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Antral pyloric hypertrophy in the dog

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Category: Schede
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  • Disciplina: Gastroenterologia
  • Specie: Cane

Antral pyloric hypertrophy (APH) is an important cause of delayed gastric emptying and is due to hypertrophy of the tunica mucosa and/or muscle layer of the pylorus1.

The term antral pyloric hypertrophy is used to define a group of disorders which, over the years, have been called antral pyloric hypertrophy syndrome, chronic hypertrophic pyloric gastropathy, antral hypertrophy and pyloric stenosis. Although this last name has been used to indicate APH, in the author’s opinion it should be reserved to those pathological conditions in which the thickening of the smooth muscle of the pylorus causes mechanical stenosis. In contrast, in APH it is the hypertrophic, polypoid-appearing mucosa that hampers, to the point of completely preventing, passage of the ingesta through the pylorus. Pyloric stenosis is reported mainly in Boxers and Boston Terriers,1,2 with the symptoms often already present at the time of weaning.2

 

SIGNALMENT AND PATHOGENESIS

APH is a relatively common pathological condition in some brachycephalic breeds such as the Lhasa Apso, Maltese, Pekingese, Shih Tzu, French Bulldog and English Bulldog,1-5 whereas it is rare in other breeds. APH is found mainly in young and adult male dogs.1-5 The condition is reported rarely in cats, because most of the disorders of the pyloric region are functional rather than anatomical.2

Antral pyloric hypertrophy is usually manifested as a polypoid-appearing hypertrophy of the gastric mucosa in the area around the pylorus; less frequently there are multiple polypoid lesions of the antrum or peripyloric region or thickening of the mucosal folds which occupy the antrum.2,6

There are congenital and acquired forms; however, it has been hypothesised that the acquired forms are evolutions of a mild congenital form that was initially asymptomatic.2

 

PATHOPHYSIOLOGY

 

The pathophysiological mechanism underlying APH is not yet completely understood. Some authors have hypothesised that increased secretion of gastrin is the determinant pathophysiological factor.2-4 Gastrin is the main regulator of the secretion of gastric acid and has trophic effects on the mucosa of the body of the stomach and on smooth muscle. The sympathetic nervous system is stimulated in various conditions, such as stress, inflammatory disorders and trauma, causing a reduction in gastric motility and consequent retention of material.2-4 Furthermore, there are idiopathic forms of delayed gastric emptying, presumably secondary to neurological abnormalities. The retention of food associated with prolonged gastric distension leads to increased secretion of gastrin and, therefore, to mucosal hypertrophy (Fig. 1). Gastrin does, however, have a greater trophic action on the mucosa of the body of the stomach than on the antrum; it is, therefore, possible that some other neuroendocrine factor is involved in the pathophysiology of APH.2-4On the basis of these considerations, some authors have suggested that a subclinical form of congenital APH causes retention of gastric material which then induces chronic secretion of gastrin2-4 and, consequently, manifest APH.

This hypothesis is credible in that it is not uncommon to find mild or moderate hypertrophy of the pyloric mucosa in young, brachycephalic dogs of small breeds when these animals are evaluated by endoscopy. This hypertrophy could progress slowly until it becomes obstructive and causes clinical signs in adulthood. This author has personally detected mild mucosal hypertrophy at the level of the pylorus in two young French Bulldogs which underwent endoscopy for staging of brachycephalic syndrome. At 4 and 5 years of age, these same two animals manifested clinical signs of APH, which was then confirmed endoscopically.

 

CLINICAL SIGNS

The clinical signs of APH are related to the delayed gastric emptying. The most frequent clinical sign is vomiting of undigested food, which can occur even as long as 6-12 hours after the meal. According to Guilford,2in 25% of cases the vomiting is projectile, i.e., there is forceful ejection of the vomited material, but this characteristic is not pathognomonic of APH. Subjects with continuous and recurrent vomiting may develop signs of oesophagitis such as dysphagia, anorexia and regurgitation. More severe and later manifestations include loss of weight, dehydration, depression, abdominal distension and, in the case of erosive/ulcerative lesions of the gastric mucosa, haematemesis and melaena.2,3-5,7-9 Rarely there may be respiratory signs, such as a nasal discharge or cough, secondary to inhalation and/or aspiration of the vomited material.

 

DIAGNOSIS

The diagnosis of APH is based primarily on a careful evaluation of the signalment and history. A combination of vomiting food long after a meal and belonging to one of the breeds predisposed to APH must raise the suspicion of APH among the main differential diagnoses. The clinical condition of the patient can vary greatly depending on the severity of the pyloric obstruction and the duration of the pathological process. The clinical examination is normal in some subjects, whereas weight loss, dehydration, depression and abdominal tenderness and/or dilation may be found in others. The clinical examination may reveal severe abdominal distension, which must not be confused with ascites, even if ballottement may be positive.

Laboratory investigations (full blood count and blood biochemistry) are usually normal or there are mild signs of dehydration. In the presence of marked vomiting and obstruction of gastric outflow, hypochloraemic metabolic alkalosis may be found together with hypernatraemia and hypokalaemia.1,2,5 In the case of aspiration pneumonia there is usually leucocytosis[6], which can be considerable, and a left shift.

Plain X-rays may appear normal or show gastric dilation, sometimes of considerable size, and retention of material (fluids, gas and food) more than 6-12 hours after a meal1,3,4,9,10 (Fig. 2). X-ray procedures with contrast agents are performed to evaluate the kinetics of gastric emptying. Unfortunately, neither the method of performing these studies nor the interpretation of the findings has been standardised. Furthermore, there is a large physiological variability between animals of different sizes, ages and breeds. In the case of suspected APH it is possible, indeed advisable, to carry out contrast radiography using liquid barium or a barium meal. The examination should be performed with the animal conscious and fasted for at least 12-16 hours. Subjects with APH  have delayed gastric emptying; the typical X-ray image is the so-called “beak sign” which shows the narrowed passage through which the barium passes at the pylorus2 (Figs. 3 and 3a). APH cannot, however, be excluded from the differential diagnosis if this sign is not present.

Administration of barium impregnated polyspheres (BIPS) is another method used in contrast radiography. The spheres are of different sizes and are administered together with a meal; if there is delayed gastric emptying of mechanical or functional nature, retention of all the spheres or of only the smaller or larger ones may be seen. The real usefulness and applicability of BIPS in veterinary medicine have yet to be established and evaluated precisely.1,2,11,12

Scintigraphy could be used to show delayed gastric emptying but requires the administration of radioactive markers and standardised techniques are not yet present for its use in veterinary medicine.

Ultrasonography is certainly the best consolidated diagnostic technique for detecting abnormalities of the gastric wall in the antral and pyloric regions and for measuring contractile and peristaltic activity (Figs. 4 and 4a). The presence of gas and ingesta in the gastric lumen can complicate ultrasound evaluation and, therefore, reduce its diagnostic sensitivity. It is important to carry out the examination when the animal has fasted for at least 12-24 hours. The finding of a distended, hyperkinetic stomach with a fluid pattern, together with ultrasonographically normal anatomy of the duodenum, should raise the suspicion of an obstructive disorder of the pylorus. The typical ultrasound appearance is a symmetrical increase in the diameter of the wall of the pyloric canal; asymmetrical wall thickening and nodular lesions of the pyloric antrum may also be found.13

An endoscopic examination enables full evaluation of the gastric lumen and confirmation of the suspected diagnosis. This investigation usually shows a stomach full of fluid, which must be aspirated to allow exploration of the antral and pyloric regions.1-3,11,12,14-16 APH is manifested as a polypoid (Figs. 5 and 6) or nodule-like lesion of the mucosa of the pyloric sphincter or the peripyloric mucosa. The mucosa usually appears pink and shiny, although it may also be irregular and hyperaemic and have small, surface erosions.2,3,14,17 The volume of the mucosa varies; the tissue can have a pedunculated or sessile base and is usually mobile. The hypertrophic mucosa completely obstructs access to the pylorus; the endoscopist must try to advance the endoscope beyond the sphincter in order to determine whether a pyloric stenosis is also present. It is possible, and relatively easy, to cross the pylorus in cases of APH. When there is hypertrophy of the antral folds, the antrum, which normally has a smooth tube-like appearance, contains mucosal folds that jut into the lumen thus markedly reducing the antral space (Figs. 7 and 7a). The folds remain even if air is insufflated and hamper normal peristalsis. In some subjects, hypertrophy of the antral folds is associated with hypertrophy of the pylorus.

A biopsy of the hypertrophic tissue must always be performed to confirm the benign nature of the lesion.2,3,14-17In fact, neoplastic conditions may have a similar appearance. Biopsy samples should also be taken from the gastric and duodenal mucosa in order to stage the gastrointestinal condition completely. Histopathology studies usually show benign hyperplasia with or without a mixed, non-specific inflammatory picture.

The diagnosis of pyloric hypertrophy should not be made exclusively on histological findings, but should be based on an overall evaluation of the history, signalment and radiographic, ultrasound, endoscopic and histological findings.

 

TREATMENT

The therapeutic approach to APH depends above all on the clinical picture. Patients with hypertrophy of the antral folds which have mild, occasional, clinical signs may benefit from appropriate medical and dietary treatment. Dietary treatment – frequent administration of small, highly digestible, liquid or semiliquid meals with a low lipid content – is aimed at facilitating gastric emptying. Histological examination of the duodenum may provide further information regarding the choice of foodstuffs to use for a targeted diet.1,2

The pharmacological treatment is very varied and involves the use of antacids and prokinetics (metoclopramide at a dose from 0.2 to 0.5 mg/kg t.i.d., cisapride at a dose from 0.1 to 0.5 mg/kg per os t.i.d., and erythromycin at a dose from 0.5 to 1 mg/kg t.i.d.), which contribute to promoting gastric emptying.1-4 In cases of hypertrophy of antral folds, medical treatment and dietary management usually lead to remission of the signs or at least to their partial improvement.

If the obstructive picture in APH is marked and the patient has metabolic alkalosis with hypokalaemia, hypochloraemia and hypernatraemia, the animal must first be stabilised and given appropriate medical treatment to restore the electrolyte balance. Surgical or endoscopic correction is performed as soon as possible after the patient’s condition has been stabilised.

Surgery is aimed at removing the pathological tissue and restoring adequate pyloric transit. Pyloroplasty is usually associated with removal of the thickened mucosa. The technique of choice is Y-U pyloroplasty which can restore adequate gastric emptying with correct functioning of the pylorus. On the basis of the surgical evaluation, in some cases pylorectomy can be performed with gastroduodenostomy (Billroth I) or a Heineke-Mikulicz pyloroplasty.2,4-6,8,18,19 In contrast, pyloromyotomy is ineffective and is not, therefore, recommended.2,4,18

 

The patient must be given intravenous fluid therapy with appropriate integrations for at least 48 hours after the operation as well as medical treatment with antibiotics, antacids and prokinetics. Signs of oesophagitis, ileus and vomiting may occur during the post-operative period.20 Surgery usually resolves the problem, but some patients may have residual pyloric dysmotility and, therefore, require continued dietary and medical treatment. In some subjects, when the polypoid growth is pedunculated, a less invasive approach can be used, consisting of asportation of the excess tissue under endoscopic vision following polypectomy with a diathermy loop (Fig. 8).14,17

This mini-invasive technique can restore the patency of the pylorus while avoiding  surgery and related post-operative complications. In the author’s experience this procedure can resolve the APH and the post-intervention period of recovery is much shorter than after surgery. The author found a case of recurrent APH 3 years after a polypectomy performed under endoscopic control.

 

References

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