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.
+
[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]
  
−
'''Chronic''' pancreatitis is continued inflammation leading to irreversible pathological changes (fibrosis, atrophy) and possible decreases in function.
+
==Signalment==
 +
*Predisposed breeds include:
 +
<gallery>
 +
Image:Labrador.jpg|Labradors
 +
Image:Yorkshire Terrier.jpg|Yorkshire terriers
 +
Image:Miniature schnauzer.jpg|Miniature Schnauzers
 +
Image:Miniature Poodle.jpg|Miniature Poodles
 +
</gallery>
 +
*Middle-old aged dogs
 +
*Increased risk with obesity, [[DM|diabetes mellitus]], [[Adrenal Glands - Pathology#Adrenal Hyperfunction|hyperadrenocorticalism]], prior [[Alimentary - Anatomy & Physiology|GIT]] disease or epilepsy.
 +
*Male and speyed females > intact females.
  
−
The specific cause is usually idiopathic but several risk factors exist including:
+
==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.
  
−
A '''Nutritional''' basis which refers to obesity, low protein and high fat diets, feeding of ethionine and hypertriglyceridaemia.
+
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|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, 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.
−
'''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''': 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.
−
'''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.  
 
−
 
 
−
'''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.
 
Cats mainly suffer from mild chronic interstitial pancreatitis.
 +
==Diagnosis==
 +
===History and Clinical Signs===
 +
*History of eating a fatty meal
 +
*Anorexia
 +
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]]
 +
*Abdominal pain
 +
*Lethargy
 +
*Depression
 +
*Nausea
 +
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (sometimes with blood, fresh or melaena, 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, 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
 +
*Mild ascites
 +
*Dehydration (Mild to moderate)
 +
*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 and an increased PCV due to dehydration.
  
 +
'''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))
  
−
== Acute Haemorrhagic Pancreatitis ==
+
===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.  
−
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.
 
−
 
 
−
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.  
 
−
 
 
−
=== Cats and Dogs===
 
−
 
 
−
See [[Pancreatitis - Cat]] and  [[Pancreatitis - Dog]]
 
  
−
=== Other Animals ===
+
'''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 '''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.  
+
'''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:
 +
##Increased density
 +
##Decreased contrast
 +
##Decreased granularity
 +
#Stomach displaced to left
 +
#Angle widened between pyloric antrum and proximal duodenum
 +
#Involving the Descending duodenum:
 +
##Displacement to the right
 +
##Prescence of a medial mass
 +
##Gas pattern
 +
##Thickened walls
 +
#Gastric distension
 +
#Delayed barium passage indicating abnormal peristalsis
 +
However these findings are generally subjective so radiography is used to rule out differentials.
  
−
In '''pigs''' suppuration of the pancreas can occasionally arise as an extension from nearby infection, eg. peritonitis and perforated oesophageal ulcers.
+
'''Abdominal Ultrasound''': Highly specific with a sensitivity of 70% in dogs and 30% in cats. Findings include:
 +
*Pancreatic enlargement
 +
*Peritoneal effusion
 +
*Hypoechogenic pancreas (pancreatic necrosis)
 +
*Hyperechogenic surronding tissue
 +
*Chronic pancreatitisand fibrosis may be hyperechogenic
  
−
== Chronic Interstitial Pancreatitis ==
+
===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
  
−
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.
+
==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.  
  
−
=== Cats and Dogs===
+
'''Antibiotics''': if a pancreatic infection is suspected then [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.
  
−
See [[Pancreatitis - Cat]] and  [[Pancreatitis - Dog]]
+
'''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.
  
−
=== Other Animals ===
+
'''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.
  
−
'''In sheep'''
+
'''Corticosteroids''':for short term use in fulminating pancreatitis to be given alongside fluids. Long term treatment may lead to unwanted complications.
  
−
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.
+
'''Dopamine''': helps reduce feline pancreatitis at doses of 5µg/kg/min i.v.
  
−
'''In horses'''
+
'''Secretion prevention''': Has been found to have limited clinical use but high intravenous doses of secretin has been beneficial in rat models of pancreatitis.
  
−
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.
+
'''Enzyme inhibitors''': are at the experimental stage.
  
−
'''In cattle'''
+
'''Peritoneal dialysis''': May be of value in removing toxic material in certain cases, especially if pancreatitis has been diagnosed by exploratory laparotomy.
  
−
Focal pancreatitis may occur during [[Foot_and_Mouth_Disease|Foot and Mouth disease]] resulting in [[DM|diabetes mellitus]] during recovery.<br>{{Learning
+
'''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.
−
|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}}
+
'''Supportive care''':
−
{{Mansonchapter
+
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.
−
|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
 
−
}}
 
  
 +
===Long-term treatment===
 +
==Prognosis==
 +
The disease varies widely and the prognosis can vary from dull recovery to death despite the presenting signs. Generally if the case is single episode and uncomplicated then most patients make a good recovery.
 
==References==
 
==References==
  
−
Andrews, A.H, Blowey, R.W, Boyd, H and Eddy, R.G. (2004) '''Bovine Medicine''' (Second edition), ''Blackwell Publishing''
+
Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''
−
 
 
−
Bertone, J. (2006) '''Equine Geriatric Medicine and Surgery''', ''Elsevier''
 
−
 
 
−
Blood, D.C. and Studdert, V. P. (1999) '''Saunders Comprehensive Veterinary Dictionary''' (2nd Edition), ''Elsevier Science''
 
−
 
 
−
Brown, C.M, Bertone, J.J. (2002) '''The 5-Minute Veterinary Consult- Equine''', Lippincott, ''Williams & Wilkins''
 
−
 
 
−
Cowart, R.P. and Casteel, S.W. (2001) '''An Outline of Swine diseases: a handbook,''' ''Wiley-Blackwell''
 
−
 
 
−
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''
 
−
 
 
−
Jackson, G.G. and Cockcroft, P.D. (2007) '''Handbook of Pig Medicine,''' ''Saunders Elsevier''
 
−
 
 
−
Knottenbelt, D.C. '''A Handbook of Equine Medicine for Final Year Students University of Liverpool'''
 
−
 
 
−
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''
 
−
 
 
−
 
 
−
{{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]]
+
Merck & Co (2008) '''The Merck Veterinary Manual'''

Revision as of 11:23, 17 August 2009


 This article is still under construction.


See also Pancreas pathology

Signalment

  • Predisposed breeds include:

  • Labradors

  • Yorkshire terriers

  • Miniature Schnauzers

  • Miniature Poodles

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:

  1. Nutritional: including obesity, low protein and high fat diets, feeding of ethionine, hypertriglyceridaemia and fatty meals.
  2. 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.
  3. Pancreatic Duct obstruction: caused by biliary calculi, sphincter spasm, duct wall oedema, duodenal wall oedema, neoplasia, parasites, trauma and iatrogenic reasons.
  4. Duodenal juice reflux, Pancreatic trauma, ischaemia and reperfusion: including duodenal juice reflux into the pancreatic duct, surgical intervention, shock, anaemia, venous occlusion and hypotension.
  5. 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
  • Vomiting
  • Abdominal pain
  • Lethargy
  • Depression
  • Nausea
  • Diarrhoea (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
  • Mild ascites
  • Dehydration (Mild to moderate)
  • 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 and an increased PCV due to dehydration.

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:

  1. In the right cranial abdomen:
    1. Increased density
    2. Decreased contrast
    3. Decreased granularity
  2. Stomach displaced to left
  3. Angle widened between pyloric antrum and proximal duodenum
  4. Involving the Descending duodenum:
    1. Displacement to the right
    2. Prescence of a medial mass
    3. Gas pattern
    4. Thickened walls
  5. Gastric distension
  6. 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. 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

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

Prognosis

The disease varies widely and the prognosis can vary from dull recovery to death despite the presenting signs. Generally if the case is single episode and uncomplicated then most patients make a good recovery.

References

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

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