Introduction
Hepatic lipidosis is the most common liver disease affecting cats in the US. Although inflammatory liver disease is reported to be more common in the UK, the true incidence of hepatic lipidosis in this country has not been established. Cats are particularly prone to hepatic lipidosis due to their obligatory carnivore status. During times of adequate or excessive nutrition, fat is stored in adipocytes. When nutrition is inadequate, the fat is mobilised from fat stores to the liver. Processing of triglycerides in the liver requires protein and vitamins that are depleted as a result of inadequate intake and excessive utilisation. As a result triglycerides become 'trapped' in the liver, preventing their metabolism to more useful products. This leads to the 'fatty liver' that is typical of hepatic lipidosis. In a lean cat the fat content of the liver comprises 2.5%, with this figure increasing to 5% in obese cats. In cats with hepatic lipidosis the fat content may increase to 50%, with the total liver mass doubling, or even trebling as a result of fat deposition.
Hepatic lipidosis may arise as a primary condition, in which the cat is otherwise healthy but has suffered a significant weight loss, for example as a result of an inappropriate weight reduction regime. However, in approximately 95% of cases hepatic lipidosis arises as a result of anorexia due to some other illness: secondary hepatic lipidosis. Conditions that may be associated with hepatic lipidosis include diabetes mellitus, pancreatitis and neoplasia.
Diagnosis
History
Cats with hepatic lipidosis will typically have a history of weight loss, often of more than 25% of body weight. Anorexia may be partial or complete. Other historical findings may reflect concurrent medical problems, with nearly 40% of affected cats vomiting.
Physical Examination
Approximately 70% of affected cats are jaundiced. The liver is generally enlarged, but feels smooth on palpation. Cats are often dehydrated and ventroflexion of the neck may indicate weakness.
Haematology
Nearly a quarter of affected cats are anaemic at time of presentation. This figure may increase during treatment as a result of rehydration and repeated blood sampling. Abnormally shaped red blood cells and the presence of increased Heinz bodies are common findings.
Biochemistry
Elevations in the liver enzymes ALT, ALKP and AST are typically seen. GGT may be increased if there is a concurrent hepatopathy, but a normal or mildly elevated GGT in association with marked increases in the other liver parameters may be suggestive of hepatic lipidosis. Bilirubin is elevated in >95% of cases. Urea may be reduced, as a result of reduced hepatic synthesis, and albumin is reduced in >60% of cases. Electrolytes such as potassium, magnesium and phosphate are often low, either at presentation or following treatment.
Coagulation Tests
Prolongation in prothrombin time (PT) and activated partial thromboplastin time (aPTT) may reflect reduced synthesis of clotting factors by the liver. The PIVKA test is a more sensitive method of detecting these abnormalities.
Urinalysis
Lipid droplets may be detected in urine sediment, and bilirubin may be detected on dipstick examination.
Ultrasonography
On ultrasound the liver appears enlarged and hyperechoic, in comparison to the falciform ligament (the kidneys will also be hyperechoic due to fat deposition). Other abnormalities relating to primary diseases may also be detected by abdominal ultrasonography.
Biopsy Sampling
Confirmation of hepatic lipidosis requires cytology or histopathology. Cytology is often preferred due to the compromised nature of these patients, but may miss underlying, focal disease.
Treatment
Cats affected with hepatic lipidosis may vary from mild, subclinically affected cases to severely ill cats that require intensive treatment and prolonged hospitalisation, and therefore the treatment has to be tailored on an individual basis. However, one universal truth is that the key to management of this condition is adequate nutrition. Whilst some cats may respond to tempting, hand feeding or syringe feeding, many cats may require placement of feeding tubes. In the first instance, naso-oesophageal tubes are preferred, as they are easy to place and do not require anaesthesia. In addition, the risk of haemorrhage is minimal. However, the narrow diameter of the feeding tube limits the type of diet that can be administered via the tube, and irritation of the nasal passages may develop with prolonged use. An oesophagostomy tube is easy to place, once the cat is tolerant of general anaesthesia, and allows for more prolonged feeding, potentially in the home environment. If the underlying disease merits it, a gastrostomy tube may be placed, although this is a more complicated technique requiring a more prolonged anaesthetic.
Caloric requirement should be calculated for the cat, based on basal energy requirement. Only one-third of this should be fed on day 1, two-thirds on day 2 and the full requirement on day 3. This reduces the risk of metabolic complications associated with the re-feeding syndrome. The volume of liquid feed required for the day should be divided into four to six small feeds. Additional supplementation of vitamins, antioxidants and other nutritional cofactors may be required (Figure 1), along with treatment of any underlying conditions e.g., metoclopramide infusions for vomiting/nausea or analgesia for pancreatitis. Appetite stimulants are generally unsuccessful in management of this condition, and may cause adverse side effects.
Figure 1. Medications used in the treatment of feline hepatic lipidosis.
|
Medication |
Dose |
Comments |
|
0.9% NaCl |
Depends on degree of dehydration, concurrent cardiac disease etc. |
Lactate-containing fluids (e.g Hartmann's) should be avoided, as lactate requires hepatic metabolism |
|
Potassium chloride |
Depends on degree of hypokalaemia |
Hypokalaemia may develop with re-feeding. Monitor daily for first 72 hours. Do not exceed 0.5 mmol/kg/hr |
|
Potassium phosphate |
0.01-0.06 mmol/kg/hr
Give as constant-rate infusion in NaCl |
Hypophosphataemia may develop with re-feeding. Supplementation indicated if <0.7 mmol/l. Reevaluate after 6 hours. Will precipitate with calcium-containing fluids |
|
Magnesium sulphate |
0.3-0.5 mmol/kg/day
Give as constant rate infusion in NaCl |
Hypomagnesaemia may develop with re-feeding and may contribute to hypokalaemia. Monitor every 12-24 hours. Will precipitate with calcium-containing fluids |
|
Thiamine (vitamin B1) |
50-100 mg/cat/day |
Anaphylaxis may be seen with injectable preparations; use oral instead |
|
Cobalamin (vitamin B12) |
1 mg/cat s.c. q7-14d |
Liver cobalamin stores may be depleted in the face of normal serum cobalamin |
|
Multivitamin preparations |
1-2 ml per 500 ml bag of fluids |
Protect from light once added to bag |
|
Vitamin K1 |
0.5-1.0 mg/kg q12h for three doses |
Give orally, or by subcutaneous injection using a 25 gauge needle. Vitamin K required for clotting factors II, VII, IX and X |
|
Vitamin E |
10 IU/kg/day |
Antioxidant often depleted with anorexia or malabsorption |
|
L-carnitine |
250-500 mg/cat/day |
Promotes utilisation of fatty acids by mitochondria |
|
Taurine |
250-500 mg/cat/day |
High dietary requirement, as used for bile acid conjugation |
|
S-adenosyl methionine |
20-40 mg/kg/day 90 mg/cat/day |
Higher dose required if enteric coated tablets are crushed for administration via feeding tube. Precursor for L-carnitine and glutathione; antioxidant and hepatoprotective properties |
|
N-acetyl cysteine |
140 mg/kg; dilute 1:4 with NaCl and give over 20 minutes |
Subsequent doses may be given after 8-12 hours at 70 mg/kg. Precursor for glutathione |
Prognosis
Prognosis may depend, in part, on the aetiology of the condition. Severe hepatic lipidosis was previously associated with a poor prognosis, and whilst this is still a potentially fatal condition the recognition of the importance of nutrition, and more aggressive management has led to improved success rates.
References
1. Center SA. Feline hepatic lipidosis. Veterinary Clinics of North America 2005; 35(1): 225-269.
2. Han E. Oesophageal and gastric feeding tubes in ICU patients. Clinical Techniques in Small Animal Practice 2004; 19(1): 22-31.
3. Zoran DL. The carnivore connection to nutrition in cats. Journal of the American Veterinary Medical Association 2004; 221(11): 1559-1567.