Difference between revisions of "Pancreatitis"

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==Introduction==
 
[[Image:Pancreatitis.jpg|right|thumb|200px|<small><center>Pancreatitis (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
Pancreatitis occurs following activation of digestive enzymes within the [[Pancreas - Anatomy & Physiology|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 occurring post recovery. This may completely resolve or 'wax and wane' in the future.  
+
 +
==Description==
 +
Occurs following activation of digestive enzymes within the [[Pancreas - Anatomy & Physiology|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' in the future.  
  
'''Chronic''' pancreatitis is continued inflammation leading to irreversible pathological changes (fibrosis, atrophy) and possible decreases in function.
+
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 including:
+
The specific cause is usually idiopathic but several risk factors exist including
  
A '''Nutritional''' basis which refers to obesity, low protein and high fat diets, feeding of ethionine and hypertriglyceridaemia.
+
A '''Nutritional''' basis which refers to 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|tetracyclines]], [[Sulphonamides|sulphonamides]], vinca alkaloids, zinc toxicosis, cholinesterase inhibitor insecticides, cholinergic agonist and hypercalcaemia.
 
'''Drugs and toxins''' including L-asparginase, oestrogen, azathioprine, potassium bromide, furosemide, thiazide diuretics, salicylates, [[Tetracyclines|tetracyclines]], [[Sulphonamides|sulphonamides]], vinca alkaloids, zinc toxicosis, cholinesterase inhibitor insecticides, cholinergic agonist and hypercalcaemia.
  
'''Pancreatic duct obstruction''' which is caused by biliary calculi, sphincter spasm, duct wall oedema, duodenal wall oedema, neoplasia, parasites, trauma and iatrogenic reasons.
+
'''Pancreatic Duct obstruction''' which is 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''' which includes duodenal juice reflux into the pancreatic duct, surgical intervention, [[shock]], [[Regenerative and Non-Regenerative Anaemias|anaemia]], venous occlusion and hypotension.  
+
'''Duodenal juice reflux, Pancreatic trauma, ischaemia and reperfusion''' which includes duodenal juice reflux into the pancreatic duct, surgical intervention, shock, anaemia, venous occlusion and hypotension.  
  
 
'''Other''' risk factors include parasitic (babesiosis), viral, mycoplasmal, end stage renal disease, liver disease and auto-immune diseases.
 
'''Other''' risk factors include parasitic (babesiosis), viral, mycoplasmal, end stage renal disease, liver disease and auto-immune diseases.
Line 22: Line 22:
 
Cats mainly suffer from mild chronic interstitial pancreatitis.
 
Cats mainly suffer from mild chronic interstitial pancreatitis.
  
 +
==Signalment==
 +
Predisposed breeds include:
 +
<gallery>
 +
Image:Labrador.jpg|'''Labradors''' <br> Ellen Levy Finch (2004) WikiMedia Commons
 +
Image:Miniature Poodle.jpg|'''Miniature Poodles''' <br> Belinda (2005) WikiMedia Commons
 +
Image:Miniature schnauzer.jpg|'''Miniature Schnauzers''' <br> MagnusK (2006) WikiMedia Commons
 +
Image:Yorkshire Terrier.jpg|'''Yorkshire terriers''' <br> Jlcerso (2007) WikiMedia Commons
 +
</gallery>
  
== Acute Haemorrhagic Pancreatitis ==
 
  
This term is often interchangeable with [[Pancreatic Necrosis, Acute|acute pancreatic necrosis]] or '''acute pancreatitis'''. The condition can be mild or severe, non-fatal or fatal. It usually occurs as a sudden onset condition, often after ingestion of a meal rich in fat, but this depends on what species the condition occurs.  
+
Increased risk of disease occurs with obesity, [[Diabetes Mellitus|diabetes mellitus]], [[Adrenal Glands - Pathology#Adrenal Hyperfunction|hyperadrenocorticalism]], prior gastrointestinal disease or [[CNS Seizures - Pathology|recurrent seizures]].
  
The [[Pancreas - Anatomy & Physiology#Endocrine|Islets of Langerhans]] may become involved thus causing the signs if insulin insufficiency. Pancreatitis may be initiated by trauma which initiates the leakage of enzymes. It can also present as recurrent acute pancreatitis - repeated inflammation with minimal permanent pathology. In the disease process, proteolytic degradation of pancreatic parenchyma, vascular damage and haemorrhage occur as well as necrosis of fat by lipolytic enzymes in the pancreas and surrounding omentum. These changes are concentrated at the periphery of lobules and infiltration by leukocytes indicates inflammation. In mild cases oedema of the interstitial tissue occurs. In more severe cases the [[Pancreas - Anatomy & Physiology|pancreas]] is haemorrhagic and oedematous with greyish white areas of necrosis and this may be interspersed with normal parenchyma. The [[Peritoneal Cavity - Anatomy & Physiology|peritoneal cavity]] may contain blood-stained fluid sometimes with droplets of fat. Due to these large amounts of necrotic debris, infection by microorganisms from the [[Alimentary System Overview - Anatomy & Physiology|GIT]] is likely, causing abscesses.  
+
Additonally middle aged dogs are more commonly affected and Male and speyed females are affected more frequently than entire females.
  
=== Cats and Dogs===
+
==Diagnosis==
 +
===History and Clinical Signs===
 +
There is often a history of eating a fatty meal.
  
See [[Pancreatitis - Cat]] and [[Pancreatitis - Dog]]
+
Clinical signs include anorexia, vomiting, abdominal pain, lethargy, depression and Nausea.
 +
[[Diarrhoea|Diarrhoea]] is also a common feature sometimes with blood, fresh or melaena this occurs due to the proximity of inflamed pancreas to the [[Duodenum - Anatomy & Physiology|duodenum]] and [[Colon - Anatomy & Physiology|colon]].
 +
More severe cases may present in [[Shock - Pathology|shock]], [[Kidney Renal Failure - Pathology#Acute|acute renal failure]], [[Icterus|jaundiced]] (due to focal hepatic necrosis), or with cardiac arrhythmias. Pulmonary oedema, pleural effusions, widespread haemorrhage, [[Disseminated Intravascular Coagulation|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.
  
=== Other Animals ===
+
 +
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 occuring in 68% of affected cats. Mild chronic pancreatitis may show anorexia and weight loss.
  
In '''horses''', necrosis and inflammation results due to migration of parasites, usually strongyle larvae, releasing pancreatic enzymes causing autodigestion. Destructive granulomatous pancreatitis is a part of multisystemic eosinophilic epitheliotrophic syndrome.  
+
===Laboratory Tests===
 +
On Haematology there may be a leucocytosis, an increased Packed Cell Volume due to dehydration, thrombocytopaenia, [[Neutrophilia|neutrophilia]] and a left shift.
  
In '''pigs''' suppuration of the pancreas can occasionally arise as an extension from nearby infection, eg. peritonitis and perforated oesophageal ulcers.
+
On Biochemistry changes may include an [[Azotaemia|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.  
  
== Chronic Interstitial Pancreatitis ==
+
An increase in pancreatic digestive enzymes (amylase, lipase, trypsin-like immunoreactivity (TLI), phospholipase A2 and pancreatic lipase immunoreactivity (PLI) will also be present.
  
Chronic pancreatitis often occurs following ongoing inflammation with progression to irreversible damage and impaired function. There is usually fibrosis and reduction in acinar mass. This condition can occur in all species as a consequence of obstruction of the pancreatic ducts, [[Vitamin A Deficiency|vitamin A deficiency]] may predispose to this. The condition is most common in the dog, but also in cat, horse and cattle. The [[Pancreas - Anatomy & Physiology#Endocrine|islets of Langerhans]] tend to be preserved. If chronic pancreatitis persisits it can lead to [[Exocrine Pancreatic Insufficiency]] (EPI). In cats, chronic pancreatitis can also lead to [[Diabetes Mellitus]] developing.
+
===Pancreas-specific laboratory tests===
 +
All pancreatic enzymes increase following [[Kidney Renal Failure - Pathology|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.  
  
=== Cats and Dogs===
+
'''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.
  
See [[Pancreatitis - Cat]] and [[Pancreatitis - Dog]]
+
'''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.
  
=== Other Animals ===
+
===Diagnostic Imaging===
 +
'''Survey Radiography''' 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.
  
'''In sheep'''
+
Radiography is useful to rule out differentials.
  
Necrosis of [[Pancreas - Anatomy & Physiology#Exocrine|exocrine pancreatic cells]] followed by fibrosis can be caused by zinc toxicosis. Focal pancreatitis may occur during [[Foot_and_Mouth_Disease|Foot and Mouth disease]] resulting in [[DM|diabetes mellitus]] during recovery.
+
'''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.
  
'''In horses'''
+
===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 [[Haemorrhage - Pathology|haemorrhages]] and areas of fat necrosis.
  
Chronic pancreatitis can occur sporadically and is usually a consequence of [[Pancreas - Parasitic Pathology|parasitic migration]] or from ascending bacterial infection of pancreatic ducts. It can occur alongside '''chronic eosinophilic gastroenteritis''' and is usually clinically silent. Organ tends to be replaced by scar tissue.
+
A biopsy should be taken to provide evidence of inflammation.
  
'''In cattle'''
+
==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.
  
Focal pancreatitis may occur during [[Foot_and_Mouth_Disease|Foot and Mouth disease]] resulting in [[DM|diabetes mellitus]] during recovery.<br>{{Learning
+
Analgesia should always be given even without signs of pain. Recommended options include subcutaneous [[Opioids#Pethidine|pethidine]], intravenous or continuous rate infusion [[Opioids#Morphine|morphine]] or transdermal [[Opioids#Fentanyl|fentanyl]]. Dogs can also be given intraperitoneal [[Local Anaesthetics#Lidocaine|lidocaine]] or [[Local Anaesthetics#Bupivicaine|bupivicaine]].
|Vetstream = [https://www.vetstream.com/felis/search?s=pancreatitis Pancreatitis]
 
|literature search = [http://www.cabdirect.org/search.html?q=title%3A%28%22pancreatitis%22%29+AND+%28od%3A%28cats%29+OR+title%3A%28dogs%29%29&fq=sc%3A%22ve%22 Pancreatitis in cats and dogs publications]
 
}}
 
  
{{Chapter}}
+
If a pancreatic infection is suspected then [[Antibiotics|antibiotics]]  should be administered, [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.
{{Mansonchapter
 
|chapterlink = http://www.mansonpublishing.co.uk/book-images/9781840761115_sample.pdf
 
|chaptername = Acute Pancreatitis
 
|book = Clinical Medicine of the Dog and Cat, 2nd edition
 
|author = Michael Schaer
 
|isbn = 9781840761115
 
}}
 
  
==References==
+
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.
  
Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) '''Bovine Medicine''' (Second edition), ''Blackwell Publishing''
+
Cases often require supportive care, aggressive [[Principles of Fluid Therapy|fluid therapy]] will be needed to treat dehydration and fluid loss from [[Diarrhoea|diarrhoea]] and vomiting. Renal function and potassium levels should be monitored and if necessary pottasium should be supplemented.
 +
Patients may also develop a metabolic acidosis in acute pancreatitis or be alkalotic due to vomiting. Should [[Diabetes Mellitus|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.
  
Bertone, J. (2006) '''Equine Geriatric Medicine and Surgery''', ''Elsevier''
+
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.
  
Blood, D.C. and Studdert, V. P. (1999) '''Saunders Comprehensive Veterinary Dictionary''' (2nd Edition), ''Elsevier Science''
+
For short term use in fulminating pancreatitis [[Steroids|Corticosteroids]] can be given alongside fluids. Long term treatment may lead to unwanted complications.
  
Brown, C.M, Bertone, J.J. (2002) '''The 5-Minute Veterinary Consult- Equine''', Lippincott, ''Williams & Wilkins''
+
===Long-term treatment===
 +
In most patients that have one episode, they may only need to avoid fatty foods. Recurrent hypertriglyceridaemia may need pharmacological intervention.
  
Cowart, R.P. and Casteel, S.W. (2001) '''An Outline of Swine diseases: a handbook,''' ''Wiley-Blackwell''
+
==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.
  
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''
+
==References==
 
 
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''
+
For further information on canine pancreatitis see: [http://inpractice.bvapublications.com/cgi/reprint/26/2/64?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=feline+pancreatitis&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT Pancreatitis in the dog:. dealing with a spectrum of disease] In Practice article
  
Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition),''' ''BSAVA''
+
For further information on feline pancreatitis see: [http://inpractice.bvapublications.com/cgi/reprint/29/8/470?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=feline+pancreatitis&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT Feline pancreatitis: current concepts and treatment guidelines] In Practice article
  
Jackson, G.G. and Cockcroft, P.D. (2007) '''Handbook of Pig Medicine,''' ''Saunders Elsevier''
+
Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''
 
 
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students University of Liverpool'''
 
  
 
Merck & Co (2008) '''The Merck Veterinary Manual''' ''Merial''
 
Merck & Co (2008) '''The Merck Veterinary Manual''' ''Merial''
 
+
[[Category:Pancreas_-_Inflammatory_Pathology]][[Category:Dog]][[Category:Cat]]
Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine''' (Fourth Edition) ''Mosby Elsevier''
+
[[Category:To_Do_-_Caz]]
 
 
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''
 
 
 
 
 
{{review}}
 
 
 
{{OpenPages}}
 
 
 
[[Category:Pancreas_-_Inflammatory_Pathology]][[Category:Pancreatic Diseases - Dog]][[Category:Pancreatic Diseases - Cat]]
 
 
 
 
 
[[Category:Pancreatic_Diseases_-_Pig]] [[Category:To_Do_-_Review]] [[Category:Pancreatic_Diseases_-_Horse]][[Category:Pancreatic_Diseases_-_Sheep]]
 

Revision as of 18:05, 9 August 2010




Description

Occurs following 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' in 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 including

A Nutritional basis which refers to 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 which is 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 which includes duodenal juice reflux into the pancreatic duct, surgical intervention, shock, anaemia, venous occlusion and hypotension.

Other risk factors include parasitic (babesiosis), viral, mycoplasmal, end stage renal disease, liver disease and auto-immune diseases.

Cats mainly suffer from mild chronic interstitial pancreatitis.

Signalment

Predisposed breeds include:


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

Additonally middle aged dogs are more commonly affected and Male and speyed females are affected more frequently than entire females.

Diagnosis

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 occuring 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 Radiography 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 pottasium 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.

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 Merial