Pancreatitis - Dog
Predisposed breeds include: Labradors, Miniature Poodles, Miniature Schnauzers, Yorkshire Terriers
Additionally, middle aged dogs are more commonly affected and male and spayed females are affected more frequently than entire females.
History and Clinical Signs
There is often a history of eating a fatty meal.
Clinical signs include anorexia, vomiting, abdominal pain, lethargy, depression and nausea.
Diarrhoea is also a common feature sometimes with blood, fresh or melaena this occurs due to the proximity of inflamed pancreas to the duodenum and colon. More severe cases may present in shock, acute renal failure, jaundiced (due to focal hepatic necrosis), or with cardiac arrhythmias. Pulmonary oedema, pleural effusions, widespread haemorrhage, DIC, mild ascites, dehydration (mild to moderate) and pyrexia may also be present.
Acute haemorrhagic pancreatitis may present as shock and collapse.
A cranial abdominal mass may be palpated.
Affected cats have a very varied presentation. If severe, they present with lethargy and anorexia with vomiting and abdominal pain being reported less than in the dog, hypothermia is also common sign occurring in 68% of affected cats. Mild chronic pancreatitis may show anorexia and weight loss.
On Biochemistry changes may include an azotaemia, increased liver enzymes, hyperbilirubinaemia, hyperglycaemia in cases of nectrotizing pancreatitis and hypoglycaemia in cats with suppurative pancreatitis. In dogs hypercholesterolaemia and hypertriglyceridaemia are also common changes.
An increase in pancreatic digestive enzymes (amylase, lipase, trypsin-like immunoreactivity (TLI), phospholipase A2 and pancreatic lipase immunoreactivity (PLI) will also be present.
Pancreas-specific laboratory tests
All pancreatic enzymes increase following renal failure (apart from PLI) making it difficult to determine the true cause of the increase. However increases of three fold are mainly due to pancreatitis, whereas five fold increases are rarely not found to be pancreatitis. Rises in lipase, amylase and phospholipase A2 may also be hepatic, gastric, intestinal or neoplastic in origin.
In cats: Amylase and lipase are of no diagnostic value. Serum feline trypsin-like immunoreactivity (fTLI) is a specific test for exocrine pancreatic function but the test's sensitivity varies between 30% and 60%. In comparison, the serum feline pancreatic lipase immunoreactivity test (fPLI) has been found to be more specific and sensitive in diagnosing feline pancreatitis.
In dogs: Marked increases in serum lipase is a more reliable marker than amylase. However corticosteroid administration raises lipase activity by up to five fold. Serum canine pancreatic lipase immunoreactivity (cPLI) is the most sensitive and specific test for diagnosing canine pancreatitis.
Survey Radiographs are rarely helpful but findings may include an increased density in the right cranial abdomen, decreased contrast, decreased granularity and the stomach may be displaced to the left. Additionally the descending duodenum may be displaced to the right, with the presence of a medial mass and thickened walls. Gastric distension may be visible and barium passage may be delayed indicating abnormal peristalsis.
Radiography is useful to rule out differentials.
Abdominal Ultrasound is highly specific with a sensitivity of 70% in dogs and 30% in cats but is operator-dependant. Findings include pancreatic enlargement, peritoneal effusion, hypoechogenic pancreas (pancreatic necrosis) and hyperechogenic surrounding tissue.
Exploratory Laparotomy/Necropsy Findings
The pancreas will be oedematous and soft with fibrinous attachments to surrounding organs, there may be free fluid within the peritoneal cavity and pancreas liquefaction if severe enough. Pseudocysts may be present, as well as omental and pancreatic haemorrhages and areas of fat necrosis.
A biopsy should be taken to provide evidence of inflammation.
Acute Pancreatitis in Dogs
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.
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 are acute in onset and include severe abdominal pain, vomiting, diarrhoea and anorexia. There may or may not be a presence of icterus.
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
Chronic Pancreatitis in Dogs
Repeated mild episodes of acute pancreatitis and pancreatic necrosis results in progressive destruction and pancreatic fibrosis and chronic pancreatitis. If a significant proportion of pancreas is affected, signs of EPI develop +/- DM. the pancreas appears distorted ans shrunken. A nodular mass with fibrous adhesions to adjacent tissue may be present. The condition may be an incidental finding on necropsy. Focal pancreatitis may occur during canine parvovirus and distemper virus infection.
Clinical Signs include chronic abdominal pain, anorexia and intermitant vomiting and diarrhoea. There may also be there presence of icterus.
Diagnosis is usually by blood tests. These may show lipase to be normal or elevated. In dogs a 3-5 fold increase in lipase is indicative of pancreatitis. Amylase levels are usually normal and not much help. Serum trypsin-like immunoreactivity (TLI) is normal or raised in chronic disease and is also of limited value. Serum pancreatic lipase immunoreactivity (PLI) will be raised and cPLI & fPLI look promising as sensitive and specific markers for pancreatic inflammation.
Treatment and Control
Fluids may be required and analgesia. Placing the dog onto a low fat diet is useful in controlling the disease. It may be important to perform follow up blood tests at a later date to test for EPI as this is often a consequence of chronic pancreatitis.
Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
Pancreatitis in cats and dogs publications
Update on pancreatitis in dogs. Simpson, K. W.; Svoboda, M. ; Czech Small Animal Veterinary Association, Prague, Czech Republic, 2006 World Congress Proceedings. 31st World Small Animal Association Congress, 12th European Congress FECAVA, & 14th Czech Small Animal Veterinary Association Congress, Prague, Czech Republic, 11-14 October, 2006, 2006, pp 382-389 - Full Text Article
For further information on canine pancreatitis see: Pancreatitis in the dog:. dealing with a spectrum of disease In Practice article
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