Pancreatitis - Dog
Signalment
Predisposed breeds include: Labradors, Miniature Poodles, Miniature Schnauzers, Yorkshire Terriers
Increased risk of disease occurs with obesity, diabetes mellitus, hyperadrenocorticalism, prior gastrointestinal disease or recurrent seizures.
Additionally, middle aged dogs are more commonly affected and male and spayed females are affected more frequently than entire females.
Acute Pancreatitis in Dogs
Introduction
In dogs, the condition is possibly caused by reflux of duodenal content into pancreatic duct causing release and activation of enzymes through inflammation and therefore leakage . Most cases show necrosis and fibrosis and only 3% had acute suppurative pancreatitis.
This condition is quite common in dogs and is caused by the sudden ingestion of a fatty meal. The risk, however, is increased when concurrent conditions such as obesity, diabetes mellitus, hyperadrenocorticalism, prior GIT disease or epilepsy are present as these have a relationship with the pancreas in some way.
Signalment
Yorkshire terriers, labs, minature poodles are predisposed. It is most common in middle-old dogs. Males and speyed females are of greater risk than intact females.
Clinical Signs
Clinical signs are acute in onset and include severe abdominal pain, vomiting, diarrhoea and anorexia. There may or may not be a presence of icterus.
Diagnosis
Clinical signs and history e.g. if the dog is a scavenger etc, or knowledge of underlying conditions are suggestive of the disease.
Measuring lipase may produce normal or raised results in pancreatitis. In dogs, you would expect to see a 3- 5 fold increase in lipase i acute pancreatitis and this is indicative of the disease.
Amylase is non-specific in dogs and is not commonly used to diagnose this disease. Serum trypsin-like immunoreactivity (TLI) is also of limited value. Serum pancreatic lipase immunoreactivity (PLI) will usually be raised and cPLI & fPLI look promising as sensitive and specific markers for pancreatic inflammation.
Treatment and Control
Intitially the animal should be starved for 1- 2 days maximum and placed on intravenous fluid therapy (crystalloids, colloids or plasma). Stop precipitating therapies (azathioprine) and anti-emetics and gut protectants may be given.
The dog will need analgesia. If the condition is very severe, surgery may be indicated to remove necrotic tissue.
Control may include changing the diet to a low fat diet