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.

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.

Laboratory Tests

On Haematology there may be a leucocytosis, an increased Packed Cell Volume due to dehydration, thrombocytopaenia, neutrophilia and a left shift.

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.

Diagnostic Imaging

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.

Treatment

Acute Treatment

The general treatment involves fluid correction and maintenance while any underlying cause is treated. Support is then given to allow the inflammatory process to subside. Oral feeding should be witheld for a short period in vomiting patients but enteral and parenteral feeding can be well tolerated.

Analgesia should always be given even without signs of pain. Recommended options include subcutaneous pethidine, intravenous or continuous rate infusion morphine or transdermal fentanyl. Dogs can also be given intraperitoneal lidocaine or bupivicaine.

If a pancreatic infection is suspected then antibiotics should be administered, trimethoprim-sulphonamide and enrofloxacin have good penetration to the pancreas.

Food can be gradually introduced with a low protein and fat content as these are more likely to cause signs. Fat can be further introduced if symptoms have still not returned. If signs reoccur then further starvation should be carried out. Total parenteral nutrition can be used to sustain animals that are unable to tolerate food at all.

Cases often require supportive care, aggressive fluid therapy will be needed to treat dehydration and fluid loss from diarrhoea and vomiting. Renal function and potassium levels should be monitored and if necessary potassium should be supplemented. Patients may also develop a metabolic acidosis in acute pancreatitis or be alkalotic due to vomiting. Should diabetes mellitus develop, this may require treatment with insulin. Further management may be required for respiratory distress, bleeding disorders, renal failure, cardiovascular problems and neurological disorders.

Additionally a whole blood or plasma transfusion can be given with severe disease to replace α-macroglobulins. Albumin also provides oncotic support and limits pancreatic ischaemia and oedema.

For short term use in fulminating pancreatitis, corticosteroids can be given alongside fluids. Long term treatment may lead to unwanted complications.

Long-term treatment

In most patients that have one episode, they may only need to avoid fatty foods. Recurrent hypertriglyceridaemia may need pharmacological intervention.

Prognosis

The disease varies widely and the prognosis can vary from full recovery to death. Generally if the case is an uncomplicated single episode patients will make a good recovery.

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

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

Clinical Signs include chronic abdominal pain, anorexia and intermitant vomiting and diarrhoea. There may also be there presence of icterus.

Diagnosis

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.

Literature Search

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

References

For further information on canine pancreatitis see: Pancreatitis in the dog:. dealing with a spectrum of disease In Practice article

Blood, D.C. and Studdert, V. P. (1999) Saunders Comprehensive Veterinary Dictionary (2nd Edition), Elsevier Science

Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition), W.B. Saunders Company

Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2), W.B. Saunders Company

Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition), Mosby Elsevier

Hall, E.J, 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 Merial

Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier

Tilley, L.P. and Smith, F.W.K.(2004) The 5-minute Veterinary Consult (Third edition) Lippincott, Williams & Wilkins