Changes

==Treatment==

==Treatment==

Intensive treatment of cats is required as the disease has a high mortality if not managed aggressively.

Intensive treatment of cats is required as the disease has a high mortality if not managed aggressively. Owners should be warned that long-term nutritional support will be required to achieve a successful outcome.  In cases of secondary lipidosis, the underlying cause of disease should be treated.

 

===Nutritional Support===

===Nutritional Support===

[[File:FelineHepaticLipidosisEsophagealFeedingTube.jpg|thumb|Image of a cat receving nutritional support via an oesophagostomy tube<br><small>Released into the Public Domain]]</small>

[[File:FelineHepaticLipidosisEsophagealFeedingTube.jpg|thumb|Image of a cat receving nutritional support via an oesophagostomy tube<br><small>Released into the Public Domain]]</small>

*For a period of 4 - 6 weeks.

Nutritional support is generally required for a period of 4 - 6 weeks but longer durations may be necessary if the animal fails to eat voluntarily.  The two major considerations are the route of feeding and the composition of the diet that is fed.

*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.

Naso-oesophageal feeding tubes may be used temporarily to stabilise affected animals but this type of tube is likely to discourage voluntary feeding and it may traumatise the oesophagus.  Oesophagostomy tube or gastrostomy tubes are better suited to long-term management of patients with hepatic lipidosis and both may be placed during a short general anaesthetic.  Gastrostomy tubes may be placed under endoscopic guidance and these represent the best option if the animal has evidence of [[Oesophagitis|oesophagitis]] or chronic [[Vomiting|vomiting]].   

 

The fat content of the diet should be restricted to limit post-prandial hypertriglyceridaemia and the carbohydrate content should be limited as high concentrations will reduce the oxidation of fatty acids.  In cats, a diet of the '''highest possible protein content''' is indicated unless the animal is showing signs of hepatic encephalopathy.  Even in this situation, it is preferable to attempt to manage the signs of encephalopathy medically while continuing to feed a diet with a moderate protein content.

 

Specific nutrients such as arginine, taurine, or carnitine may also be added and there is some evidence to suggest that carnitine supplementation may be beneficial in cats with hepatic lipidosis.

===[[Hepatic Encephalopathy #Medical Management|Hepatic Encephalopathy]]===

===[[Hepatic Encephalopathy #Medical Management|Hepatic Encephalopathy]]===

===Gastro-intestinal Drugs===

===Gastro-intestinal Drugs===

*Anti-emetics and porkinetics such as [[Gastroprotective Drugs #Histamine (H2) Receptor Antagonists|ranitidine]] and [[Drugs Acting on the Intestines#Drugs Acting on 5-HT4 Receptors|metoclopromide]] if vomiting for delayed gastric emptying is present

Episodes of vomiting may cause dehydration and electrolyte imbalances and it is therefore important that this is prevented.  '''Maropitant''' (an NK1 receptor antagonist) is often used as an anti-emetic as it has both central and peripheral actions and this is often combined with [[Gastroprotective Drugs #Histamine (H2) Receptor Antagonists|'''ranitidine''']] which acts as a gastric acid secretory inhibitor and a prokinetic (by preventing the degradation of intestinal acetylcholine).  Ranitidine or [[Drugs Acting on the Intestines#Drugs Acting on 5-HT4 Receptors|'''metoclopromide''']] may also be appropriate if the vomiting is thought to result from delayed gastric emptying or intestinal ileus.

===Fluid Therapy===

===Fluid Therapy===

*Intravenous fluid therapy in early stages of disease.

Intravenous fluid therapy is often warranted in the early stages of disease when the patient is likely to be dehydrated and to have marked electrolyte imbalances. Blood glucose concentration should be monitored but supplementation with dextrose solutions should be sparing as this is likely to inhibit fatty acid oxidation.  Of the electrolytes, potassium and chloride are most likely to be deficient at presentation and potassium should be supplemented if its concentration can be measured regularly.  As feeding is introduced, hypophosphataemia may occur as part of a '''refeeding syndrome''' and this should be supplemented as necessary.

*Blood glucose and electrolytes especially potasium and phosphate should be monitored.

===Coagulopathy===

===Coagulopathy===

*Vitamin K supplement may be required if coagulopathy is significant.

Supplementation with '''vitamin K''' may be required by subcutaneous injection if the coagulopathy is significant.  Most coagulopathies are responsive to vitamin K supplementation even if this is not the primary cause.

==Prognosis==

==Prognosis==

This is dependent on the underlying cause.  If treated appropriately, 85% of severely affected animals will recover.

This is dependent on the underlying cause and the way in which the patient is managed.  If treated appropriately, 85% of severely affected animals will recover.

==References==

==References==