WikiVet English - User contributions [en]

WikiClinical Page Template

2009-08-28T14:59:43Z

Dmassey:

The page should include as many of the below titles but if they are not relevant they can be deleted.
{{cat}}
{{dog}}

==Signalment==
Predisposed breeds can be put into a page gallery like the one below:
<gallery>
Image:Labrador.jpg|Labradors
</gallery>
This section should include the common presentation of animals with the condition such as species, age, sex and breed. Any predilections should be included here.

==Description==
This should give a definition/brief description of the condition including the aetiology and pathogenesis. Any predispositions or risk factors may also be included in this section.
==Diagnosis==
This should incorporate the following subheadings and include the relevant findings that are associated with the condition. Any other tests that may aid diagnosis may be included as further subheadings .
===History and Clinical Signs===
*

===Haematology===
*

===Biochemistry===
*

===Urinalysis===

===Plain radiography===

===Positive contrast radiography===

===Ultrasonography===

===Endoscopy and Biopsy===

==Treatment==
This should include the general aims of the treatment. It may be subdivided into medical and surgical treatment options and any possible complications should be included here. Please do not include the dosages or rates of drugs.

===[[Fluid Therapy]]===

===Acid-base correction===

===Analgesia===

===[[Antibiotics]]===

===Surgery===

==Prognosis==
A brief summary of the prognosis associated with the condition.

==References==
Any sources of information that were used when writing the page must be included here.

Images can be included anywhere on the page so long as copyright has been agreed and it is recognised. The images must first be uploaded using the 'Upload File' Tab located in the toolbox. The following script may be useful: The size of the picture can be changed by altering the number infront of px.
[[Image:stomach diaphragmatic hernia.jpg|thumb|right|150px|Displacement of stomach into thorax (Courtesy of BioMed Image Archive)]]

WikiClinical Page Template

2009-08-28T14:50:28Z

Dmassey:

The page should as many of the below titles but if they are not relevant they can be deleted.
{{cat}}
{{dog}}

==Signalment==
Predisposed breeds can be put into a page gallery like the one below:
<gallery>
Image:Labrador.jpg|Labradors
</gallery>
This section should include the common presentation of animals with the condition such as species, age, sex and breed. Any predilections should be included here.

==Description==
This should give a definition/brief description of the condition including the aetiology and pathogenesis. Any predispositions or risk factors may also be included in this section.
==Diagnosis==
This should incorporate the following subheadings and include the relevant findings that are associated with the condition. Any other tests that may aid diagnosis may be included as further subheadings .
===History and Clinical Signs===
*

===Haematology===
*

===Biochemistry===
*

===Urinalysis===

===Plain radiography===

===Positive contrast radiography===

===Ultrasonography===

===Endoscopy and Biopsy===

==Treatment==
This should include the general aims of the treatment. It may be subdivided into medical and surgical treatment options and any possible complications should be included here. Please do not include the dosages or rates of drugs.

===[[Fluid Therapy]]===

===Acid-base correction===

===Analgesia===

===[[Antibiotics]]===

===Surgery===

==Prognosis==
A brief summary of the prognosis associated with the condition.

==References==
Any sources of information that were used when writing the page must be included here.

Images can be included anywhere on the page so long as copyright has been agreed and it is recognised. The images must first be uploaded using the 'Upload File' Tab located in the toolbox. The following script may be useful: The size of the picture can be changed by altering the number infront of px.
[[Image:stomach diaphragmatic hernia.jpg|thumb|right|150px|Displacement of stomach into thorax (Courtesy of BioMed Image Archive)]]

WikiClinical Page Template

2009-08-28T14:46:47Z

Dmassey: New page: The page should as many of the below titles but if they are not relevant they can be deleted. {{cat}} {{dog}} ==Signalment== Predisposed breeds can be put into a page gallery like the one...

Sandpit

2009-08-28T14:32:05Z

Dmassey:

[{{SERVER}}/index.php?title=Special:Upload&wpDestFile=WikiPath_Nervous_System_Content_Map.zip Upload New File] 
http://w01.rvcwiki.wf.ulcc.ac.uk/index.php?title=Special:Upload&wpDestFile=WikiPath_Nervous_System_Content_Map.zip

==WMV Extension==
<wmvplayer>file=http://stream2.rvc.ac.uk/Anatomy/bovine/Pot0048.wmv|width=300|height=300</wmvplayer>
===Old Stuff===
====RVC page====
====Edinburgh====
*[[Jorge]]
====Practice Pages====
*[[Steph]]
*[[Kim]]
*[[Chris]]
*[[Kate]]
*[[Matt]]
*[[Dave]]
====Other Pages====
*[[Moira Duplicate Page]]
*[[Donkey Page]]

[[WikiClinical Page Template]]

Pancreatitis

2009-08-28T11:19:01Z

Dmassey: /* Acute Treatment */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 - Pathology|shock]], [[Kidney Renal Failure - Pathology#Acute|acute renal failure]], [[Liver General Pathology - Pathology#Jaundice (Icterus)|jaundiced]] (due to focal hepatic necrosis), or with [[Altered Impulse Formations - WikiClinical|cardiac arrhythmias]] or [[Lungs Circulatory - Pathology#Pulmonary oedema|pulmonary oedema]] or pleural effusions, widespread haemorrhage or [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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]].

'''Transfusion''': [[Plasma - WikiBlood|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.

'''[[Steroids|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.

'''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|fluid therapy]] will be needed to treat dehydration and fluid loss from [[Intestine Diarrhoea - Pathology|diarrhoea]] and [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]]. Monitoring of renal function and potassium levels which may need supplementing. Patients may also have metabolic acidosis in acute pancreatitis or be alkalotic due to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]]. Should [[Diabetes mellitus - WikiClinical|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: [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

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

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'''

Pancreatitis

2009-08-28T11:18:50Z

Dmassey: /* Acute Treatment */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 - Pathology|shock]], [[Kidney Renal Failure - Pathology#Acute|acute renal failure]], [[Liver General Pathology - Pathology#Jaundice (Icterus)|jaundiced]] (due to focal hepatic necrosis), or with [[Altered Impulse Formations - WikiClinical|cardiac arrhythmias]] or [[Lungs Circulatory - Pathology#Pulmonary oedema|pulmonary oedema]] or pleural effusions, widespread haemorrhage or [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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]].

'''Transfusion''': [[Plasma - WikiBlood|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.

'''[[Steroids|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.

'''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|fluid therapy]] will be needed to treat dehydration and fluid loss from [[Intestine Diarrhoea - Pathology|diarrhoea]] and [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]]. Monitoring of renal function and potassium levels which may need supplementing. Patients may also have metabolic acidosis in acute pancreatitis or be alkalotic due to [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomiting]]. Should [[Diabetes mellitus - WikiClinical|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: [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

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

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'''

Pancreatitis

2009-08-28T11:10:32Z

Dmassey: /* History and Clinical Signs */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 - Pathology|shock]], [[Kidney Renal Failure - Pathology#Acute|acute renal failure]], [[Liver General Pathology - Pathology#Jaundice (Icterus)|jaundiced]] (due to focal hepatic necrosis), or with [[Altered Impulse Formations - WikiClinical|cardiac arrhythmias]] or [[Lungs Circulatory - Pathology#Pulmonary oedema|pulmonary oedema]] or pleural effusions, widespread haemorrhage or [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Pancreatitis

2009-08-28T11:07:56Z

Dmassey: /* History and Clinical Signs */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 - Pathology|shock]], [[Kidney Renal Failure - Pathology#Acute|acute renal failure]], [[Liver General Pathology - Pathology#Jaundice (Icterus)|jaundiced]] (due to focal hepatic necrosis), or with [[Altered Impulse Formations - WikiClinical|cardiac arrhythmias]] or pulmonary oedema or pleural effusions, widespread haemorrhage or [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Pancreatitis

2009-08-28T11:06:45Z

Dmassey: /* History and Clinical Signs */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 - Pathology|shock]], [[Kidney Renal Failure - Pathology#Acute|acute renal failure]], jaundiced (due to focal hepatic necrosis), or with [[Altered Impulse Formations - WikiClinical|cardiac arrhythmias]] or pulmonary oedema or pleural effusions, widespread haemorrhage or [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Pancreatitis

2009-08-28T11:05:54Z

Dmassey: /* History and Clinical Signs */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 [[Altered Impulse Formations - WikiClinical|cardiac arrhythmias]] or pulmonary oedema or pleural effusions, widespread haemorrhage or [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Pancreatitis

2009-08-28T11:04:47Z

Dmassey: /* History and Clinical Signs */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 [[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Acute haemorrhagic pancreatitis may present as [[Shock - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Pancreatitis

2009-08-28T11:04:16Z

Dmassey: /* History and Clinical Signs */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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 [[Disseminated Intravascular Coagulation - Pathology|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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Pancreatitis

2009-08-28T11:02:59Z

Dmassey: /* Description */

{{review}}

{{cat}}
{{dog}}

[[Pancreas Inflammatory - Pathology|See also Pancreas pathology]]

==Signalment==
*Predisposed breeds include:
<gallery>
Image:Labrador.jpg|Labradors
Image:Miniature Poodle.jpg|Miniature Poodles
Image:Miniature schnauzer.jpg|Miniature Schnauzers
Image:Yorkshire Terrier.jpg|Yorkshire terriers
</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.

==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|tetracyclines]], [[Sulphonamides|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%)
*[[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|Vomiting]] (Dog - 90%)
*Abdominal pain (Dog - 58%)
*Lethargy (Dog - 79%, Cat - 100%)
*Depression
*Nausea
*[[Intestine Diarrhoea - Pathology|Diarrhoea]] (Dog - 33%) (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
*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:
##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 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 [[Potentiated-Sulphonamides|trimethoprim-sulphonamide]] and [[Fluoroquinolones|enrofloxacin]] have good penetration to the pancreas.

'''Analgesia''': should 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 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: [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

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

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'''

Acknowledgements

2009-08-27T13:36:30Z

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{{toplink
|linkpage =Main Page
|linktext =MAIN PAGE
}}
 
=== Thank you ===

This WikiPath project originated from an initial collaboration between the Veterinary Schools at the University of Cambridge, Edinburgh and London before spreading to other institutions and organisations. We would like to acknowledge the contributions made by everyone involved in the project - it has been a true community and collaborative effort.

Specific contributors are listed below, with the proviso that anyone who is missing from this list or would like to be on this list (we welcome veterinary contributors/editors/etc) should either add themselves or request to be added by emailing bcox@rvc.ac.uk.

* '''Cambridge Vetschool'''
** [[Tim Scase]]
** [[User:Alexm1983|Alex Morley]]
** Kate Read

* '''Edinburgh Royal Dick School of Veterinary Studies'''
** [[Susan Rhind]]
** [[Lizzie Slack]]
** [[Sarah McFarland]]
** [[Linda Morrison]]

* '''London Royal Veterinary College'''
** [[Ken Smith]]
** [[Alun Williams]]
** [[Barbora Stanikova]]
** [[Elisabeth Bachynsky]]
** [[Nick Short]]
** [[Brian Cox]]
** [[Vicki Dale]]
** [[Kim Whittlestone]]
** [[Freya Lawrence]]
** [[Simon Priestnall]]
** [[Sophie Stenner]]
** [[Natalie Brown]]
** [[Lois Wilkie]]
** [[Laura-Jayne Bown]]
** [[Maura Ambron]]
** Jenny Sanders
** [[Amy Cartmel]]
** Edward Ayton
** [[Rebecca Pocock]]
** [[Sarah Hamilton]]
** [[Katherine Grace]]
** [[John Tulloch]]
** Matt Field
** Dave Massey

[[image: logo.gif|thumb|right|All staff and students at Nottingham are very grateful for their funding from the Learning and Teaching Development Fund, University of Nottingham that enabled Nottingham to contribute towards the initial development of Wikivet]]
* '''Nottingham School of Veterinary Medicine and Science'''
** [[Richard Hammond]]
** [[Mike Targett]]
** [[David Gardner]]
** [[Julia Kydd]]
** [[Asher Allison]]
** [[Carolyn Harvey-Myers]]
** [[Thomas Iveson]]
** [[Rachael Wallace]]
** [[Jo Henstock]]
** [[Jo Hinsley]]
** [[Kirsty Ranson]]
** [[Naomi Ragsdell]]
** [[Stephanie Smith]]
** [[Chris Burton]]

* '''HEA''' ''Centre for Medicine, Dentistry & Veterinary Education''
** [[Gillian Brown]]

Intestinal Conditions Canine

2009-08-24T14:00:45Z

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{{dog}}

[[Alimentary Lymphoma - WikiClinical|Alimentary Lymphoma]]

[[Haemorrhagic Gastroenteritis - WikiClinical|Haemorrhagic Gastroenteritis]]

[[Inflammatory Bowel Disease - WikiClinical|Inflammatory Bowel Disease]]

[[Intestinal Adenocarcinoma - WikiClinical|Intestinal Adenocarcinoma]]

[[Intestinal Leiomyoma/Leiomyosarcoma - WikiClinical|Intestinal Leiomyoma/Leiomyosarcoma]]

[[Intestinal Obstruction - WikiClinical|Intestinal Obstruction]]

[[Intussusception - WikiClinical|Intussusception]]

[[Lymphangiectasia - WikiClinical|Lymphangiectasia]]

[[Protein-Losing Enteropathy - WikiClinical|Protein-Losing Enteropathy]]

[[Short Bowel Syndrome - WikiClinical|Short Bowel Syndrome]]

[[Small Intestinal Bacterial Overgrowth and Antibiotic Responsive Diarrhoea - WikiClinical|Small Intestinal Bacterial Overgrowth and Antibiotic Responsive Diarrhoea]]

Intestinal Adenocarcinoma

2009-08-24T14:00:06Z

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Intestinal tumours are uncommon accounting for less than 10% of all tumours in dogs and cats and 22% of gastrointestinal tumours in dogs and 35% in cats. It has been reported that the jejunum, ileum and caecum are the most frequent sites affected in the dog. Intestinal tumours in dogs and cats are usually malignant, [[Intestine Proliferative - Pathology #Adenocarcinoma|Adenocarcinoma]]/carcinoma being the most common malignant tumour in dogs and accounting for 17% of intestinal tumours in cats.

==Signalment==
* Dogs:
** Mean age: 6-9 years
** Minor male predisposition
** Large breeds may predominate particularly Collies, German Sheperds and Boxers

* Cats:
** Mean age: 10-12 years
** There are conflicting reports of whether there is a minor male predisposition
** Siamese may have a breed predisposition

==Description==
* No organism or chemical agent has been identified that will induce spontaneous intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]].
* The gross appearance of colorectal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] vary from pedunculated, particularly in the distal rectum, cobblestone, in particularly the middle rectum, and annular, also usually in the middle recutum, and may also have associations with tumour behaviour and prognosis.
* In cats, [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] have been reported to have been found in the ileum and ileocaecal region. Another study reports the jejunum to be the most common site.
* Metastasis occurs via lymphatic and vascular routes. For small intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] the most frequent sites of metastasis are the mesenteric lymph nodes. Other sites include the liver, kidneys, peritoneal cavity, omentum and lungs. Metastatic spread is commonly encountered at time of diagnosis.
* Large intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] often metastasise to the deep inguinal lymph nodes. The liver is less frequently affected. These tumours also undergo aggressive local growth and local recurrence after resection frequently occurs.

==Diagnosis==
===Clinical Signs===
Usually chronic and often dependent on the site of the tumour within the gastrointestinal tract. Signs include:
* For more proximal lesions:
** Vomiting
* For lesions within the small intestine:
** Weight loss
* For tumours in the more distal tract:
** Tenesmus
** Hematochezia
** Faeces may be altered in shape with constricting lesions
* Other signs reported include:
** Anorexia
** Diarrhoea
** Signs associated with acute intestinal obstruction (usually when the tumour has grown in an annular form), perforation and peritonitis
Associated paraneoplastic abnormalities include:
* Neutrophilia
* Monocytosis
* Eosinophilia
* Cutaneous disease
* Hyperviscosity syndromes

===Physical Examination===
* An abdominal mass may be palpable
* A rectal mass, and potentially a lower colonic lesion, may be palpable digitally via rectal examination
* Cats may be dehydrated

===Haematology and Biochemistry===
Abnormalities observed include:
* Anaemia
* Leukocytosis
* Left shift
* Monocytosis
* Hypoproteinemia
* Raised hepatic enzymes
* High cholesterol
* Raised BUN - may be due to concurrent renal insufficiency, dehydration or absorption following intestinal bleeding
* Electrolyte abnormalities - due to intestinal obstruction

===Abdominal Radiography===
* An abdominal mass may be visible with plain radiography
* Alternatively, evidence of obstruction may be observed
* Poor serosal detail may be apparent
* Contrast radiography can be useful for localising masses, revealing obstructions and filling defects and for intestinal areas more difficult to visualise via ultrasonography due to the accumulation of air.

===Thoracic Radiography===
This is highly advised though presentation with pulmonary metastasis is infrequent.

===Abdominal Ultrasonography===
Is more sensitive than radiography in localising a mass and can assess involvement of surrounding structures. In addition, guided needle aspiration or biopsy may be taken at this time. Findings may include the following:
* Intestinal wall thickening with loss of wall layering - dogs with loss of layering are over 50 times more likely to have neoplastic disease rather than enteritis
* In dogs, [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] have been described as being usually hypoechoic and most dogs have reduced gut motility
* In cats, [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] have been described as being of mixed echogenicity and are often asymmetric

===Endoscopy and Laparoscopy===
Allow visualisation of the lesion. In addition, biopsies may be taken at this time. Open proctoscopes are more useful than fibreoptic scopes for colorectal lesions as direct visualisation of the mass is possible and deeper biopsies can be obtained. Nevertheless, often only small superficial samples can be obtained on biopsying the gut thus there can be significant variation in the interepretation of the findings.

===Exploratory Laparotomy===
Definitive diagnosis requires an excisional biopsy. All abdominal tissues should be assessed and full thickness biopsies taken. Resection of the mass and intestinal anastomosis may be performed at this time.

==Treatment==
===Surgery===
Surgical excision is advised as primary treatment for intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]]. Extraserosal invasion or adhesions may cause difficulties and care must be taken to ensure there is no iatrogenic damage to the biliary and pancreatic ducts for duodenal lesions. In the small intestine, wide local resection (4-8cm margins) can usually be achieved via enterectomy and anastomosis. Stapling and suturing by hand have been shown to be equally efficient for this procedure. If appropriate, regional lymph nodes should also be removed. Large margins may be more difficult to achieve for colorectal lesions due to access issues. Perioperative complications include peritonitis and sepsis.

===Adjuvant Chemotherapy===
Doxirubicin has been shown to significantly improve survival times for cats with colonic [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] with median durations of 56 and 280 days for those not receving and those receiving chemotherapy respectively. No other evidence exists to confirm the benefits of adjuvant chemotherapy in dogs or cats. Piroxicam, a non-steroidal anti-inflammatory drug may have beneficial effects for rectal lesions.

===Radiotherapy===
Rarely reported due to concerns of intolerance of surrounding tissues leading to for example perforations and adhesions. In addition it cannot be relied upon that the same target will be irradiated each day due to intestinal mobility. There has been a report of single high-dose irradiation being used for anorectal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinomas]] which had been surgically exposed and no long-term side effects were observed.

==Prognosis==
If no metastasis has occurred long term survival may be achieved following wide excision of a well differentiated small intestinal tumour. The rate of metastasis of [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] to the local lymph nodes for both dogs and cats is approximately 50%. Without surgical intervention, the mean survival of dogs with small intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] is 12 days and reports varying from 114 days to 7-10 months for those who receive surgical treatment. In one study males with small intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] had a significantly better prognosis than females with the same disease though the sample size was small. Intensity of treatment is prognostic for colorectal tumours with palliative care carrying a poorer prognosis than local excision. Local excision of colorectal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] has a median survival time of 22 months while the use of stool softeners alone has a median survival time of 15 months.

There is significant perioperative risk associated with cats with small intestine [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] with a high mortality rate within the first two weeks following surgery. However, after these two weeks long term control may be achieved. For cats with large intestinal [[Intestine Proliferative - Pathology #Adenocarcinoma|adenocarcinoma]] survival time after surgery alone has been reported as approximately 4.5 months.

==References==
* Liptak J. M, Withrow S.J, (2007), Cancer of the Gastrointestinal Tract, in Withrow and MacEwen's Small Animal Clinical Oncology, fourth edition, Eds Withrow S.J, Vail D.M, Missouri, Saunders Elsevier, pp 491-501
* White, R. A. S, (2003), Tumours of the intestines, in BSAVA Manual of Canine and Feline Oncology, second edition, Eds Dobson J. M, Lascelles B. D. X, Gloucester, British Small Animal Veterinary Association, pp 229-233

Recto-anal Conditions Canine

2009-08-24T13:58:19Z

Dmassey:

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[[Anal Sac Abscessation - WikiClinical|Anal Sac Abscessation]]

[[Anal Sac Adenocarcinoma - WikiClinical|Anal Sac Adenocarcinoma]]

[[Anal Sacculitis - WikiClinical|Anal Sacculitis]]

[[Anal Sac Disease - General - WikiClinical|Anal Sac Disease - General]]

[[Anal Sac Impaction - WikiClinical|Anal Sac Impaction]]

[[Caecocolic Intussusception - WikiClinical|Caecocolic Intussusception]]

[[Colitis - WikiClinical|Colitis]]

[[Perianal Fistulae - WikiClinical|Perianal Fistulae]]

[[Perianal Gland Tumours - WikiClinical|Perianal Gland Tumours]]

[[Perineal Hernia - WikiClinical|Perineal Hernia]]

[[Rectal Polyps - WikiClinical|Rectal Polyps]]

[[Rectal Prolapse - WikiClinical|Rectal Prolapse]]

[[Rectal Strictures - WikiClinical|Rectal Strictures]]

Anal Sac Disease - General

2009-08-24T13:58:00Z

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Below is an overview of Anal sac disease presenting signs and disease factors.
For individual disease information see the pages under [[Recto-anal Conditions]]

Presenting signs:
*Excessive licking or chewing around tail base or anus
*Reluctance to sit or discomfort when sitting
*Scooting
*Dyschezia if extreme
*Tenesmus
*Draining tracts

Disease factors:
*Faecal consistency
*Diet
*Poor muscle tone
*Inactivity
*Obesity
*Generalized seborrhoea
*Oestrus
*Anal furunculosis
*Small toy breeds
*German Shepherd Dogs

Peritoneal Conditions Canine

2009-08-24T13:56:16Z

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[[Abdominal Haemangiosarcoma - WikiClinical|Abdominal Haemangiosarcoma]]

[[Haemoabdomen - WikiClinical|Haemoabdomen]]

[[Mesothelioma - WikiClinical|Mesothelioma]]

[[Peritonitis - WikiClinical|Peritonitis]]

Hepatic Neoplasia

2009-08-24T13:55:00Z

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* Primary hepatic tumours are rare (less than 1.5% of all canine tumours and 1.0-2.9% of all feline tumours) * However, the liver is a common site of metastatic tumours due to the rich blood supply (hapatic portal vein and hepatic artery)
* In dogs, metastasis to the liver is 2.5 times more likely than primary neoplasia
* In cats, primary hepatobillary tumours are more frequent than metastatic tumours
* Malignant tumours are more common in dogs
* Benign tumours are more common in cats
* Malignant primary tumours include:
** [[Liver Proliferative - Pathology #Hepatocytic|Hepatocellular carcinoma]]
** [[Liver Proliferative - Pathology #Cholangiocellular|Cholangiocellular carcinoma]]
** Gall bladder carcinoma
** [[Liver Proliferative - Pathology #Haemangiosarcoma|Haemangiosarcoma]]
** Mast cell tumour
** Hepatic carcinoids (neuroendocrine)
* Benign tumours include:
** [[Liver Proliferative - Pathology #Hepatocytic|Hepatocellular adenoma]] (hepatoma)
** [[Liver Proliferative - Pathology #Cholangiocellular|Cholangiocellular adenoma]]
** Gall bladder adenoma
Note: Distinction must be made between all hepatic tumours and [[Liver Unknown Aetiology - Pathology #Nodular hyperplasia|benign nodular hyperplasia]] that is frequently observed in the older canine. The most significant primary tumours in the dog are hepatomas, [[Liver Proliferative - Pathology #Hepatocytic|Hepatocellular]] and [[Liver Proliferative - Pathology #Cholangiocellular|Cholangiocellular]] carcinomas and hepatic carcinoids. [[Liver Proliferative - Pathology #Hepatocytic|Hepatocellular carcinoma]] and [[Liver Proliferative - Pathology #Cholangiocellular|Cholangiocellular carcinoma]] are the most significant in cats.

==Diagnosis==
Symptomatic in approximately 75% of dogs and 50% of cats, particularly if malignant.
===Clinical signs===
* Usually non-specific:
** Weight loss
** Inappetance
** Lethargy
** Polyuria-Polydipsia
** Vomiting
** Ascites
* Neurological Signs - seizures, ataxia and weakness occur less frequently. They may be due to metastasis to the central nervous system, [[Hepatic Encephalopathy|hepatic encephalopathy]] or hypoglycaemia which can occur as a paraneoplastic syndrome
* Icterus - Particularly in dogs with extrahepatic cholangiocellular carcinomas and diffuse carcinoids

===Physical Examination===
* Cranial abdominal mass - palpable in up to 75% of cats and dogs

===Haematology and Biochemistry===
* Usually non-specific. The following are frequently observed in dogs:
** Mild non-regenerative anaemia - cause idiopathic, however anaemia of chronic disease, inflammation, red blood cell sequestration and iron deficiency may play roles
** Leukocytosis - resulting from the associated inflammation and necrosis that can occur with large liver masses
** Thrombocytosis - potential causes include production of thrombopoietin as a parneoplastic syndrome, iron deficiency, inflammatory cytokines and anaemia
* Elevated hepatic enzymes - likely due to hepatocellular damage or biliary stasis though the extent of enzyme increase is not proportional to severity of liver damage
* Hypoalbuminaemia
* Hyperglobulinaemia
* Hypoglycaemia - can occur as a paraneoplastic syndrome where there is increased utilisation of glucose or increased production of hormones with insulin-like activity.
* Elevated pre- and postprandial bile acids

* The following have been observed in cats:
** Azotaemia
** Elevated hepatic enzymes
** Elevated serum bilirubin - particularly in those with hepatocellular carcinoma

===Plain Abdominal Radiography===
Hepatomegaly and rounding of the margins of the liver may be observed. Alternatively a cranial abdominal mass may be visible with displacement of the stomach caudally and laterally with massive hepatic neoplasms. Occasionally mineralisation of the biliary tree is observed in dogs with cholangiocellular carcinoma. Three thoracic views should also be taken to assess lung metastasis although this is uncommon at the time of diagnosis.

===Ultrasonography===
Advised to evaluate the condition of surrounding structures. It also allows classification of the mass as massive, nodular or diffuse. Doppler techniques can also be utilised to assess the vascular structure of tumours. Guided fine-needle aspirates or core biopsies can also be taken at this time (a coagulation profile is highly recommended prior to performing a liver biopsy due to risk of haemorrhage). If the lesion is solitary and massive surgical resection without preoperative biopsy is usually undertaken as diagnosis and treatemnt are accomplished in one procedure.

===Advanced Imaging===
CT and MRI are more sensitive in detecting small lesions and confirming the relationship of the mass with surrounding tissues and vasculature.

===Abdominocentesis===
Cytological examination of the sediment may reveal neoplastic cells. Effusions are usually modified transudates and haemorrhage may indicate tumour rupture.

==Signalment and Description==
===Hepatocellular Tumours ([[Liver Proliferative - Pathology #Hepatocytic|Hepatocellular carcinomas]] (HCC) and [[Liver Proliferative - Pathology #Hepatocytic|Hepatomas]])===
* HCC occurs more frequently in dogs and hepatomas more commonly in cats. They are the most common primary liver tumour in dogs and the second most common in cats.
* Male dogs over 10 years old are the most frequently affected by HCC and Miniature schnauzers may have a breed predisposition.
* Regional lymph nodes (hepatic and diaphragmatic nodes), peritoneum and lungs are the most frequent sites of metastasis in dogs with nodular and diffuse HCC.
* Metastatic rate for dogs with massive HCC: 0-37%
* Metastatic rate for dogs with nodular and diffuse HCC: 93-100%
* [[Liver Proliferative - Pathology #Hepatocytic|Hepatomas]]) are usually incidental findings and non-significant

===Cholangiocellular Tumours (Bile duct carcinomas and adenomas)===
* Bile duct carcinomas are the most common malignant hepatobillary tumours in cats and the second most frequent in dogs and females may be predisposed
* Intrahepatic carcinomas are more frequent in dogs. In cats there have been reports of both equal occurrence of intra-and extrahepatic tumours and of a extrahepatic dominance.
* Bile duct carcinomas are aggressive with metastasis to particularly the regional lymph nodes and lungs frequently being observed in dogs and diffuse intraperitoneal metastasis and carcinomatosis being common in cats.
* Bile duct adenomas (also known as biliary or hepatobiliary cystadenomas) are common in cats, particularly males.
* Bile duct adenomas are non-significant unless they of sufficient size to compress surrounding soft tissue structures

===Carcinoids (Neuroendocrine Tumours)===
* Usually occur in younger animals compared with other primary hepatobiliary tumours.
* Primary tumours are aggressive and often affect more than one liver lobe and metastasise most frequently to the regional lymph nodes, the lungs and peritoneum.

===Sarcomas ([[Liver Proliferative - Pathology #Haemangiosarcoma|Haemangiosarcoma]] (HSA), Leiomyosarcoma, Fibrosarcoma)===
* HSA is the most common hepatic sarcoma in cats
* Leiomyosarcoma is the most common hepatic sarcoma in dogs
* These tumours are aggressive and metastasis to the spleen and lungs is frequently observed.

==Treatment==
===Surgery===
Surgical excision is advised for hepatic adenomas, bile duct adenomas and massive [[Liver Proliferative - Pathology #Hepatocytic|hepatocellular carcinomas]]. Nodulectomy or lobectomy can be used for focal tumours of one or more lobes. Diffuse tumours and widespread nodular disease carry a worse prognosis.

===Chemotherapy===
Not currently recommended for primary hepatic neoplasia. Some metastatic sarcomas, for example [[Liver Proliferative - Pathology #Haemangiosarcoma|haemangiosarcomas]], may show some response.

===Radiotherapy===
Not reported. Surrounding abdominal organs may show poor tolerance.

==Prognosis==
The mean survival time for massive [[Liver Proliferative - Pathology #Hepatocytic|hepatocellular carcinomas]] following surgery is approximately 1 year. Otherwise the prognosis is poor for other malignant and metastatic tumours. If successfully excised the prognosis for benign tumours is good.

==References==

* Morris J, Dobson J (2001) Gastrointestinal Tract, in Small Animal Oncology, Blackwell Science, pp 137-140
* Liptak J. M, Withrow S.J, (2007), Cancer of the Gastrointestinal Tract, in Withrow and MacEwen's Small Animal Clinical Oncology, fourth edition, Eds Withrow S.J, Vail D.M, Missouri, Saunders Elsevier, pp 483-489

Liver Conditions Canine

2009-08-24T13:54:20Z

Dmassey:

{{unfinished}}
{{dog}}

[[Chronic Hepatitis]]

[[Hepatic Encephalopathy]]

[[Hepatic Lipidosis - WikiClinical|Hepatic Lipidosis]]

[[Hepatic Neoplasia - WikiClinical|Hepatic Neoplasia]]

[[Portosystemic Shunt]]

Liver Conditions Canine

2009-08-24T13:53:36Z

Dmassey:

{{unfinished}}
{{dog}}

[[Cholangitis/Cholangiohepatitis- WikiClinical|Cholangitis/Cholangiohepatitis]]

[[Chronic Hepatitis]]

[[Hepatic Encephalopathy]]

[[Hepatic Lipidosis - WikiClinical|Hepatic Lipidosis]]

[[Hepatic Neoplasia - WikiClinical|Hepatic Neoplasia]]

[[Portosystemic Shunt]]

Exocrine Pancreatic Neoplasia - Dogs and Cats

2009-08-24T13:52:21Z

Dmassey:

{{Unfinished}}

{{cat}}
{{dog}}

Primary pancreatic tumours are rare (accounting for less than 0.5% of all cancers in the dog), however the pancreas is also a site for metastasis from particularly gastro-intestinal neoplasms. Primary tumours include:
* [[Pancreas Hyperplastic and Neoplastic - Pathology #Carcinomas|Carcinomas]]
* Adenocarcinomas
* [[Pancreas Hyperplastic and Neoplastic - Pathology #Adenomas|Adenomas]]

It is important to make the distinction between pancreatic neoplasia and [[Pancreas Hyperplastic and Neoplastic - Pathology #Nodular hyperplasia|pancreatic nodular hyperplasia]] which frequently occurs in older dogs and cats and is non-significant.

==Signalment==
[[Pancreas Hyperplastic and Neoplastic - Pathology #Carcinomas|Carcinomas]]:
* Usually female dogs with a mean age of 10 years
* Spaniels and Airedale terriers may have breed predispositions
* Affected cats have a mean age of 12 years

==Description==
Aetiology is idiopathic. [[Pancreas Hyperplastic and Neoplastic - Pathology #Adenomas|Adenomas]], although they do not metastasise and are frequently small and focal, can compress the surrounding pancreas. [[Pancreas Hyperplastic and Neoplastic - Pathology #Carcinomas|Carcinomas]] are aggressive with local invasion of the stomach or duodenum and metastasis to the liver, regional lymph nodes (hepatic and splenic), lungs, periotoneal surface and other abdominal organs usually occurring prior to a diagnosis being reached. Other complications include blockage of the common bile duct and [[Exocrine Pancreatic Insufficiency - WikiClinical|exocrine pancreatic insufficiency]]. [[Pancreatitis - WikiClinical|Pancreatitis]] can also occur where pancreatic atrophy results in tumour necrosis and an inflammatory response.

==Diagnosis==
===Clinical Signs===
Non-specific including:
* Lethargy
* Weight loss - marked in cats
* Anorexia - marked in cats
* Vomiting
* Diarrhoea
* Constipation
* Abdominal pain/distension due to mass effect or abdominal effusions
* Jaundice - if biliary obstruction
* Alopecia - as a paraneoplastic syndrome, occurring ventrally, facially and on the limbs in cats with adenocarcinoma
Such signs may also occur with concurrent [[Pancreatitis - WikiClinical|pancreatitis]]. Alternatively clinical signs may reflect those of metastatic disease.

===Physical Examination===
In cats, an abdominal mass may be palpable.

===Haematology and Biochemistry===
Potential abnormalities include:
* Mild anaemia
* Neutrophilia
* Elevated hepatic enzymes or bilirubinaemia - if there is cholestasis or biliary obstruction
* Hyperglycaemia - If there is concurrent beta cell destruction
* Hypokalaemia

===Plain and Contrast Radiography===
Plain abdominal radiography may reveal a mass or mottled appearance on account of local peritonitis. In addition, there may be diplacement of the descending duodenum and pylorus. Where there is peritoneal metastasis and effusion loss of serosal detail and increased radiodensity may be observed. Thoracic radiography is also advised for pulmonary metastases.

Positive contrast radiography can be used to evaluate gastric emptying which can be delayed with pancreatic neoplasia. Compression or invasion of the duodenum may also be seen.

===Ultrasonography===
Provides information on the extent of the tumour and its invasiveness. A guided fine needle aspirate may be taken at this time, however, cytological examination is often unrewarding as pancreatic tumour cells do not exfoliate well.

===Exploratory Celiotomy===
Excising the whole tumour if operable or taking a sample via shave biopsy or crush ligation allows histopathological confirmation.

==Treatment==
===Surgery===
Usually at the time of diagnosis adenocarcinomas have already metastasised or local invasion has already taken place. If metastasis has no yet occurred surgical resection may be attempted with care to avoid iatrogenic trauma to the vascular supply to the proximal duodenum and obstruction of the main pancreatic duct. Total pancreatectomy and pancreaticoduodenectomy (Whipple's procedure) are not advised. Tumours of the body or base of the pancreas are inoperable. Gastrojejunostomy (gastrointestinal bypass) may be performed for short term palliation. Small pancreatic adenomas may be removed via partial pancreatectomy.

===Chemotherapy===
Not recommended.

===Radiotherapy===
Not recommended.

==Prognosis==
Poor for adenocarcinomas on account of their invasiveness and early metastasis. Survival time is less than 1 year for such tumours regardless of treatment.

==References==
* Morris J, Dobson J (2001) Gastrointestinal Tract, in Small Animal Oncology, Blackwell Science, pp 140-142
* Liptak J. M, Withrow S.J, (2007), Cancer of the Gastrointestinal Tract, in Withrow and MacEwen's Small Animal Clinical Oncology, fourth edition, Eds Withrow S.J, Vail D.M, Missouri, Saunders Elsevier, pp 479-480

Pancreatic Conditions Canine

2009-08-24T13:52:02Z

Dmassey:

{{unfinished}}
{{dog}}

[[Exocrine Pancreatic Insufficiency - WikiClinical|Exocrine Pancreatic Insufficiency]]

[[Exocrine Pancreatic Neoplasia - WikiClinical|Exocrine Pancreatic Neoplasia]]

[[Insulinoma - WikiClinical|Insulinoma]]

[[Pancreatitis - WikiClinical|Pancreatitis]]

Pancreatic Conditions Canine

2009-08-24T13:51:16Z

Dmassey:

{{unfinished}}
{{dog}}

[[Exocrine Pancreatic Insufficiency - WikiClinical|Exocrine Pancreatic Insufficiency]]

Exocrine Pancreatic Insufficiency

2009-08-24T13:50:38Z

Dmassey:

{{review}}

{{cat}}
{{dog}}

==Signalment==
*Most common in dog:
**German Shepherd Dogs
**Rough Collie
*Occurs occasionally in other species including calves with [[Pancreas Developmental - Pathology#Pancreatic hypoplasia|pancreatic hypoplasia]] and in cats ([[Pancreas Inflammatory - Pathology#Chronic Pancreatitis|chronic pancreatitis]])
*In contrast, '''horses''' with very little pancreatic tissue develop '''hypoinsulinism''' but rarely EPI

==Description==
'''Exocrine pancreatic insufficiency (EPI)''' is a syndrome caused by insufficient synthesis and secretion of digestive enzymes by the exocrine portion of the pancreas
*Leading to insufficient activity of digestive enzymes in the lumen of the small intestine
*Pancreas has considerable functional reserve, large proportion needs to be non-functional to show signs of EPI
*In dog it is mostly caused by [[Pancreas Degenerative - Pathology|pancreatic atrophy]] or Pancreatic Acinar Atrophy (PAA)
*In the cat it is usually associated with [[Pancreas Inflammatory - Pathology#Chronic Pancreatitis|chronic pancreatitis]]

==Diagnosis==
===History===
*Weight loss with or without polyphagia (usually ravenous with scavenging)
*Coprophagia and pica
*Polyuria and polydipsia due to Diabetes Mellitus
*Varible diarrhoea (large volumes of semi-formed faeces)
*Vomiting
*Borborygmus and flatulance
===Clinical Signs===
*Steatorrhoea
*Diarrhoea
*Mild to marked weight loss
*Muscle wastage
*Polyphagia
*Poor haircoat
*Flatulance
===Laboratory Tests===
Routine tests are generally unhelpful. Serum alanine aminotransferase (ALT) can have mild to moderate elevations. Other biochemical results include reductions in total lipid, polyunsaturated fatty acid concentraions and cholesterol.
The most sensitive and specific test for the diagnosis of EPI is the '''TLI''' serum assay. The values are greatly reduced as compared to normal animals. Values '''<2µg/l''' in dogs and '''<8µg/l''' in cats are considered diagnostic. This test must be carried out after withdrawing food for several hours. Serum fTLI is only available from specialist laboratories.
Other tests are available but are often inconvenient and expensive.

===Other===
Atrophy of the pancreas seen via exploratory laparotomy or laparoscopy
==Treatment==
===Enzyme replacement===
EPI can be managed with the supplementation of pancreatic enzymes from dried pancreatic extracts. Meals should be fed '''twice a day''' to allow weight gain. Many clinical signs resolve within 5 days. Doses can then be lowered to a minimum effective dose which is different for each animal. Cheaper alternatives include chopped raw cow or pig pancreas.

===Dietary modification===
*Diets containing high volumes of non-fermentable fibre should be avoided
*Low fat diets should not be fed
*Certain studies show that:
**animals may do better with a highly digestible diet
**the animals may also benefit from readily hydrolysed and absorbed medium chain triglycerides within the diet
===Vitamin supplementation===
Levels of vitamin B12 (cobalamin) and vitamin E (tocopherol) are often found to be low.
*Tocopherol should be supplemented for 1 month
*Cobalamin weekly for several weeks. Long term monitoring should be carried out in cats.

===Antibiotic therapy===
Dogs with EPI often have Small Intestinal Bacterial Overgrowth (SIBO). This can be treated with oral oxytetracycline, tylosin or metronidazole.

===Glucocorticoid therapy===
This is a last line treatment.
*Oral prednisolone. Long term treatment is usually not needed

==Prognosis==
EPI is a life-long condition and so is the treatment. However recoveries have been reported. The prognosis is generally good so long as the owner understands the longevity of the disease and the cost involved with treating it.

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

Gastric Dilatation and Volvulus

2009-08-24T09:30:15Z

Dmassey:

{{review}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*[[Altered Impulse Formations - WikiClinical|Cardiac arrythmias]] (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen - WikiClinical|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*[[Gastric Motility Disorders - WikiClinical|Abnormal gastric motility]]
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T09:29:31Z

Dmassey:

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*[[Altered Impulse Formations - WikiClinical|Cardiac arrythmias]] (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach. (GDV x-ray from WikiCommons[[http://commons.wikimedia.org/wiki/File:GDV_x-ray.JPG]])
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen - WikiClinical|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*[[Gastric Motility Disorders - WikiClinical|Abnormal gastric motility]]
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T09:12:31Z

Dmassey: /* Post-operative complications */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*[[Altered Impulse Formations - WikiClinical|Cardiac arrythmias]] (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen - WikiClinical|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*[[Gastric Motility Disorders - WikiClinical|Abnormal gastric motility]]
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T09:10:09Z

Dmassey: /* Other treatment */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*[[Altered Impulse Formations - WikiClinical|Cardiac arrythmias]] (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen - WikiClinical|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure [[Opioids|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T09:09:32Z

Dmassey:

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*[[Altered Impulse Formations - WikiClinical|Cardiac arrythmias]] (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.)

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or [[Haemoabdomen - WikiClinical|haemoabdomen]]. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]] disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], [[Opioids#Fentanyl|fentanyl]] or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: [[Steroids|Prednisolone sodium succinate]] or [[Steroids|dexamethasone sodium phosphate]].
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, syncope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology#Acid / Base|acid-base]], [[Essential Ion and Compound Balance and Homeostasis - Anatomy & Physiology|electrolyte]] and [[Haemostasis - Pathology|haemostatic]] disturbances. The treatment is [[Local Anaesthetics#Lidocaine|lidocaine]] by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure [[Opiods|opioid]] of [[Opioids#Morphine|morphine]], [[Opioids#Methadone|methadone]] or [[Opioids#Fentanyl|fentanyl]].
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included [[Opioids#Fentanyl|fentanyl]] and [[Benzodiazepines#Diazepam|diazepam]] bolus or titrated [[Propofol|propofol]]. Maintenance can be achieved with the use of [[Isoflurane|isoflurane]] and [[Sevoflurane|sevoflurane]] in oxygen however [[Nitrous Oxide|nitrous oxide]] should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, [[Blood Pressure#Central Venous Pressure|central venous pressure]], PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial [[Blood Pressure|blood pressure]].

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T08:47:53Z

Dmassey: /* History and Clinical signs */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*[[Altered Impulse Formations - WikiClinical|Cardiac arrythmias]] (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T08:45:16Z

Dmassey: /* References */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/2/66?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation]]''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T08:44:11Z

Dmassey: /* References */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''[[http://inpractice.bvapublications.com/cgi/reprint/31/3/114?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=brockman&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT|Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management]]''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T08:43:00Z

Dmassey: /* Post-operative complications */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*[[Lungs Inflammatory - Pathology#Aspiration pneumonia|Aspiration pneumonia]]
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T08:41:08Z

Dmassey:

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*Aspiration pneumonia
*Abnormal gastric motility
*Gastric necrosis
*[[Disseminated Intravascular Coagulation - Pathology|DIC]]
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-24T08:40:10Z

Dmassey:

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40-50% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgical aims include:
*Gastric decompression and repositioning
*Assessing the organ viability
*Removing necrotic tissue
*Gastropexy (can perform incisional, tube, belt-loop and circumcostal techniques) to prevent recurrence

If gastric necrosis (happens in 10-37% of patients) is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

===Post-operative complications===
These are wide and varied and include:
*Hypoperfusion
*Hypotension
*Cardiac arrythmias
*Aspiration pneumonia
*Abnormal gastric motility
*Gastric necrosis
*DIC
*Systemic Inflammatory Response Syndrome (SIRS)

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation''' 31(2):66 ''In Practice''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndromein dogs 2. Surgical and postoperative management''' 31(3):114 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-21T10:15:11Z

Dmassey: /* References */

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgery is aimed to reposition the stomach and spleen whilst preventing recurrence by performing a gastropexy. If gastric necrosis is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Tivers, M. and Brockman, D. (2009) '''Gastric dilation–volvulus syndrome in dogs 1. Pathophysiology, diagnosis and stabilisation''' 31(2):66 ''In Practice''

Gastric Dilatation and Volvulus

2009-08-21T10:13:17Z

Dmassey:

{{unfinished}}

{{dog}}

==Signalment==
*Large deep chested breeds including:
<gallery>
Image:Akita.jpg|Akitas
Image:Bloodhound.jpg|Bloodhounds
Image:Smooth Collie.jpg|Collies
Image:Greatdane.jpg|Great Danes
Image:Irish Setter.jpg|Irish Setters
Image:Irish Wolfhound.jpg|Wolfhounds
Image:Newfoundland.jpg|Newfoundlands
Image:Rottweiler.jpg|Rottweilers
Image:Stbernard.jpg|Saint Bernards
Image:Standard poodle.jpg|Standard Poodles
Image:Weimaraner.jpg|Weirmaraners
</gallery>

==Description==
Gastric dilatation (GD) and Gastric dilatation and volvulus (GDV) are caused by the stomach distending with air. In GDV the stomach twists around its axis mainly in a clockwise direction with both conditions leading to compression of the caudal vena cava. GDV can lead to [[Shock - Pathology#Hypovolaemic shock|hypovolaemic shock]], splenic torsion, gastric wall ischaemia, abdominal viscera congestion, [[Shock - Pathology#Endotoxic shock|endotoxic shock]] and [[Disseminated Intravascular Coagulation - Pathology|disseminated intravascular coagulation (DIC)]]. The exact pathogenesis is unclear but risk factors for GDV include age, fast eating, once- daily feeding, aerophagia, raised feeding bowl and a close relative with GDV.

==Diagnosis==
===History and Clinical signs===
*Abdominal distension
*Non-productive retching
*Weakness
*Collapse
*Salivation
*Abdominal tympany
*Tachycardia
*Pallor
*Hypothermia
*Cardiac arrythmias (present in 40% of patients) ([[Altered Impulse Formations - WikiClinical#2. Ventricular Premature Complexes (VPCs)|ventricular premature beats]], [[Altered Impulse Formations - WikiClinical#1. Ventricular Tachycardia|ventricular tachycardia]])

===Haematology===
*Increased haematocrit
*DIC (thrombocytopaenia, increased firbin degradation products, prolonged patial thromboplastin time and reduced antithrombin III.

===Biochemistry===
Most commonly find hypokalaemia and metabolic acidosis. The acidosis is caused hypoperfusion and anaerobic metabolism leading to lactic acid accumulation. Respiratory acidosis and alkalosis may also be present due to hypo- and hyperventilation.

===Diagnostic imaging===
Best performed after fluid therapy and gastric decompression. It allows distinction between GD and GDV:
*Gastric dilatation: gas distension, on right lateral shows air in the fundus.
*Gastric dilatation and volvulus: pylorus moves dorsally and left with a compartmentalized stomach.
A right lateral view will show a large fundus ventrally, with a smaller gas filled pylorus located dorsally to that. These are seperated by a soft tissue strip. The contrast of the abdomen may be lost indicating peritonitis or haemabdomen. Gastric rupture would show as pneumoperitoneum and increased contrast.

==Treatment==
The most important first line treatments are [[Principles of Fluid Therapy|fluid therapy]] and gastric decompression.

===Fluid therapy===
Should be individualised to the patient due to the varying nature of the acid-base disturbances. Large bore (16 or 18 gauge) catheters should be placed into cephalic or jugular veins (ideally two into both cephalic veins). Shock doses of Compound Sodium Lactate (Lactated Ringer's Solution) (60-90ml/kg/h). Hypertonic saline can also be used. Monitoring of the situation should be done by regular blood pressure measurements, heart rates, PCV and total solids and urine output. Potassium can be supplemented to bags in the form of KCl after the initial shock doses.

===Gastric decompression===
Performed by introduction of a lubricated premeasured (from nostril to last rib) stomach tube or by trocharizing the most tympanic area caudal to the ribs with a 14 to 16 gauge catheter. Sedation may be required to allow the passage of the stomach tube. Suitable drugs for this include [[Opioids#Butorphanol|butorphanol]], fentanyl or oxymorphone and [[Benzodiazepines#Diazepam|diazepam]].

===Other treatment===
*For shock: Prednisolone sodium succinate or dexamethasone sodium phosphate.
*For bacterial translocation and endotoxaemia: Broad spectrum antibiotics (e.g. [[Cephalosporins|cephalosporin]] and a [[Fluoroquinolones|fluoroquinolone]]) should also be given at surgical induction through to the postoperative period.
*For cardiac arrythmias: indicated if weakness, sycope, tachycardia runs with R on T complexes, ventricular tachycardia at rates >150bpm. Treated by correcting acid-base, electrolyte and haemostatic disturbances. The treatment is lidocaine by bolus or continuous rate infusion or procainamide if they persist.
*For analgesia: Pure opiod of morphine, methadone or fentanyl.
*General: Oxygen supplementation if possible

===Anaesthesia===
Anaesthesia must be carried out with care even after the patient has been stabilised. There are limited protocols but included fentanyl and diazepam bolus or titrated propofol. Maintenance can be achieved with the use of isoflurane and sevoflurane in oxygen however nitrous oxide should be avoided due to third spacing. Regular routine monitoring of urine production, blood pressure, central venous pressure, PCV, total solids, blood gas and serum electrolytes. High rates of fluids should be used to maintain tissue perfusion and arterial blood pressure

===Surgery===
Surgery is aimed to reposition the stomach and spleen whilst preventing recurrence by performing a gastropexy. If gastric necrosis is present (discoloured dark purple or grey/green, don't bleed when incised or feel paper thin) then a parital gastrectomy is required. Damage to the spleen via avulsion or torsion may need partial or complete splenectomy.

==Prognosis==
Simple GDV mortality rates are around 15%. Patients suffering from gastric necrosis, gastric resection or splenectomy have a higher mortality rate at over 30%. Gastric necorsis can be predicted by measuring plasma lactate. Values >6mmol/l indicates necrosis (Specificity 88%, Sensitivity 66%)

==References==

Hall, E.J, Simpson, J.W. and Williams, D.A. (2005) '''BSAVA Manual of Canine and Feline Gastroenterology (2nd Edition)''' ''BSAVA''

King, L. and Hammond, R. (1999) '''BSAVA Manual of Canine and Feline Emergency and Critical Care''' ''BSAVA''

Gastric Dilatation and Volvulus

2009-08-21T09:53:41Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T09:42:38Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T09:35:13Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T09:30:58Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T09:18:58Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T09:09:41Z

Dmassey: /* Diagnostic imaging */

Gastric Dilatation and Volvulus

2009-08-21T09:07:42Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T08:50:20Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T08:49:31Z

Dmassey:

Gastric Dilatation and Volvulus

2009-08-21T08:39:15Z

Dmassey:

Gastric Ulceration - Dog

2009-08-20T13:30:29Z

Dmassey:

{{review}}

{{cat}}
{{dog}}
See also [[Stomach and Abomasum Inflammation - Pathology#Erosive and Ulcerative Gastritis|Pathology in WikiPath]]

[[Image:Gastric ulceration.jpg|thumb|right|250px|Gastric Ulceration - Copyright David Walker RVC]]
==Signalment==
*Sled dogs

==Description==
Is a round or oval punched out lesions ranging from 1-4 cm in diameter caused by damage to the gastric mucosa.

There are many disease associations including:

{| style="width:100%; height:200px" border="1"

! '''Disease type'''
! '''E.g.'''

|-
|'''Hypotension'''
|[[Shock - Pathology|Shock]], Sepsis
|-
|'''Drug - induced'''
|[[NSAIDs|Non-steroidal anti-inflammatory drugs (NSAIDs)]]
|-
|'''Idiopathic'''
|Stress, exercise induced
|-
|'''Inflammatory'''
|[[Acute Gastritis - WikiClinical|Gastritis]], [[Pancreatitis - WikiClinical|Pancreatitis]]
|-
|'''Neoplastic'''
|Adenocarcinoma, lymphosarcoma, leiomyoma, gastrinoma (Zollinger-Ellison syndrome),
|-
|'''Metabolic/endocrine'''
|[[Hypoadrenocorticism - Addison's Disease|Hypoadrenocorticism]], liver disease, uraemia, [[Disseminated Intravascular Coagulation - Pathology|Disseminated Intravascular Coagulation (DIC)]], mastocytosis and hypergastrinaemia
|}

Gastric ulceration is caused by damage to the gastric mucosa through the above mechanisms. [[NSAIDs|NSAIDs]] directly damage the mucosa and interfere with the prostaglandin synthesis. Gastric ulceration is worsened by the use of [[NSAIDs|NSAIDs]] in combination with [[Steroids|corticosteroids]]. This risk can be minimised by using cyclooxygenase-1 (COX-1) sparing [[NSAIDs|NSAIDs]] (carprofen, meloxicam and deracoxib).

Gastric acid hypersecretion following mast cell degranulation of histamine and gastrin secretion from gastrinomas is a major cause of gastric ulceration. Sled dogs and equine race horses are prone to gastric ulceration.

==Diagnosis==
===History and Clinical Signs===
History may involve:
*Access to toxins and drugs such as [[NSAIDs|NSAIDs]]
Clinical Signs:
*Vomiting
*Haematemesis
*Malaena
*Pale mucous membranes
*Abdominal pain
*Weakness
*Inappetance
*Hypersalivation
*Circulatory comprimise

===Haematology===
*[[Anaemia|Anaemia]] - regenerative initially, may progress to microcytic, hypochromic and minutely regenerative.
*Thrombocytosis
*Lack of stress leucogram (and lymphocytosis and eosinophilia) supportive of [[Hypoadrenocorticism - Addison's Disease|hypoadrenocorticism]]
*Examination of the buffy coat may detect mastocytosis
*[[Changes in Inflammatory Cells Circulating in Blood - Pathology#Neutrophilia|Neutrophilia]] and a left shift - signs of inflammation or gastric perforation
*May show abnormalities in [[Haemostasis - Pathology|haemostasis]]

===Biochemistry===
*Dehydration - azotaemia
*Hepatic disease - increased liver enzymes and bilirubin, decreased urea, albumin and cholesterol
*Renal disease - azotaemia
*[[Hypoadrenocorticism - Addison's Disease|Hypoadrenocorticism]] - Sodium:Potassium ratio of less than 27:1
*Vomiting will lead to electrolyte and acid-base abnormalities - metabolic alkalosis, hypokalaemia and hypochloraemia

===Urinalysis===
*Dehydration - Hypersthenuria
*Renal disease - Isosthenuria

===Plain radiography===
[[Image:Gastric ulceration.png|thumb|right|250px|Gastric Ulceration - Copyright David Walker RVC]]
Not usually diagnostic but rules out differentials.

===Positive contrast radiography===
May show filling defects.

===Ultrasonography===
Shows gastric thickening and rules out differentials.

===Endoscopy and Biopsy===
Diagnostic test of choice and allows biopsies to be taken. [[NSAIDs|NSAID]] related ulcers are reguarly located in the antrum and there is limited mucosal thickening or irregularity whereas ulcerated [[Gastric Neoplasia - WikiClinical|gastric tumours]] will have thickened mucosa and edges. Any biopsies should be taken at the edge of normal and diseased to avoid further deepening or perforation.

==Treatment==
The main aim is to treat any primary underlying cause whilst giving general support. This may be hydrating, restoring electrolytes and acid-base and also helping the gastric lining to recover. Anti-ulcerative therapy should be continued for up to 6-8 weeks.

===[[Fluid Therapy]]===
Depends upon degree of dehydration, prescence of shock and any other diseases that are affected by volume. Prolonged vomiting or anorexia may lead to hypokalaemia so KCl may need adding to any fluids given. Normal rates for treatment of shock apply with dehydration being overcome by a fluid rate over 24 hours to replace the defecits along with a maintenance rate.

===Acid-base correction===
Imbalances should be corrected after taking a blood gas reading.
*If metabolic acidotic: give sodium bicarbonate but do repeated blood gas
*If metabolic alkalosis: replace volume defecit with intravenous NaCl and KCl.
*Blocking of acid secretion:
**[[Gastroprotective Drugs#Histamine (H2) Receptor Antagonists|Histamine receptor antagonists]]:
***cimetidine
***ranitidine
***famotidine
**Gastrin antagonists:
***proglumide
**Acetylcholine receptor antagonists:
***atropine
***pirenzepine
**Adenyl cyclase inhibitors:
***[[Gastroprotective Drugs#Prostaglandin E Analogues|prostaglangin E2 (PGE) analogues]] (misoprostol)
**[[Gastroprotective Drugs#Proton Pump Inhibitors|H+:K+ATPase inhibitors ]]:- for use when patient is refractory to histamine antagonists
***omeprazole - good for exercise induced gastric ulceration

===Mucosal protectants===
Such as misoprostol can be given alongside [[NSAIDs|NSAIDs]] to decrease the risk of ulceration. '''[[Gastroprotective Drugs#Binding Agents|Sucralfate]]''' which is polyaluminium sucrose sulphate, binds to damaged mucosa and assists in the treatment of gastric ulceration. It is best given 2 hours after acid inhibitors to prevent interference.

===Prophylaxis===
Prophylactic treatment has been shown not to prevent gastric ulceration. [[Gastroprotective Drugs#Binding Agents|Sucralfate]] is reported to be the best drug in patients receiving high doses of glucocorticoids.

===[[Emetics and Anti-Emetic Drugs#Anti-Emetics|Anti-emetics]]===
Indicated if vomiting is severe causing fluid and electrolyte imbalances and discomfort. See [[Emetics and Anti-Emetic Drugs#Anti-Emetics|Anti-emetics]] for drug details.

===Analgesia===
Is best provided by [[Opioids|opiods]] such as buprenorphine, pethidine and fentanyl.

===[[Antibiotics]]===
Animals suffering from shock and gastric barrier dysfunction may require prophylactic antibiotic cover. First line drugs include [[Penicillins|ampicillin]] or a [[Cephalosporins|cephalosporin]] which are effective against Gram-positive, some Gram-negative and some anaerobes. These can be combined with an [[Aminoglycosides|aminoglycoside]] which are effective against Gram-negative aerobes if sepsis is present. [[Fluoroquinolones|Enrofloxacin]] can also be used instead of an [[Aminoglycosides|aminoglycoside]] in skeletally mature animals

===Surgery===
May be required to investigate or to resect peforating ulcers which may lead to [[Peritonitis - WikiClinical|peritonitis]].

==Prognosis==
For animals with peptic ulcers is good. Prognosis is poorer for patients with renal or hepatic failure related ulcers. It is also poor for animals with gastric carcinoma and gastrinoma.

==References==

Hall, J.E., 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'''