Hepatic lipidosis, aka, fatty liver syndrome, is a common cause of liver disease in cats. The initial trigger for this disease is rapid weight loss, typically 25% or more loss of body weight within a 2 week period. This disease occurs most commonly in obese cats that suddenly go into a cycle of rapid weight loss, but can happen occasionally in average to slightly heavier built cats as well. While the hepatic lipidosis by itself can make the affected cat very sick, even die in its own right, in treating hepatic lipidosis, it is necessary to figure out and treat the cause for whatever caused the kitty to lose weight and/or stop eating so suddenly.
It may seem unusual to pet owners that such a serious problem can result from rapid weight loss, as we generally view weight loss in the context of ourselves, where many people and their doctors would embrace the concept of timely weight loss for the purpose of better health and aesthetics. To understand why rapid weight loss in cats can lead to such devastating liver disease, one must first understand the unique physiology of the feline.
Cats evolved as predators of small mammals and birds, eating multiple small meals as they hunted throughout the day. Their physiology is therefore geared towards a nearly completely carnivorous diet and with the notion that cats would live lean and not really have the opportunity to develop excessive stores of fat.
This of course drastically changed as the feline became domesticated. In having their food essentially provided for them and existing more on a” rest and digest” state of being, the opportunity to become overweight became quite common, while their physiology remained geared toward the subsistence hunters they descended from. On a day to day basis, this does not necessarily cause big problems, but when these overweight house cats suddenly stop eating or experience disease that causes rapid weight loss, hepatic lipidosis can result.
In this subsequent starvation mode, the body mobilizes fat body fat stores for energy and the maintenance of metabolism. This mobilized first moves to the liver to be processed into lipoproteins, however, the feline liver is not physiologically equipped to handle such large amounts of mobilized fat, so it becomes infiltrated with fat, leading to inflammation and eventually failure if not treated. Since it is the accumulation of fat in the liver that is the direct insult to the liver, the resultant common name of this disease is “fatty liver” or “fatty liver syndrome.”
As previously mentioned, one of the hallmark signs of hepatic lipidosis is a
substantially built cat experiencing rapid weight loss over a short period of time. The affected cat in most cases is not eating, and sometimes will exhibit vomiting, diarrhea, and marked depression. Many affected cats will have a yellow pallor to the whites of the eyes, the skin, and the gums, a clinical condition known as jaundice. The appearance of jaundice is caused by the accumulation of a yellow pigment called bilirubin, which is typically kept in check by the liver.
Blood work results will typically reveal elevation of the liver enzymes and total bilirubin. Imaging is often an essential component to confirming disease, with x-rays commonly showing an enlarged, dense liver, and ultrasound actually revealing brightly appearing plaques of fat on the liver surface.
The primary treatment goal aside from supportive care is to stop the negative energy balance thereby stopping the mobilization of body fat that is clogging the liver tissue. In mild cases, this consists of supporting the patient with IV fluids, anti-nausea injectable medication, antibiotics, and syringe feeding the cat an entire 3 ounce can of food per day. My preference for diet is a highly palatable and syringable diet that packs a lot of calories called Hills A/D. A/D is a prescription veterinary recovery diet, densely packed with nutrients and calories.
If a cat is either too sick or too stressed to accept syringed food, then it is best to have a feeding tube placed. These can be placed in the esophagus (called an esophageal tube), in the back of the throat (called a pharyngostomy tube), or guided up the nostril, down the back of the throat and into the esophagus (called a nasogastric tube). Any of these are acceptable and the best one is really whatever the attending veterinarian is most comfortable with. Any one of these can be placed with a brief course of general anesthesia and with minimal trauma. The feeding tubes can stay in for 2 weeks, providing the owner the ability to syringe feed the kitty with minimal stress. At the end of two weeks, feeding tubes can be removed without sedation or need for further anesthesia.
Supportive care for the liver is often of benefit as well. SAM-E and milk thistle both protect liver cells and promote liver regeneration. Ursodiol helps to increase bile flow thought the liver to expel excess bilirubin and other accumulated liver toxins.
Prognosis for hepatic lipidosis is guarded because of the variability of what caused the affected cat to stop eating and/or drop rapid weight in the first place. The hepatic lipidosis itself is resolvable with aggressive feeding and supportive care as described in 90% of cases.
As previously mentioned, it was initially a stoppage of eating or lack of ability to absorb dietary nutrients that led down a slippery slope to hepatic lipidosis. The Cornell University College of Veterinary Medicine Internal Medicine department published a study of cats affected with hepatic lipidosis and found primary conditions that led to hepatic lipidosis in the first place in the following percentages:
•28% had inflammatory bowel disease
•20% had a second type of liver disease (typically cholangiohepatitis)
•14% had cancer
•11% had pancreatitis
•5% had social problems (new cat, new dog, new home, new furniture, etc.)
•4% had respiratory disease
•2% were diabetic
For full recovery, any of these possible underlying possible primary conditions needs to be addressed.
Roger L. Welton, DVM
Founder and Chief Editor, Web-DVM.net
President, Maybeck Animal Hospital
Article updated 10/30/2012