Ulcers are uncommon in the dog. They are usually ‘peptic’ which means they develop in the presence of acid and pepsin, and are most commonly located in the body, antrum, pylorus or proximal duodenum. Normally the stomach can resist damage through protection from the gastric mucosal barrier. Anything which damages this barrier will lead to inflammation and ulceration. Acute lesions are often manifest as multiple superficial erosions, while chronic lesions are single circumscribed deep ulcers with raised margins. Location, morphology and clinical manifestations vary with underlying pathogenesis. All the agents which cause acute and chronic gastritis together with anything which increases gastric acid production, changes the acid — base balance or effects the nutritional status can cause ulceration. The aetiology is large and complex and may be described as follows:
- Drugs — such as aspirin, flunixin and phenylbutazone. They act by interfering directly with the mucosal barrier and not by increased acid production. Corticosteroids also cause ulceration by decreasing mucosal cell turnover, reducing mucus production both of which lead to loss of protection of the mucosa. In addition they increase gastrin levels, which stimulate acid production.
- Shock, hypotension, trauma, central nervous system disease and severe illness. These are stress ulcers which occur as multiple small superficial erosions mainly in the body of the stomach.
- Bile reflux. Bile acids are ulcerogenic and work together with factors inducing gastric ischaemia, excess acid and pepsin secretions to damage the gastric mucosal barrier. The prevalence of bile acid reflux is not clear but may be quite common.
- Neuroendocrine. Stress causes release of cortisol and catecholamines which are thought to be ulcerogenic. If this occurs in conjunction with increased sympathetic drive causing vasoconstriction and thus mucosal ischaemia there is a real probability of ulcer formation.
- Neurological disease. Dogs with spinal cord lesions undergoing surgery and receiving corticosteroids may develop haemorrhagic gastritis or deep ulceration of gastric mucosa often with high mortality. The spinal cord lesions are thought to lead to altered sympathetic/parasympathetic balance and stress ulceration. Vagal stimulation leads to vasodilation, increases acid and enzyme secretion. In addition to these changes animals with cord lesions often receive corticosteroids and this compounds the ulcerogenic effect.
- Metabolic disease. In renal disease elevated blood urea and urea products occur. These toxins may damage, among many tissues, the gastric mucosa. Renal disease also delays excretion of gastrin and this continues to stimulate acid production. Ulcers may also occur in liver disease although the cause is not known but may be associated with catabolism of gastrin or other toxins. Murray et al. () described 22 dogs with gastric ulcers, of which 16 had concurrent liver disease.
- Hyperacidity. There are many conditions which increase acid production and hence increase risk of gastric ulceration. Increased vagal stimulation and elevated gastrin or histamine levels will have this effect. These peptic ulcers tend to be confined to the antrum and proximal duodenum. Increased gastrin comes from gastrin secreting tumours found in either the stomach or pancreas. The condition is similar to Zollinger—Ellison syndrome observed in man and dogs (). Secondary increases in gastrin levels occur when gastrin is retained in renal disease. Further parietal cells are stimulated to produce more acid by elevated histamine levels. Such levels originate from systemic mastocytomas or mast cell tumours in the liver ().
- Ulceration can be associated with the presence of gastric neoplasia where the tumour involves the mucosa and there is a breakdown of the gastric mucosal barrier. For this reason it is essential to biopsy any dog or cat with gastric ulceration to determine if neoplasia is present.
Gastric ulceration: Clinical diagnosis
Vomiting with the presence of blood usually indicates ulceration. Blood may be present in small amounts, as large clots or occur as ‘coffee grounds’ if retained in the stomach for some time prior to vomition. A microcytic anaemia may be observed in chronic ulceration as may dark tarry faeces if blood passes through the pylorus and intestinal tract. Nausea, variable appetite, weight loss, polydipsia and gastric pain, manifest by assuming the praying position, may all occur (). Some dogs exhibit marked salivation particularly in advanced cases, while other dogs show no clinical signs at all ().
Contrast studies may reveal filling defects or barium retention. Endoscopy is the best confirmatory method of diagnosis. Chronic ulcers show little inflammation but appear as craters with raised peripheries and may bleed easily. Stress ulcers appear as small punctate submucosal haemorrhages scattered over the stomach surface. Biopsy via exploratory laparotomy or endoscopy (Plate 2) is essential as ulcers may be associated with malignant neoplasia. Plasma gastrin levels should be checked, the normal fasted range for the dog being 20 to 70pg/ml. Results should be interpreted carefully as gastrin levels may be increased in renal or hepatic disease, gastric retention and gastritis ().
Gastric ulceration: Treatment
The prognosis depends on the underlying cause and also whether the most frequent complication, namely perforation and peritonitis has occurred (). An underlying cause should be determined and further mucosal damage prevented. If no obvious cause is found then the symptoms should be treated, thus improving the mucosal environment. The diet should be changed to a low fat diet fed as frequent small meals. In addition metaclopramide (Emequell; SmithKline Beecham) at 0.5 to 1.0mg/kg every 8h may be used to reduce vomiting. Oral antacids may be used to neutralize the acid and to inactivate the pepsin (Table Antacids available to control the production or effects of gastric acid). Non-systemic antacids must be given frequently as infrequent use often leads to rebound hyperacidity. This occurs because of the failure in the negative feedback reflex where low pH reduces gastrin and hence acid production. The maximum frequency of dosing should be every 2h. At this dose rate there are risks of sodium overload, alkalosis and diarrhoea from magnesium salts. Aluminium hydroxide may lead to phosphate deficiency. Gastric acidity may also be reduced using systemic H2 blockers which block the histamine receptor on the parietal cell. These drugs are useful in idiopathic ulceration, gastritis, mast cell tumour, gastrinomas and in uraemia. Cimetidine (Tagamet; SmithKline Beecham) at 5mg/kg tid has been shown to be effective with no apparent toxicity. Anticholinergic drugs reduce vagal stimulation of acid production, and allow smooth muscle relaxation, but also reduce gastric emptying. This causes distention of the stomach which in turn stimulates acid production. Carbenoxolone (Winthrop) is a drug which protects gastric/duodenal mucosa by promoting mucus production and prolonging the life of epithelial cells. Sucralfate is a new drug given orally to coat and seal gastric ulcers, effectively ‘bandaging’ the ulcer. This prevents any further inflammation from acid or pepsin activity. It is a human preparation and as yet there is no suitable data for veterinary use.
Table Antacids available to control the production or effects of gastric acid
|Non-systemic antacids||Aluminium hydroxide, calcium carbonate Magnesium hydroxide:
|Systemic antacids||H2 blockers:
Z an tec
Gastric haemorrhage may be treated with oral iced water and noradrenaline 8mg/500ml by stomach tube. Any absorbed noradrenaline is removed by passage through the liver. The lavage should be left in the stomach for 5 to 30min, then removed to assess for further bleeding. Surgical resection of ulcers may be required especially in cases where tumour is involved.
Selections from the book: “Digestive Disease in the Dog and Cat” (1991)