Difference between revisions of "Hepatic Lipidosis"

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*Disturbances in the neurohormonal control of appetite resulting in inappropriate anorexia.
 
*Disturbances in the neurohormonal control of appetite resulting in inappropriate anorexia.
  
'''Secondary hepatic lipidosis''' is a neuroendocrine response in dogs and cats to other diseases for example, pacreatitis, diabetes mellitus, inflammatory bowel disease and primary hyperlipidaemia.  Secondary hepatic lipidosis is therefore less closely correlated with obesity and be seen in normal or even thin cats.
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'''Secondary hepatic lipidosis''' is a neuroendocrine response in dogs and cats to other diseases for example, [[Pancreatitis - WikiClinical|pacreatitis]], diabetes mellitus, inflammatory bowel disease and primary hyperlipidaemia.  Secondary hepatic lipidosis is therefore less closely correlated with obesity and be seen in normal or even thin cats.
  
 
Factors which contribute to hepatic lipidosis are:
 
Factors which contribute to hepatic lipidosis are:

Revision as of 16:43, 13 August 2009



Category:WikiClinical FelineCow
Category:WikiClinical CanineCow


Signalment

Indoor cats are more prone to primary hepatic lipidosis. Middle-aged cats are more prone.

Description

Hepatic lipidosis is the derangement of lipid and protein metabolism, which occurs cats and dogs, but more clinically significant in cats. It is important to differentiate primary or idiopathic hepatic lipidosis from secondary hepatic lipidosis.

Primary or idiopathic hepatic lipidosis is most recognised in obese indoor cats following anorexia. It is the most common hepatic disease in North America but it is also becoming more common in Europe. It is an acute hepatopathy with a large accumulation of lipid in hepatocytes, causing the liver to lose its function. The mortality rate is high unless the disease is treated aggressively. The pathogenesis includes a number of factors:

  • Excessive lipid mobilisation which is induced by anorexia, illness or stress.
  • Deficiency of dietary proteins and other nutrients, which reduces the liver's capacity to produce transport proteins and to metabolise fat. Recognised nutrient deficiencies include arginine, carnitine, taurine and methionine.
  • Disturbances in the neurohormonal control of appetite resulting in inappropriate anorexia.

Secondary hepatic lipidosis is a neuroendocrine response in dogs and cats to other diseases for example, pacreatitis, diabetes mellitus, inflammatory bowel disease and primary hyperlipidaemia. Secondary hepatic lipidosis is therefore less closely correlated with obesity and be seen in normal or even thin cats.

Factors which contribute to hepatic lipidosis are:

Diagnosis

Clinical Signs

  • Often obese cats following a sudden starvation
  • Anorexia and lethargy
  • Jaundice
  • Hepatic Encephalopathy
  • Diarrhoea (sometimes)
  • Palpable hepatomegaly (sometimes)
  • Coagulopathies (sometimes)

Laboratory Tests

Haematology

Biochemistry

  • Markedly increased level in alanine
  • Low gamma-glutamyltransferase (GGT) concentration
Hepatic Lipidosis Histology - Copyright Karin Allenspach's lecture RVC

Diagnostic Imaging

Abdominal radiography shows a marked hepatomegaly. On ultrasound, an enlarged and diffusely hyperechoeic liver is seen.


Histopathology

Fine needle aspirate of the liver is normally sufficient for a diagnosis. Cytology demonstrates hepatocytes swollen with lipid. Biopsy and culture of the liver tissue is always indicated to determine the underlying cause of the disease.

Treatment

  • Intensive treatment of cats is required for best outcome
  • Nutritional support for 4 - 6 weeks.
    • This is the most important treatment in hepatic lipidosis. It is vital to ensure that the diet is of adequate calorific content with an increase in protein content. Specific nutrients such as arginine, taurine, or carnitine may also be added.
    • This can be done via different feeding systems such as naso-oesophageal tube, oesophagostomy tube, gastrostomy tube.
  • Treat for Hepatic Encephalopathy if presented.
  • Anti-emetics and porkinetics such as ranitidine and metaclopromide if vomiting for delayed gastric emptying is present
  • Intravenous fluid therapy in early stages of disease.
    • Blood glucose and electrolytes especially potasium and phosphate should be monitored.
  • Vitamin K supplement may be required if coagulopathy is significant.


Prognosis

References

  • Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company.
  • 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.