Changes

==Description==

==Description==

Hepatic encephalopathy is charaterised by a complex of neurological abnormalities that may occur in the presence of advanced liver disease.  By far the most common cause in dog and cat is [[Portosystemic Shunt]] (PSS) although a marked reduction in functional mass of hepatic tissue can also leads to hepatic encephalopathy.  In rare cases, if severe acquired shunt due to hepatobiliary disease and congenital PSS have been been ruled out, congenital urea enzyme cycle deficiencies and organic acidaemias, where there is lack of ability to degrade ammonia to urea, can be considered.

Hepatic encephalopathy is characterised by a complex of neurological abnormalities that may occur in the presence of advanced liver disease.  By far the most common cause in dog and cat is [[Portosystemic Shunt]] (PSS), although a marked reduction in functional mass of hepatic tissue can also lead to hepatic encephalopathy.  In rare cases, when severe acquired shunt due to hepatobiliary disease and congenital PSS have been ruled out, congenital urea enzyme cycle deficiencies and organic acidaemias, where there is lack of ability to degrade ammonia to urea, can be considered.

This is a reversible abnormality of the cerebral metabolism.  Its pathogensis is not yet fully understood.  Increased concentration of ammonia level is most common cause of this disease manifestations due to the toxic effect it has on brain cells.  Due to the lack of urea cycle in the brain, ammonia in cerebrospinal fluid (CSF) is detoxified into glutamine.  Level of glutamine can be shown to correlate with clinical signs.  Aromatic amino acids, especially tryptophan and its metabolites, share an antiport transporter with ammonia in CSF.  Consequently, dogs with congenital PSS are reported to have an increased aromatic amino acid concentrations in CSF.  Increased ammonia concentrations also have a number of other effects on the central nervous system, including a reduction in serotonin activity, an increased in NMDA (N-methyl-D-aspartic acid) and peripheral-type benzodiazepine receptors.

This is a reversible abnormality of the cerebral metabolism.  Its pathogenesis is not yet fully understood.  Increased concentration of ammonia level is the most common cause of this disease manifestation, due to its toxicity effect on brain cells.  Due to the lack of urea cycle in the brain, ammonia in cerebrospinal fluid (CSF) is detoxified into glutamine.  Level of glutamine can be shown to correlate with clinical signs.  Aromatic amino acids, especially tryptophan and its metabolites, share an antiport transporter with ammonia in CSF.  Consequently, dogs with congenital PSS are reported to have increased aromatic amino acid concentrations in CSF.  Increased ammonia concentrations also have a number of other effects on the central nervous system, including a reduction in serotonin activity, an increased in NMDA (N-methyl-D-aspartic acid) and peripheral-type benzodiazepine receptors.

The sources resposible for an increase in ammonia levels include:

The sources responsible for an increase in ammonia levels include:

*the bacterial and intestinal breakdown of urea by urease, which then diffuses into the colon from the blood.

*the bacterial and intestinal breakdown of urea by urease, which then diffuse into the colon from the blood.

*the bacterial breakdown of undigested amino acids and in the colon.

*the bacterial breakdown of undigested amino acids in the colon.

*the catabolic metabolism of glutamine as an enerygy source by small intestinal enterocytes.

*the catabolic metabolism of glutamine as an energy source by small intestinal enterocytes.

*endogenous hepatic protein metabolism by excess dietary protein, breakdown of lean body mass and gastrointestinal bleeding.

*endogenous hepatic protein metabolism by excess dietary protein intake, breakdown of lean body mass and gastrointestinal bleeding.

*temporary resolution of clinical signs with antimicrobial therapy

*temporary resolution of clinical signs with antimicrobial therapy

*prolonged recovery from sedation or anaesthesia

*prolonged recovery from sedation or anaesthesia

*polyuria and polydipsia in a third of cases

*polyuria and polydipsia in 33% of cases

====Cat====

====Cat====

Typical signs include:

Typical signs include:

*well grown and in good body condition which in contrast to dogs

*well grown and in good body condition which in contrast to dogs

*hypersalivation or ptyalism is the most commonly reported clinical feature, but rarely in dogs

*hypersalivation or ptyalism is the most commonly reported clinical feature, but rarely reported in dogs

*seizures reported in 50% of cases, but uncommon in dogs

*seizures, found in 50% of cases, but uncommon in dogs

*anorexia, vomiting and diarrhoea, polyuria and polydipsia is less common

*anorexia, vomiting and diarrhoea, polyuria and polydipsia are less common

*compulsive behaviour is less common compared to in dogs

*compulsive behaviour is less common compared to in dogs

===Diagnostic Imaging===

===Diagnostic Imaging===

*Abdominal radiographs shows microhepatica and often renomegaly.  Renomegally may relate to altered splanchnic blood flow or o increased metabolic activity of the kidney due to hyperammonaemia.  These findings in a young dog is highly suggestive of [[Portosystemic Shunt]].

*Abdominal radiography shows microhepatica and often renomegaly.  Renomegaly may relate to an altered splanchnic blood flow or to an increased metabolic activity of the kidney due to hyperammonaemia.  These findings in a young dog are highly suggestive of [[Portosystemic Shunt]].

*Confirmation of a [[Portosystemic Shunt]] requires visualisation of the shunting blood vessel.  This may be done with either ultrasonography or contrast portography or at surgery.

*Confirmation of a [[Portosystemic Shunt]] requires visualisation of the shunting blood vessel.  This may be done with either ultrasonography or contrast portography or at surgery.

*Oral antibiotics such as ampicillin, neomycin or metronidazole can be given initially reduce the amount of bacteria in intestines and hence decrease the production of ammonia.

*Oral antibiotics such as ampicillin, neomycin or metronidazole can be given initially reduce the amount of bacteria in intestines and hence decrease the production of ammonia.

*Lactulose PO

*Lactulose PO

**This is a synthetic disaccharide which is metabolised by the colonic bacteria, acidifying the colon.  Ammonia is converted into ammonium ions which cannot be absorbed, hence trapped in the colon and excreted in the faeces.  Lactulose also acts as a osmotic laxative, allowing more faeces and bacteria to be washed out.

**This is a synthetic disaccharide which is metabolised by the acidifying colonic bacteria.  Ammonia is converted into ammonium ions, which cannot be absorbed and hence trapped in the colon and excreted in the faeces.  Lactulose also acts as an osmotic laxative, allowing more faeces and bacteria to be washed out.

*A high carbohydrate, low protein (2g/kg/day) and low fat diet is recommended.

*A high carbohydrate, low protein (2g/kg/day) and low fat diet is recommended.

**The aim is to provide adequate nutrients and energy to support hepatic tissue repair, reduce the metabolic load on the liver and minimise the development of hepatic encephalopathy

**The aim is to provide adequate nutrients and energy to support hepatic tissue repair, reduce the metabolic load on the liver and minimise the development of hepatic encephalopathy

==Prognosis==

==Prognosis==

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

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

*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.

*Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''.