Difference between revisions of "Pancreatitis"
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| − | + | [[Pancreas Inflammatory - Pathology|See also Pancreas pathology]] | |
| − | '''Chronic''' | + | ==Signalment== |
| + | *Yorkshire terriers, Labradors, Miniature Schnauzers and Miniature Poodles are predisposed | ||
| + | *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 (?treatment associated). | ||
| + | *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 | + | 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. | |
| − | '''Drugs and toxins''' including L-asparginase, oestrogen, azathioprine, potassium bromide, furosemide, thiazide diuretics, salicylates, | + | #'''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. | |
| − | '''Pancreatic | ||
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| − | '''Duodenal juice reflux, | ||
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| − | '''Other''' | ||
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 nctrotizing 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: | ||
| + | ##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. | ||
| − | + | '''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 | |
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| + | ==Treatment== | ||
| + | ===Acute Treatment=== | ||
| + | '''Antibiotics''': | ||
| + | '''Analgesia''': | ||
| + | '''Transfusion''': | ||
| + | '''Corticosteroids''': | ||
| + | '''Somatostatin and dopamine''': | ||
| + | '''Secretion prevention''': | ||
| + | '''Enzyme inhibitors''': | ||
| + | '''Peritoneal dialysis''': | ||
| + | '''Diet changes''': | ||
| + | '''Supportive care''': | ||
| + | ===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== | ||
| − | + | Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA'' | |
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| − | Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition) | ||
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| − | + | Merck & Co (2008) '''The Merck Veterinary Manual''' | |
Revision as of 08:50, 17 August 2009
 |
This article is still under construction. |
Signalment
- Yorkshire terriers, Labradors, Miniature Schnauzers and Miniature Poodles are predisposed
- Middle-old aged dogs
- Increased risk with obesity, diabetes mellitus, hyperadrenocorticalism, prior GIT disease or epilepsy (?treatment associated).
- 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
- 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 nctrotizing 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:
- 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.
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
Antibiotics: Analgesia: Transfusion: Corticosteroids: Somatostatin and dopamine: Secretion prevention: Enzyme inhibitors: Peritoneal dialysis: Diet changes: Supportive care:
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