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| {{review}} | | {{review}} |
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| + | Also known as: '''''Portosystemic encephalopathy — Hepatic coma |
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− | {| cellpadding="10" cellspacing="0" border="1"
| + | See also: '''[[Hepatic Encephalopathy - Horse|Hepatic Encephalopathy in Horses]]''' |
− | | Also known as:
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− | | '''Portosystemic encephalopathy<br>
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− | '''Hepatic coma'''
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− | | See also:
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− | | '''[[Hepatic Encephalopathy - Horse|Hepatic Encephalopathy in Horses]]'''
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− | ==Description== | + | ==Introduction== |
| '''Hepatic encephalopathy''' (HE) is characterised by a complex of neurological abnormalities that occur due to congenital or acquired abnormalities in hepatic structure or function. HE is usually associated with some form of [[Portosystemic Shunt|'''portosystemic shunt''']] (PSS) in dogs and cats, although it may also be caused by a marked reduction in functional hepatic mass. Other causes of HE, such as [[Hepatic Microvascular Dysplasia|'''microvascular dysplasia''']], '''congenital defects of enzymes of the urea cycle''', '''arginine deficiency''' or '''organic acidaemias''', are very rare or of only experimental interest. The clinical signs of HE are associated with increases in the blood concentration of several metabolites: | | '''Hepatic encephalopathy''' (HE) is characterised by a complex of neurological abnormalities that occur due to congenital or acquired abnormalities in hepatic structure or function. HE is usually associated with some form of [[Portosystemic Shunt|'''portosystemic shunt''']] (PSS) in dogs and cats, although it may also be caused by a marked reduction in functional hepatic mass. Other causes of HE, such as [[Hepatic Microvascular Dysplasia|'''microvascular dysplasia''']], '''congenital defects of enzymes of the urea cycle''', '''arginine deficiency''' or '''organic acidaemias''', are very rare or of only experimental interest. The clinical signs of HE are associated with increases in the blood concentration of several metabolites: |
| *'''Ammonia''' is a by-product of protein degradation which is transported in the portal vein and metabolised to urea in the liver via the urea cycle. In animals with PSS, ammonia is not removed from the portal blood as this bypasses the liver, leading to an increase in its blood concentration. For ammonia generation in normal animals see [[Ammonia|ammonia]]. | | *'''Ammonia''' is a by-product of protein degradation which is transported in the portal vein and metabolised to urea in the liver via the urea cycle. In animals with PSS, ammonia is not removed from the portal blood as this bypasses the liver, leading to an increase in its blood concentration. For ammonia generation in normal animals see [[Ammonia|ammonia]]. |
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| ==Prognosis== | | ==Prognosis== |
| In cases of PSS, the prognosis in dogs for resolution of clinical signs after total surgical ligation is excellent. However, the response to surgical intervention in cats is less promising than in dogs. | | In cases of PSS, the prognosis in dogs for resolution of clinical signs after total surgical ligation is excellent. However, the response to surgical intervention in cats is less promising than in dogs. |
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| + | ==Literature Search== |
| + | [[File:CABI logo.jpg|left|90px]] |
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| + | Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation). |
| + | <br><br><br> |
| + | [http://www.cabdirect.org/search.html?q=%28%28title%3A%28%22Portosystemic+encephalopathy%22%29%29%29+OR+%28%28title%3A%28%22Hepatic+coma%22%29%29%29+OR+%28%28title%3A%28%22Hepatic+Encephalopathy%22%29%29%29 Hepatic Encephalopathy publications] |
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| ==References== | | ==References== |