Gastric Ulceration - Dog

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Gastric Ulceration - Copyright David Walker RVC

Signalment

• Sled dogs

Description

Is a round or oval punched out lesions ranging from 1-4 cm in diameter caused by damage to the gastric mucosa.

There are many disease associations including:

Disease type	E.g.
Hypotension	Shock, Sepsis
Drug - induced	Non-steroidal anti-inflammatory drugs (NSAIDs)
Idiopathic	Stress, exercise induced
Inflammatory	Gastritis, Pancreatitis
Neoplastic	Adenocarcinoma, lymphosarcoma, leiomyoma, gastrinoma (Zollinger-Ellison syndrome),
Metabolic/endocrine	Hypoadrenocorticism, liver disease, uraemia, Disseminated Intravascular Coagulation (DIC), mastocytosis and hypergastrinaemia

Gastric ulceration is caused by damage to the gastric mucosa through the above mechanisms. NSAIDs directly damage the mucosa and interfere with the prostaglandin synthesis. Gastric ulceration is worsened by the use of NSAIDs in combination with corticosteroids. This risk can be minimised by using cyclooxygenase-1 (COX-1) sparing NSAIDs (carprofen, meloxicam and deracoxib).

Gastric acid hypersecretion following mast cell degranulation of histamine and gastrin secretion from gastrinomas is a major cause of gastric ulceration. Sled dogs and equine race horses are prone to gastric ulceration.

Diagnosis

History and Clinical Signs

History may involve:

• Access to toxins and drugs such as NSAIDs

Clinical Signs:

• Vomiting
• Haematemesis
• Malaena
• Pale mucous membranes
• Abdominal pain
• Weakness
• Inappetance
• Hypersalivation
• Circulatory comprimise

Haematology

• Anaemia - regenerative initially, may progress to microcytic, hypochromic and minutely regenerative.
• Thrombocytosis
• Lack of stress leucogram (and lymphocytosis and eosinophilia) supportive of hypoadrenocorticism
• Examination of the buffy coat may detect mastocytosis
• Neutrophilia and a left shift - signs of inflammation or gastric perforation
• May show abnormalities in haemostasis

Biochemistry

• Dehydration - azotaemia
• Hepatic disease - increased liver enzymes and bilirubin, decreased urea, albumin and cholesterol
• Renal disease - azotaemia
• Hypoadrenocorticism - Sodium:Potassium ratio of less than 27:1
• Vomiting will lead to electrolyte and acid-base abnormalities - metabolic alkalosis, hypokalaemia and hypochloraemia

Urinalysis

• Dehydration - Hypersthenuria
• Renal disease - Isosthenuria

Plain radiography

Gastric Ulceration - Copyright David Walker RVC

Not usually diagnostic but rules out differentials.

Positive contrast radiography

May show filling defects.

Ultrasonography

Shows gastric thickening and rules out differentials.

Endoscopy and Biopsy

Diagnostic test of choice and allows biopsies to be taken. NSAID related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated gastric tumours will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased to avoid further deepening or perforation.

Treatment

The main aim is to treat any primary underlying cause whilst giving general support. This may be hydrating, restoring electrolytes and acid-base and also helping the gastric lining to recover. Anti-ulcerative therapy should be continued for up to 6-8 weeks.

Fluid Therapy

Depends upon degree of dehydration, prescence of shock and any other diseases that are affected by volume. Prolonged vomiting or anorexia may lead to hypokalaemia so KCl may need adding to any fluids given. Normal rates for treatment of shock apply with dehydration being overcome by a fluid rate over 24 hours to replace the defecits along with a maintenance rate.

Acid-base correction

Imbalances should be corrected after taking a blood gas reading.

• If metabolic acidotic: give sodium bicarbonate but do repeated blood gas
• If metabolic alkalosis: replace volume defecit with intravenous NaCl and KCl.
• Blocking of acid secretion:
  • Histamine receptor antagonists:
    • cimetidine
    • ranitidine
    • famotidine
  • Gastrin antagonists:
    • proglumide
  • Acetylcholine receptor antagonists:
    • atropine
    • pirenzepine
  • Adenyl cyclase inhibitors:
    • prostaglangin E2 (PGE) analogues (misoprostol)
  • H⁺:K⁺ATPase inhibitors :- for use when patient is refractory to histamine antagonists
    • omeprazole - good for exercise induced gastric ulceration

Mucosal protectants

Such as misoprostol can be given alongside NSAIDs to decrease the risk of ulceration. Sucralfate which is polyaluminium sucrose sulphate, binds to damaged mucosa and assists in the treatment of gastric ulceration. It is best given 2 hours after acid inhibitors to prevent interference.

Prophylaxis

Prophylactic treatment has been shown not to prevent gastric ulceration. Sucralfate is reported to be the best drug in patients receiving high doses of glucocorticoids.

Anti-emetics

Indicated if vomiting is severe causing fluid and electrolyte imbalances and discomfort. See Anti-emetics for drug details.

Analgesia

Is best provided by opiods such as buprenorphine, pethidine and fentanyl.

Antibiotics

Animals suffering from shock and gastric barrier dysfunction may require prophylactic antibiotic cover. First line drugs include ampicillin or a cephalosporin which are effective against Gram-positive, some Gram-negative and some anaerobes. These can be combined with an aminoglycoside which are effective against Gram-negative aerobes if sepsis is present. Enrofloxacin can also be used instead of an aminoglycoside in skeletally mature animals

Surgery

May be required to investigate or to resect peforating ulcers which may lead to peritonitis.

Prognosis

For animals with peptic ulcers is good. Prognosis is poorer for patients with renal or hepatic failure related ulcers. It is also poor for animals with gastric carcinoma and gastrinoma.

References

Hall, J.E., Simpson, J.W. and Williams, D.A., (2005) BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition) BSAVA

Merck & Co (2008) The Merck Veterinary Manual