-dense foods
  • Promotility agents (metoclopramide, cisapride 1 mg/kg PO q 8h or 1.5 mg/kg PO q 12h) can be trialed as it increases motility of the oesophageal smooth muscle, but generally the response to these agents seems to be poor since most of the oesophagus in the cat is composed of skeletal muscle and thus its efficacy in megaoesophagus remains questionable.

5. Oesophageal Neoplasms

Primary oesophageal neoplasms are considered ‘rare’; however, this may be an underrepresentation. Squamous cell carcinoma is the most common primary oesophageal neoplasm in elderly cats. Oesophageal neoplasia causes chronic progressive signs of oesophageal disease and presents similarly to the aforementioned conditions. Survey radiographs may be normal or may reveal a soft tissue mass in the region of the oesophagus. Endoscopically, neoplasia usually appears as a focal proliferative mass, which may partially or completely occlude the lumen, often with an accumulation of hair preceding the mass. Surgical resection is not usually feasible or successful in the long term.

6. Periesophageal Masses

Mass lesions arising from peri-oesophageal tissues may cause regurgitation due to compression of the oesophagus with partial or complete obstruction. Mediastinal lymphoma is most common, although any large tumour or abscess arising from mediastinal structures (e.g., thymus, lymph node, lung) could potentially cause secondary oesophageal compression. Lymphoma is mostly in young cats, whereas thymoma occurs in elderly cats. Survey and/or contrast thoracic radiography usually identifies the mass. Lymphoma is diagnosed by fluid or FNA cytology.

In Conclusion

Feline practitioners must remain astute when assessing cats whose owner report vomiting, ptyalism, ‘painful mouth,’ and weight loss. A structured approach based around the key questions of defining the problems/system/location/lesion provides a robust framework for the practitioner to ensure all relevant diagnostic clues have been considered. Clinical thinking/reasoning skills, once developed, will allow for time-efficient clinical assessment and to allow the practitioner to make diagnostically relevant decisions which will enhance client communication and improve the welfare of the cat.


1.  Beatty JA, Swift N, Foster DJ, et al. Suspected clindamycin-associated oesophageal injury in cats: five cases. J Feline Med Surg. 2006;8:412–9.

2.  German AJ, Cannon MJ, Dye C, et al. Oesophageal strictures in cats associated with doxycycline therapy. J Feline Med Surg. 2005;7:33–41.

3.  Melendez L, Twedt D, Wright M. Suspected doxycycline-induced esophagitis with esophageal stricture formation in three cats. Feline Pract. 2000;28:10–12.

4.  Westfall DS, Twedt DC, Steyn PF, Overhauser EB, Van Cleave JW. Evaluation of esophageal transit of tablets and capsules in 30 cats. J Vet Intern Med. 2001;15(5);467–70.

5.  Graham JP, Lipman AH, Newell SM, Roberts GD. Esophageal transit of capsules in clinically normal cats. Am J Vet Res. 2000;61(6):655–7.

6.  Bennett AD, MacPhail CM, Gibbons DS, et al. A comparative study evaluating the esophageal transit time of eight healthy cats when pilled with the FlavoRx pill glide versus pill delivery treats. J Feline Med Surg. 2010;12:286–90.

7.  Leib MS, Dinnel H, Ward DL, et al. Endoscopic balloon dilation of benign esophageal strictures in dogs and cats. J Vet Intern Med. 2001;15:547–52.

8.  Battersby I, Doyle R. Use of a biodegradable self-expanding stent in the management of benign oesophageal stricture in a cat. J Small Anim Pract. 2009;51:49–52.

9.  Moses L, Harpster NK, Beck KA, Hartzband L. Esophageal motility dysfunction in cats: a study of 44 cases. J Am Anim Hosp Assoc. 2000;36(4):309–312.

10.  Berube D, Scott-Moncrieff JC, Rohleder J, Vemireddi V. Primary esophageal squamous cell carcinoma in a cat. J Am Anim Hosp Assoc. 2009;45:291–5.


Speaker Information
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E. Robertson
Feline Vet and Endoscopy Vet Referrals
Brighton, East Sussex, UK

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