Oesophagitis

The term oesophagitis means inflammation of the mucosa (and sometimes also of the submucosa) of the oesophagus. There are various causes of oesophageal inflammation and in chronic cases the oesophatitis can cause oesophageal strictures and mega-oesophagus.

CAUSES

The commonest cause of oesophagitis is prolonged contact of the oesophageal mucosa with gastric acid following episodes of continuous vomiting, excessive production of acid (for example, in the case of tumours) or gastro-oesophageal reflux (general anaesthesia, hiatus hernia, abnormalities of the gastric cardia, etc.). Physiological oesophageal peristalsis usually ensures that gastric acid returns quickly into the stomach. However, in cases of diminished peristalsis or persistent presence of gastric acid in the stomach, the acid can reflux into the oesophagus, causing severe damage to the mucosa and submucosa. In chronic cases a vicious inflammatory circle becomes established, which is difficult to break and can lead to the formation of oesophageal stenoses.

Gastro-oesophageal reflux is not very common in anaesthetised animals, but when it does occur it is often severe and may also lead to strictures_^1-3. This complication can affect both sexes; studies have recently demonstrated that, in females, there is no relation between increased levels of reproductive hormones_⁴ and the development of strictures.

Foreign bodies (for example, bones_⁵, fish hooks_⁶ and dental sticks_⁷) can often cause oesophagitis and consequent stenosis.

Drugs that remain in the oesophagus a long time can cause local inflammation with consequent irritation: in the cat, tetracyclines in particular have been accused of having this effect_^8,9.

Some animals can ingest caustic substances from the environment or lick them directly from their skin during cleaning activities (cats), causing lesions to the mouth and oesophagus. The extent of the lesions depends above all on the caustic agent ingested.

Some neoplasms such as gastrinomas may secrete large amounts of gastric acid which can pass from the stomach to the oesophagus, causing inflammation.

The oesophagus may also be involved, and thus become inflamed, in some rare diseases (such as pythiosis and spirocercosis) and in immunosuppressed animals (such as those receiving treatment with steroids, cyclosporine, azathioprine, etc.). Oesophageal tumours are a less common cause of inflammation. 

CLINICAL SIGNS

The clinical signs vary depending on the type of local damage and the extent and degree of the inflammation_¹⁰. If the inflammation is minimal the animal may be completely asymptomatic. In the case of moderate to severe inflammation the clinical signs most frequently seen are hypersalivation, anorexia, odynophagia (painful deglutition manifested by extension of the head and neck during swallowing), dysphagia, often regurgitation (sometimes with fresh blood), weight loss and cachexia.

DIAGNOSIS

A good history_¹¹ can usually direct the diagnosis towards oesophagitis.

Blood tests (full blood count and biochemistry tests) rarely show abnormal values.

Chest X-rays are not sensitive enough to indicate a state of inflammation. Oesophagrams, which are X-rays with contrast agents, such as barium, can show retention of the contrast agent in the oesophagus, mild dilatation of the oesophagus and changes in oesophageal mucosa (Figs. 2 and 3). Usually liquid barium is administered first, then barium mixed with food (the barium meal). Rarely, liquid barium may pass through a stenotic area without demonstrating the stricture.

Fluoroscopy, being a dynamic examination, can show partial obstructions that may escape detection on radiographic examinations.

Endoscopy (without biopsy examinations) is the most sensitive and specific method for diagnosing oesophageal problems. In animals with mild inflammation, only modest erythema of the tissues may be seen (Fig. 4), but in those with severe inflammation there can be erythema, erosions and sometimes even ulcers (Fig. 5). In the case of gastro-oesophageal reflux, the lesions are more evident in the distal part of the oesophagus, close to the cardia (lower oesophageal sphincter) (Fig. 6).

TREATMENT

The treatment of oesophagitis is based on eliminating the underlying factors (for example, hiatus hernia, foreign body), appropriate medical therapy and a diet consisting of small, frequent meals with a low lipid content and high protein content to increase the tone of the cardia and minimise reflux_¹².

Sucralfate is the drug most frequently used to treat oesophagitis_¹³. The dose varies depending on the weight of the animal (dogs: < 20 kg, 0.5 g/dog and > 20 kg, 1 g/dog; cats: 250 mg/cat per os) and is given three times a day on an empty stomach. Sucralfate binds selectively to the proteins of eroded mucosa, thereby forming a barrier over exposed areas and protecting them from further damage caused by the gastric juices.

H₂ receptor antagonists (ranitidine, famotidine, cimetidine) inhibit the production of gastric acid and can also reduce oesophageal reflux well. These drugs may be given orally and parenterally. Parenteral administration is the route of choice for all patients that, because of vomiting, cannot take the drug by mouth. In humans it seems that some H₂ receptor antagonists also have prokinetic activity (e.g. ranitidine, nizatidine) and these appear to be more effective than the H₂ receptor antagonists without this property (cimetidine, famotidine)^₁₄.

Proton pump inhibitors (omeprazole, lansoprazole) are effective alone, but their efficacy in reducing the production of gastric acid and oesophageal reflux increases if they are given together with H₂ receptor antagonists.

Metoclopramide can be administered both orally and parenterally (subcutaneously and intravenously). This drug is less effective than cisapride in reducing oesophageal reflux and promoting gastric emptying, but the latter drug has been withdrawn from the market in various countries because of its cardiovascular side effects.

Other centrally acting anti-emetics (for example, maropitant, ondansetron, chlorpromazine) can be administered to inhibit vomiting.

In animals that cannot eat satisfactorily because of vomiting or an oesophageal stenosis, it is advisable to place a gastric feeding tube (for example, a percutaneous endoscopic gastrotomy [PEG]) in order to be able to feed the animal while bypassing the oesophagus, thus avoiding further oesophageal irritation (Figs. 7 and 8). Oesophageal and naso-oesophageal tubes are not recommended.

Corticosteroids are often administered systemically to reduce the risk of strictures, but their efficacy has never been scientifically demonstrated. It does however, seem that local injections of steroids during the endoscopic dilatation of severe oesophageal strictures can increase the efficacy of the dilatation and reduce the number of subsequent dilatations necessary_¹⁵.

The use of antibiotics in these cases is controversial since it has not yet been demonstrated that they are of help in healing the oesophagus. If they are administered, broad-spectrum types should be used since these are normally effective also against the anaerobic bacteria often found in the oral cavity.

If a stricture is present, endoscopic dilatation with bougies will be necessary. Surgery is rarely indicated in these cases and should be the last solution.

It is good practice to give water to animals that must take drugs (particularly tablets) by mouth in order to avoid inflammation and consequent oesophagitis.

The duration of treatment varies depending on the degree of inflammation. Endoscopic assessment a few days or weeks after the start of treatment is strongly recommended in order to evaluate the results obtained.

PROGNOSIS

The prognosis depends on the severity of the oesophagitis. The prognosis of mild and moderate cases is usually excellent with medical treatment and an appropriate diet, but the prognosis in severe cases is uncertain. This is because of the possibility of oesophageal strictures, which may not  always be resolved by multiple endoscopic dilatation. The percentage success rate in such cases has been reported to vary from 77 to 88%.^1,3,7.

In most cases early treatment of oesophagitis resolves the clinical signs and prevents the formation of oesophageal strictures.

References

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2. Adamama-Moraitou KK, Rallis TS, Prassinos NN, Galatos AD. Benign esophageal stricture in the dog and cat: a retrospective study of 20 cases.   Canadian  Journal of  Veterinary Research,  2002, 66, 55-9.
3. Wilson DV, Walshaw R Postanesthetic esophageal dysfunction in 13 dogs. Journal of  American Animal Hospital  Association, 2004, 40, 455-60.
4. Anagnostou TL, Savvas I, Kazakos GM, Ververidis HN, Haritopoulou MR, Rallis TS, Raptopoulos D Effect of endogenous progesterone and oestradiol-17beta on the incidence of gastro-oesophageal reflux and on the barrier pressure during general anaesthesia in the female dog. Veterinary  Anaesthesia and  Analgesia , 2009, 36, 308-18
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8. Melendez LD, Twedt DC, Wright M. Suspected doxycycline induced esophagitis with esophageal stricture formation in 3 cats. Feline Practice, 2000, 28, 100
9. McGrotty YL, Knottenbelt CM: Esophageal stricture in a cat due to oral administration of tetracycline.  Journal of Small Animal Practice, 2002; 43:221-223.
10. Glazer A, Walters P. Esophagitis and esophageal strictures. Compendium of Continuing Education Practising Veterinary, 2008 30:281-92.
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12. Jergens AE: Diseases of the esophagus, in Textbook of Veterinary Internal Medicine, Ed.Ettinger SJ, Feldman EC, Saunders Elsevier, Missouri, USA, 2010 1487-1499.
13. Katz PO, et al: Acid-induced esophagitis in cats is prevented by sucralfate but not synthetic prostaglandin E. Digestive  Disease  Sciencei  1988; 33:217
14. Hamamoto N, Hashimoto T, Adachi K, Hirakawa K, Ishihara S, Inoue H, Taniura H, Niigaki M, Sato S, Kushiyama Y, Suetsugu H, Miyake T, Kinoshita Y. Comparative study of nizatidine and famotidine for maintenance therapy of erosive esophagitis. Journal of  Gastroenterology and  Hepatology 2005, 20, 281-6.
15. Altintas E, Kacar S, Tunc B, Sezgin O, Parlak E, Altiparmak E, Saritas U, Sahin B. Intralesional steroid injection in benign esophageal strictures resistant to bougie dilation. Journal of  Gastroenterology and  Hepatology 19 1388-91.