Pancreatitis - Cat

Introduction

See Pancreatitis for general overview of the disease.

Cats mainly suffer from mild chronic interstitial pancreatitis.

General Disease

Signalment

Increased risk of disease occurs with obesity, diabetes mellitus, hyperadrenocorticalism, prior gastrointestinal disease or recurrent seizures.

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.

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.

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

Introduction

Cats occasionally get the acute necrotizing form seen in dogs, but acute interstitial pancreatitis in seen mainly with systemic toxoplasmosis. Cats mainly get chronic pancreatitis, rather than the acute form. Pyogranulomatous pancreatitis occurs in FIP. Serum amylase and lipase are unreliable (extrahepatic sources and both are excreted by the kidneys). There is usually a high serum glucose and cholesterol, with low serum potassium and calcium present on blood tests. Serum feline tryspin-like immunoreactivity is poorly associated with histopathological diagnosis.

Clinical Signs

Signs are very vaue and may include vomiting, diarrhoea and anorexia.
Acute haemorrhagic pancreatitis may present as shock and collapse.

Diagnosis

In cats it is a much less common disease and so therefore more difficult to diagnose, especially as the clinical signs are so vague. In cats lipase, amylase and Serum trypsin-like immunoreactivity (TLI) have little value. Serum pancreatic lipase immunoreactivity (PLI) is usually raised and cPLI & fPLI look promising as sensitive and specific markers for pancreatic inflammation.

Treatment

Do not starve cats. Intravenous fluid therapy is required and a feeding tube may be placed (risk of hepatic lipidosis if do not eat).

Chronic Pancreatitis

Image of chronic pancreatitis and fibrosis in a cat from Cornell Veterinary Medicine

This chronic, relapsing condition is more common than the acute condition in cats. Fibrosis, ductular ectasia with cyst formation and inflammation will be present on the pancreas. The condition has been associated with hepatic lipidosis, cholangiohepatitis and inflammatory bowel disease.

Clinical Signs

Clinical signs are vague and may include vomiting, diarrhoea, anorexia, lethargy and icterus.

Diagnosis

Blood tests for lipase may be normal or elevated in cats and therfore may or may not be any use. Amylase and Serum trypsin-like immunoreactivity (TLI) are not useful in cats. Serum pancreatic lipase immunoreactivity (PLI) will be raised and cPLI & fPLI look promising as sensitive and specific markers for pancreatic inflammation.

Treatment

Treat the underlying cause if there is one. Treatment may include placing the animal on a low fat diet and giving supportive care such as fluids and analgesia. If the cat is not eating, place a feeding tube as starvation may cause hepatic lipidosis in cats.

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

Pancreatitis in cats. Graves, T. K.; Ontario Veterinary Medical Association, Milton, Canada, Ahead of the curve: OVMA Conference Proceedings, 26-28 January, 2006, 2006, pp 158-163 - Full Text Article

References

For further information on feline pancreatitis see: Feline pancreatitis: current concepts and treatment guidelines 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

Sturgess, K. (2003) Notes on Feline Internal Medicine Blackwell Publishing

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