Pancreatitis

Signalment

Predisposed breeds include:

Labradors
Miniature Poodles
Miniature Schnauzers
Yorkshire terriers

Middle-old aged dogs
Increased risk with obesity, diabetes mellitus, hyperadrenocorticalism, prior GIT disease or epilepsy.
Male and speyed females > intact females.

Description

Is due to the activation of digestive enzymes within the pancreas leading to autodigestion of the gland. Can be referred to as Acute or chronic pancreatitis.

Acute Pancreatitis is rapid onset inflammation of the pancreas with little or no pathological changes occuring post recovery. This may completely resolve or 'wax and wane' into the future.
Chronic Pancreatitis is continued inflammation leading to irreversible pathological changes (fibrosis, atrophy) and possible decreases in function.

The specific cause is usually idiopathic but several risk factors exist:

Nutritional: including obesity, low protein and high fat diets, feeding of ethionine, hypertriglyceridaemia and fatty meals.
Drugs and toxins: including L-asparginase, oestrogen, azathioprine, potassium bromide, furosemide, thiazide diuretics, salicylates, tetracyclines, sulphonamides, vinca alkaloids, zinc toxicosis, cholinesterase inhibitor insecticides, cholinergic agonist and hypercalcaemia.
Pancreatic Duct obstruction: caused by biliary calculi, sphincter spasm, duct wall oedema, duodenal wall oedema, neoplasia, parasites, trauma and iatrogenic reasons.
Duodenal juice reflux, Pancreatic trauma, ischaemia and reperfusion: including duodenal juice reflux into the pancreatic duct, surgical intervention, shock, anaemia, venous occlusion and hypotension.
Other: including parasitic (babesiosis), viral, mycoplasmal, end stage renal disease, liver disease and auto-immune diseases.

Cats mainly suffer from mild chronic interstitial pancreatitis.

Diagnosis

History and Clinical Signs

History of eating a fatty meal
Anorexia (Dog - 91%, Cat - 97%)
Vomiting (Dog - 90%)
Abdominal pain (Dog - 58%)
Lethargy (Dog - 79%, Cat - 100%)
Depression
Nausea
Diarrhoea (Dog - 33%) (sometimes with blood, fresh or melaena, 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 or pulmonary oedema or pleural effusions, widespread haemorrhage or DIC
Acute haemorrhagic pancreatitis may present as shock and collapse.
Cranial abdominal mass
Hypothermia (Cat - 68%)
Mild ascites
Dehydration (Mild to moderate) (Dog - 46%, Cat - 92%)
Febrile
A cats presentation is more variable. If severe, they present with lethargy and anorexia with vomiting (35%) and abdominal pain (25%) being reported less than in the dog. Mild chronic pancreatitis may show anorexia and weight loss.

Laboratory Tests

Haematology:

Leucocytosis
Increased PCV due to dehydration
Thrombocytopaenia
Neutrophilia and a left shift

Biochemistry:

Azotaemia
Increased liver enzymes
Hyperbilirubinaemia
Hyperglycaemia in cases of nectrotizing pancreatitis
Hypoglycaemia in cats with suppurative pancreatitis
Hypercholesterolaemia is very common in dogs
Hypertriglyceridaemia is very common in dogs
Hyperlipaemia may inhibit accurate evaluation of biochemical values
Hypocalcaemia
Increase in pancreatic digestive enzymes (amylase, lipase, trypsin-like immunoreactivity (TLI), phospholipase A2 and pancreatic lipase immunoreactivity (PLI))

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 fTLI is a specific test for exocrine pancreatic function without azotaemia buts the test's sensitivity varies between 30% and 60%. In comparison, the serum 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 cPLI is the most sensitive and specific test for diagnosing canine pancreatitis but serum cTLI can be used if there is no azotaemia.

Diagnostic Imaging

Survey Radiography: Rarely helpful but findings may include:

In the right cranial abdomen:
1. Increased density
2. Decreased contrast
3. Decreased granularity
Stomach displaced to left
Angle widened between pyloric antrum and proximal duodenum
Involving the Descending duodenum:
1. Displacement to the right
2. Prescence of a medial mass
3. Gas pattern
4. Thickened walls
Gastric distension
Delayed barium passage indicating abnormal peristalsis

However these findings are generally subjective so radiography is used to rule out differentials.

Abdominal Ultrasound: 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)
Hyperechogenic surronding tissue
Chronic pancreatitisand fibrosis may be hyperechogenic

Exploratory Laparotomy/Necropsy Findings

The pancreas will be oedematous, soft with fibrinous attachments to surrounding organs
Free fluid within the peritoneal cavity
Pancreas liquefaction if severe enough
Formation of pseudocysts
Omental and pancreatic haemorrhages
Areas of fat necrosis

However 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 a period as possible in patients that are vomiting but enteral and parenteral feeding can be well tolerated.

Antibiotics: if a pancreatic infection is suspected then trimethoprim-sulphonamide and enrofloxacin have good penetration to the pancreas.

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

Transfusion: Plasma or whole blood can be given with severe disease to replace α-macroglobulins. Albumin also provides oncotic support and limits pancreatic ischaemia and oedema.

Corticosteroids:for short term use in fulminating pancreatitis to be given alongside fluids. Long term treatment may lead to unwanted complications.

Dopamine: helps reduce feline pancreatitis at doses of 5µg/kg/min i.v.

Secretion prevention: Has been found to have limited clinical use but high intravenous doses of secretin has been beneficial in rat models of pancreatitis.

Enzyme inhibitors: are at the experimental stage.

Peritoneal dialysis: May be of value in removing toxic material in certain cases, especially if pancreatitis has been diagnosed by exploratory laparotomy.

Diet changes: Small amounts of water offered once the patient has stopped vomiting. 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 ahve still not returned. If sugns 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.

Supportive care: Mild cases may only require 1 or 2 days of supportive treatment. Aggressive fluid therapy will be needed to treat dehydration and fluid loss from diarrhoea and vomiting. Monitoring of renal function and potassium levels which may need supplementing. Patients may also have metabiolic 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 although these all carry a poor prognosis.

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 despite the presenting signs. Generally if the case is single episode and uncomplicated then most patients make a good recovery.

References

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

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

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