Oesophageal strictures are uncommon in both dogs and cats. Strictures can be congenital or acquired: most of the former are caused by vascular ring anomalies and, in rare cases, by abnormal development of embryonic rudiments that become fibrous rings located at various sites along the organ. The clinical signs associated with oesophageal strictures usually develop between the 4th and 6th week of life, in the period of changing from a fluid diet to semisolid and solid food. The signs include regurgitation occurring at various times during the day, extreme greed for food, thinness associated with delayed growth and, sometimes, cough. The acquired oesophageal strictures are divided into malignant and benign. The malignant forms are very uncommon and are caused by primary or metastatic neoplastic disease in the oesophagus. These strictures are defined as intramural when the neoplasm originates from the mucosa, submucosa or muscle layer of the oesophagus. If the stricture is caused by a tumour outside the oesophagus, which compresses the organ from the exterior, the stricture is defined extramural.
Possible reported causes of malignant extramural oesophageal strictures include thyroid, laryngeal and tonsillar cancers, thymoma, intrathoracic lymphoma, chemodectoma (paraganglioma) and large lung tumours. Acquired benign oesophageal strictures are the most common types of stricture in both the dog and cat. In these types of stricture, the lumen of the oesophagus is narrowed as the result of formation of fibrous tissue.
AETIOLOGY AND PATHOPHYSIOLOGY
It has been hypothesised that oesophageal strictures occur following an episode of severe oesophagitis which also involves the submucosal layers. Whatever the origin of the mucosal damage, in patients predisposed to the formation of oesophageal strictures, a process of intense reactive fibroplasia develops, which leads to the formation of variably sized rings or tunnels of scar tissue at various sites. The strictures may be single or multiple, simple or tortuous. There are numerous potential primary causes of strictures: gastro-oesophageal reflux of gastric juices and enzymes during anaesthesia, mucosal erosion due to foreign bodies in the oesophagus or to their removal, persistent vomiting in debilitated patients, administration of drugs that can potentially damage tissues and prolonged contact of such drugs with the mucosa (tablets of doxycycline-clindamycin and chloramphenicol in cats and tablets of non-steroidal anti-inflammatory drugs in dogs), trauma caused by trichobezoars in the cat, ingestion of irritant acid and/or alkali substances, thermal damage to the mucosa secondary to the ingestion of very hot food and various types of oesophageal trauma.
In cases of gastro-oesophageal reflux, the hydrochloric acid contained in the gastric juices exposes the oesophageal mucosa to an acid pH; this causes denaturation of the mucosal proteins and the transformation of salivary pepsinogen into pepsin, which also has proteolytic properties. If the regurgitated fluid also contains pancreatic enzymes or bile acids, the tissue damage is even more severe; if the submucosal layers down to the oesophageal musculature are involved, a marked fibroblastic reaction can be induced which, in a period varying from 2 to 15 days, induces the formation of scar tissue and a consequent oesophageal stricture. Gastro-oesophageal reflux can occur during anaesthesia, with intra-abdominal surgery of the genital apparatus being reportedly the most common cause of oesophageal strictures. Numerous studies have been performed to identify the variables that can influence or cause the development of strictures, including the anaesthetic protocol, the age of the patient, the duration of pre-operative fasting and the type of handling and position of the patient during the operation. Although it has been demonstrated that the duration of fasting can increase the intensity of gastro-oesophageal reflux and that the administration of omeprazole prior to the anaesthesia can decrease the acidity of the reflux, no factors have been found to have a statistically significant effect on promoting or inhibiting the formation of strictures. However, epidemiologically, oesophageal strictures secondary to reflux occur rarely with respect to the number of anaesthetics administered. This suggests that there are other causes, as yet unknown, and that individual predisposition is presumably the determinant factor in the onset of oesophageal strictures. Furthermore, gynaecological operations are the most frequently performed type of surgery. Drug-induced strictures in the cat are related to the particular anatomical conformation of the oesophagus in this species and to the composition of the tablets. In the cat, the caudal third of the oesophagus is formed of smooth muscle which contracts more slowly (from 1 to 2 cm/second), so the tablets remain on the mucosa for a longer time. The chalky consistency and tissue-damaging nature of some drugs, such as tablets of doxycycline and/or clindamycin, can cause oesophageal damage. For this reason, it is preferable to give tablets to dogs, but especially to cats, together with water or food.
CLINICAL SIGNS
Whatever the event that triggers the oesophageal damage, the time between the event and the manifestation of the clinical signs can vary between 3 and 15 days. In the case that regurgitation occurs within 24-48 hours after the potential causative trigger, it is more likely that the regurgitation is secondary to oesophagitis rather than to a stricture. The regurgitation typically occurs immediately after ingestion of food and with a progressively increasing intensity. Some animals may regurgitate only after the ingestion of solid food and not following the intake of water or a semi-liquid diet. The regurgitation is influenced by the site and size of the stricture. Owners may confuse regurgitation with vomiting, particularly in animals with a precardial stricture. Many patients have polyphagia together with progressive weight loss, while patients which develop aspiration pneumonia may have fever, depression, cough and loss of appetite.
DIAGNOSIS
The patient’s history and clinical signs must always be evaluated with care since they often suggest the diagnosis. X-rays and endoscopic studies are used to confirm the suspected diagnosis. Plain X-rays are generally fairly uninformative, while contrast studies are usually diagnostic. These latter studies can be performed using liquid barium or a barium meal. In large dogs, the use of liquid barium could give equivocal or false negative results, since the contrast agent could pass through the stricture without showing the obstruction or slowed passage. Contrast radiography gives information on the site and the length of the stenotic tract, showing the outline of the cranial and caudal margins of the stricture and the contractile features of the oesophagus. This information is also used by the clinician to plan the therapeutic intervention (Fig. 1). Some studies have, however, shown that the radiographic evaluation of the length of the oesophageal stricture can be imprecise.
In doubtful cases an endoscopic examination is indispensable in order to confirm the diagnosis; furthermore, it enables staging of the pathological condition with a view to treatment. In cases in which the stricture may be of malignant origin, it is essential to take a biopsy and carry out cytological and histological studies. Since acquired benign oesophageal strictures are formed of scar tissue, they are tough and endoscopic biopsy is difficult if not impossible. Once the stricture has been identified, its macroscopic appearance and size can be evaluated. Strictures typically have a homogeneous appearance with a clear pinkish, translucent mucosa (Fig. 2); an important finding is that the oesophagus at the site of the stricture cannot be dilated and the endoscope cannot, therefore, explore the post-stenotic tract of oesophagus. Strictures defined as “tortuous” (Fig. 3) have a more irregular, apparently lumpy appearance and are extremely tough. Tortuous strictures are the most difficult to treat since they are usually long and extremely fibrous, presumably because of the chronic nature of the pathological process. The diameter of the oesophageal stricture can be determined by using biopsy forceps of known diameter as a size marker. Evaluating the length of the stricture is more complex. For strictures with a diameter greater than 5 mm a small fiberscope can be passed and the length can, therefore, be determined. Strictures are, however, very often smaller than 5 mm and, in these cases, their lengths can be determined by using flexible, smaller instruments (2.7 mm) although manoeuvres are more difficult with these since they do not have four movements and air cannot be insufflated. Alternatively, closed biopsy forceps can be introduced and, once positioned caudally to the stricture, retracted with the arms open to evaluate at what level the retraction is blocked and thereby estimate the length of the oesophageal stricture.
TREATMENT
Numerous surgical options have been described for the treatment of strictures: resection, dilatation of the narrowing using a flap of diaphragm, insertion of a prosthesis, etc. Most of these techniques have now been abandoned because of the low success rates and the high incidence of complications related to the surgery. Oesophageal dilatation under endoscopic vision is considered the treatment of choice and the success rate of this management is about 75% in most studies. Oesophageal strictures can be treated by balloon dilatation or rigid dilators (bougies). There are no studies showing that one technique is more effective than the other.
Balloon dilatation acts by delivering a radial force on the stricture, while bougies act by exploiting a longitudinal force (Fig. 4); for this reason, it is the author’s belief that bougies create a higher risk than balloons of rupturing the stricture and perforating the oesophagus. Balloon dilators come in various sizes with regards to both inflated diameter and length (Fig. 5). It is important to have instruments of different lengths and diameters in order to be able to treat the variously sized strictures in animals of different sizes. Normally air is used to expand the balloon and there are manometers or syringes with attachable manometers in order to monitor the pressure of insufflation. Balloon dilators can also be filled with water or other fluid. There are no studies demonstrating that one method of expansion of the balloons is more effective than another.
There are various different types of rigid dilators; the best known are the Savary-Gillard and Eder-Puestow dilators. It is important to have a series of these dilators, because they are of a fixed size and made of rigid material; by having a series of increasing sizes, the most suitable dilator for each, differently sized stricture can be used.
The technique of balloon dilatation involves introducing the balloon into the centre of the stricture and then expanding it with air or water to a pressure of about 40 psi, after which it is left in situ for about 5 minutes; once the balloon has been deflated, the stricture is checked to determine whether it has been unblocked and whether the diameter achieved is sufficient. Oesophageal dilatation is usually associated with superficial lacerations of the oesophageal mucosa and bleeding that resolves spontaneously and rapidly; these endoscopic findings are considered evidence of breakage of the submucosal fibrin bridges and are, therefore, evaluated positively (Fig. 6). Further dilatations can be performed in the same session or larger dilators may be used. After 2 or 3 days, it is advisable to ascertain whether the luminal diameter obtained with the preceding dilatation has been maintained or whether the fibrous stricture has re-formed and the diameter has, therefore, decreased again. Indeed, the main complication of the treatment of strictures is recurrence. In general, two or three dilatations are performed weekly, for a total of between two and eight to ten dilatations in the most complex cases. There are numerous variables involved in the balloon dilatation technique: the number of dilatations in the same session and in a week, the duration of the dilatation, the content of the balloon, treatment associated with the dilatation and the luminal diameter considered sufficient after the dilatation. No comprehensive studies have compared these variables which are, therefore, used subjectively. Conventionally, it is considered that a diameter of at least 1 cm in cats and small breeds of dogs (≤ 10 kg) and at least 1.5 cm in medium-sized and large breeds of dogs is sufficient for a functional recovery of the oesophagus.
When using rigid dilators the procedure involves introducing the narrower part of the instrument into the stricture; subsequently, the progressive longitudinal pressure and the increase in diameter of the bougie should break the fibrous tissue. The number, duration and frequency of the bougienages vary, as with the technique of balloon dilatation.
Some recent studies in both humans and animals seem to demonstrate that local application of steroids (triamcinolone) by intralesional injection through a Wang’s needle under endoscopic control is able to slow or inhibit stricture formation and limit recurrences after balloon dilatation. In the presence of severe oesophagitis associated with the stricture, it is advisable to introduce a Pezzer catheter (PEG) for gastric nutrition ]with the purpose of accelerating healing of the oesophagus.
Rare complications of endoscopic treatment of oesophageal strictures include oesophageal perforation and abundant bleeding. Unfortunately, the most frequent complication is failure, which may mean inability to dilate the stenotic tissue or uncontrollable recurrence after each treatment. Besides local treatment, a patient with an oesophageal stricture must be given appropriate systemic medical therapy in order to reduce further damage to the oesophageal mucosa caused by the dilatations and to inhibit the formation of new scar tissue. The usual medical treatment consists of prednisone (0.5 mg/kg b.i.d.), sucralfate (1 g/30 kg b.i.d.), metoclopramide (0.5 mg/kg b.i.d.) and cimetidine (1 mg/kg t.i.d.); this treatment can be continued for 7-15 days after the last dilatation. In some animals, sucralfate (1 g/30 kg b.i.d. p.o., administered at least 60-120 minutes before the antacids) and metoclopramide (0.5 mg/kg b.i.d. p.o. or s.c.) can be used, particularly if it is suspected that gastro-oesophageal reflux is an underlying cause of the formation of the stricture or a co-cause in its recurrence. Following treatment of the stricture, the patient must be fed for at least the first 30 days with a commercial semi-liquid diet or homogenised meat diluted with water. The return to solid food must be gradual, with the consistency of the patient’s food being increased progressively. Although treatment of the stricture leads to a sufficient degree of dilatation, it is possible, indeed probable, that the patient must be fed a semi-liquid diet all its life; for this reason it is very important to inform the owner of all the operative and prognostic variables related to this condition.
Suggested readings
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- Bissett SA, Davis J, Subler K, Degernes LA Risk factors and outcome of bougienage for treatment of benign esophageal strictures in dogs and cats: 28 cases (1995-2004).J Am Vet Med Assoc. 2009 Oct 1;235(7):844-50
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