Hepatic lipidosis is caused by an abnormally high accumulation of fats (triglycerides) in your cat’s liver cells. It is a disease caused by a cat’s inability to shift gears and live off of its fat reserves when it does not eat. When those fats build up rather being turned into usable energy, your cat’s liver cannot perform its other vital functions. It is the most common form of liver disease in pampered, middle-aged domestic cats. The problem is much less common in dogs. (ref1, ref2, ref3) What makes housecats so prone to developing hepatic lipidosis remains unknown. Through 2015, the many theories discussed among veterinarians remain unproven.
Fatty liver disease can be fatal if it is not quickly corrected. It can occur in a cat of any breed or age; but veterinarians in the USA and the UK see it most often in middle-aged and older cats. Some vets think that perhaps a few more female than male cats are affected. The problem is often entwined with the chronic inflammations of triad disease , diabetes or inflammatory bowel disease and, together with hepatic lipidosis (HL), they are the most common chronic problems affecting the digestive tracts of mature domestic cats. (ref)
In both human and cats, health professionals have noted an association between being overweight and these diseases. (ref1, ref2)
Some still explain hepatic lipidosis in cats as something that simple occurs when a cat will not eat. But it is more than that. The cats that gave rise to our housecats and that still roam free in Europe and Asia loose almost a third of their body weight in winters when prey is scarce without developing the disease. (ref)
The fact that all reports fined hepatic lipidosis more common in cats in the UK, Canada and the USA also leads to suspicions that diet and lifestyle play a major part in the disease.
The subcutaneous fat of overweight cats has different, unhealthy characteristics not shared by normal amounts of internal fat stores; and cats have great difficulty utilizing it to live on (for energy/calories) when they have no appetite or no access to food. Veterinarians do not know why that is - but many theories have been proposed. (ref)
Cats, particularly overweight ones that will not or cannot eat will often begin to develop in hepatic lipidosis in 3-7 days. Those eating substantially less than their normal amount can take two weeks or so to develop the problem. (ref)
When our cats (or for that mater us humans) don’t eat, our fat reserves begin to dissolve (mobilize) (=lipolysis) and free fatty acids and triglycerides, alternative forms of stored energy, are liberated to take the place of the calories we are no longer getting from food. Those fatty acids enter the blood stream where some eventually reach the liver; much of the rest is used as fuel by the muscles. In a normal liver, those fatty acids would be used to supply the great energy needs of the liver to perform its vital functions - that include processing absorbed nutrients, eliminating toxic substances and manufacturing blood proteins.
In cats, particularly fat, inactive ones, this fatty acid mobilization to the liver to produce energy fails. The fatty acids do get there, but they are not processed. They accumulate in the liver cells (hepatocytes) in their triplet triglyceride form where they block those cell’s vital functions. What we know and what some theorize is summed up in an article I mentioned earlier. (rptref) Since that article was published, it has become clearer that fat stored in different locations in your cat's body behave differently and, in overweight cats, can send signals throughout the body that interfere with the animals ability to live off of those fats in an emergency or metabolize blood sugar (increased insulin resistance). (ref) It has also become apparent that many cat owners are so attached to their pet that they are not particularly good at recognizing or won't accept the notion that their cat is too chubby for its own good. (ref)
Cats in the early stages of hepatic lipidosis can look and act surprisingly fine. What they all have in common is they will not eat their normal amounts of food. You might notice that your cat is disheveled (not grooming itself), you might notice that its eyes have mater at their corners (due to dehydration) or that its third eyelids are slightly extended and visible.
If you look at the inside of an unpigmented portion of the cat's lips, eyes or ear, you might notice a slight yellow tinge (like this). Maybe it has lost a bit of weight. Maybe its bowel habits have changed. Perhaps you recall a recent traumatic or stressful period in your cat’s life; perhaps one is ongoing. Several articles I referenced earlier speak at length about that; you can read more about it here.
When the the liver problems are more advanced, some cats bruise easily due to blood clotting problems; in others, their skin becomes fragile as it does in elderly people. (ref)
The classic position of a cat undergoing a hepatic lipidosis crisis is with its head and neck bent downward (= ventroflexion) - but such a position can accompany a number of other serious diseases as well.
There is always an underlying stress or disease process. It is very difficult to produce hepatic lipidosis in a cat that does not have underlying health issues or an obesity problem. (Even cutting the cat's food intake 25-45% did not produce HL.[ref]) In a fortunate few, it was a change in the cat’s environment that it did not like. Perhaps a new cat addition, perhaps a stay at a boarding kennel, pet "resort" or Uncle Charlie's, perhaps a new diet that did not appeal to it. Perhaps a bad reaction to a medication or supplement. (ref1, ref2)
But more often, HL is the an end result of chronic inflammatory problems affecting your cat’s digestive tract and the tract’s accessory organ (pancreas, gall bladder, bile duct and liver). In older cats, the toxic byproducts of common cancers must also be considered. Viruses can also underlie the condition. (ref) So can diabetes.
But no matter what the cause, once hepatic lipidosis begins, it appears to progress along the same biochemical and metabolic course no mater what originally instigated (caused) it.
Some veterinarians classify hepatic lipidosis as secondary (due to some underlying disease) or “primary” (idiopathic) when no underlying disease was found. Others use the term “primary” to mean the cases due to psychological stress, boarding or some physical reason why the cat can not or will not eat. But idiopathic does not mean it occurred without a cause. It just means that we could not determine what the cause was.
In 2005, Cornell University looked at 157 cats with hepatic lipidosis and determined their underlying problems. Twenty-eight percent had inflammatory bowel disease, 20% had another underlying type of liver disease (usually cholangiohepatitis), 14% had cancer, 11% had pancreatitis, 5% had social problems (a new cat in the home, move to a new home, new family members, etc.), 4% had some kind of respiratory disease and 2% were diabetic. (ref)
It is rare for a cat to recover from hepatic lipidosis if it does not receive appropriate veterinary care. Untreated, most cats will experience a downward spiral that they will not survive. The exceptions are cases where something in the home environment was to blame and where the owners or their vet recognized and eliminated that problem. But one should never attempt to treat a cat with hepatic lipidosis other than under the close supervision of a caring veterinarian.
The survival of your cat will depend on the success of three things:
2) Enteral (tube feeding) feeding - at least initially - is usually required.
3) Curing or stabilizing your cat's underlying health problem(s). Failure on any of these three fronts is unacceptable. When progress is made on all fronts, ~80% will recover. The younger the cat, the less overweight it is and the earlier it is presented to your veterinarian, the greater its chances of recovery.
The best sign of a likely recovery is the beginning of a gradual drop in your cat’s blood bilirubin levels and, of course, increased interest in food. Other blood values usually take longer to improve.
In a state of hepatic lipidosis, your cat is having problems obtaining the calories to fuel the needs of its body. Normally, those calories come from the proteins and fats in the food it eats. It has some sugar stored in its live as glycogen, but those reserves are not large. In other species of animals and in humans, it would nutritionally "switch gears" and the triglycerides stored in its fat cells would be liberated (as fatty acids) to fill its energy needs. But that doesn't work well in pampered house cats. The triglycerides and fatty acids your cat has stored away in its body fat reach its liver –but they just accumulate there in the liver cells (swell them) and are not utilized (not burned for the energy/calories they contain). Eventually this swelling causes the animal’s liver to shut down. (ref1, ref2, rptref3)
The result of that decreased liver function are abnormalities in the cat’s insulin/blood sugar interactions that deprive its body of essential energy plus high blood fatty acid and triglycerides levels without the ability to utilize them. Because the cat’s liver can no longer process the hemoglobin from obsolete red blood cells, the cat’s bilirubin levels begin to rise, eventually causing the cat’s skin to take on the yellowish tone of that compound (icterus).
Cats in this situation have no desire to eat. That is probably not just because the cat doesn't feel good. Two hormones control appetite, ghrelin, the "hunger hormone” produced mostly in the stomach and leptin the “I'm full” hormone, produced mostly by the cat’s fat. Veterinarians suspect that cats in hepatic lipidosis crisis produce too much leptin. (ref)
Cat in the midst of a major hepatic lipidosis event have high blood alkaline phosphatase (aka ALP, AP, ALKP) levels because ALP enzyme leaks out of their damaged liver cells. As I mentioned earlier, blood bilirubin values are above normal as well. Other liver-related blood enzymes, GGT, ALT and AST levels are inconsistent and variable. (Some vets associate high GGT with the likelihood that other liver problems are present along with HL. [ref]) High blood bile acid levels are also common due to the liver’s impaired ability to secrete them into the bile.
Many of these cats (about a third) develop anemia (the non-regenerative form) as toxic products normally eliminated by the liver begin to interfere with the ability of its bone marrow to produce replacement red blood cells. Others become anemic due to bleeding tendencies that are though to develop as the liver looses its ability to produce prothrombin and other clotting factor - although how these bleeding tendencies develop is complex and debatable. (ref)
There are many severe diseases that cause alterations in a cat’s blood electrolytes. Hepatic lipidosis is one of them. Those electrolyte changes, when found, are not diagnostic of HL, but any major alterations in your cat’s blood electrolyte elements (ie sodium, potassium, calcium, magnesium , chloride, phosphate or carbonate [ref] ) needs to be corrected with intravenous fluids to help your cat recover.
Ketone levels might be found to be high in your pet’s urine – although diabetes can cause that as well. (ref)
Your veterinarian might elect to confirm the diagnosis with an ultrasound-directed or fine needle liver biopsy to rule out other forms of liver injury- particularly if some of the cats examination results could have other explanations (see on how that's done ). The vet might use an ultrasound examination of the cat’s liver to confirm that the entire organ is involved (In other liver diseases, like lymphoma tumors or abscesses, the pathology damage is limited to specific portions of the liver not all of it as in HL). (ref)
You cat needs the services of a qualified veterinarian (This is not a self-help treatment manual). Let your local veterinarian decide that. In cases that are caught early, it might be possible for a house call veterinarian to provide those services. But such a person at least needs the backup option of a full staff/full-service veterinary facility that provides 24-hour care - if required. Other things being equal, my preference is to utilize feline-only practices when you are faced with HL – even if you must drive some distance to reach one. When its vaccinations or day-surgery, mixed animal facilities are fine. But your cat is under a lot of stress now. Dogs on the premises can add stress to an already stressful situation.
Your cat needs immediate nutrition. Force-feeding a cat orally at home is a very hard task for most cat owners. Many cats fight and stress out in the process. In that process, you might be bitten. Cat bites can lead to serious hand infections. (ref) But it sometimes can be done and there are veterinarians who will work with you to provide instructions. If that is not an option, search for “how to force feed a cat” on but remember I warned you. Just as important as potential bites, problem with doing things like this yourself is that although you may succeed in getting your cat to eat on its own again, you will not know what caused the problem in the first place. It’s a bit like adding air to a flat tire without finding out why the tire went flat in the first place - you may not get very far down the road.
When your cat is hospitalized it will be checked for dehydration, a common finding, and rehydrated with intravenous fluids when they are required. Other stabilization procedures include bringing the cat to normal body temperature and dealing with respiratory and circulatory issues in critical cases.
During that period, the vets will do a complete physical examination on the cat and almost certainly a blood analysis. Depending on the practice philosophy and blood work results, many might suggest any number of equipment-assisted examinations to get a complete feel for the urgency and extent of the problem. That might include x-rays, ultrasound exams, electrocardiogram, liver biopsy etc. Yet, with years of experience behind them, it may take only a few moments for a seasoned veterinarian to size up the urgency and seriousness of the problem.
In most cases, cats will need a less stressful way to obtain nutrition than force-feeding. That means inserting a feeding tube into its stomach. Some of the references in this article describe that procedure in detail. I know of no data as to what foods are best – other than they should meet the published nutritional needs of cats and either come in a liquid form or be easily liquefied to pass through a syringe and tube. Depending on the cat and the owner’s temperaments, some cats can be released from the hospital and fed through that implanted feeding tube at home where they are more at ease. You can see photos of how cat’s are fed through a tube in an article I referenced earlier (rptref). Initially, that feeding tube is often entered through the cat’s nose and down into its stomach. For longer term, it needs to exit through an incision over the neck. Most wait until the cat is strong and stable enough to receive an anesthetic. (ref) That can upset squeamish cat owners – but it is not nearly as drastic a technique as it may first appear to you.
That food is now getting to your cat’s stomach is very important - but not sufficient to be relaxed. These cat’s general condition still need to be monitored closely for possible unexpected problems. (ref)
Veterinarians have traditionally given these cats antibiotics (to prevent an infection or control one that might possibly already be present) and an injectable form of vitamin K (Aquamephyton aka phytonadione) in an attempt to combat defective blood clotting. Perhaps they will be helpful. If blood ammonia levels are found to be high (eg hepatic encephalopathy), they might consider temporarily restricting the amount of protein the cat receives or limiting proteins to egg and dairy sources (restricting the protein supply of cats can lead to its own set of problems).
Drooling and vomiting cats need medications to combat nausea. Those that are vomiting, need medications to calm their stomachs as well. There are many (= antiemetics, eg Zoetis’Cerenia=[ref]. (ref) Slow administration of food through feeding tubes in more frequent, but smaller amounts and placing the cat in optimal positions during feeding sometimes helps minimize vomiting problems.
Although I know of no studies that suggest their use in cats, there may also be a role for Ursodeoxycholic acid supplements to improve liver function in some of these cats. You can read about that compound here.
There are many additional compounds veterinarians give to cats with hepatic lipidosis. Some may be helpful, some are certainly not and none have been scientifically proven to work. They include: vitamins E, C and B12 (Cobalamin), S-adenosyl-methionine (SAMe) and/or silymarin (Milk Thistle), L-carnitine and ursodiol. Providing the amino acids, leucine, isoleucine, valine and taurine, has also been suggested. The optimal dose and dose frequency of all of them also remains unknown. Because they would not be approved by the FDA if marketed as liver medications, they are marketed as “liver support”. Don't exceed your veterinarian's suggested doses.
There are medications that are known to increase appetite and, for many years, veterinarians gave them to cats with hepatic lipidosis in an attempt to get them to eat. Many have fallen out of favor - because they seemed to have little effect in cats, because they required a healthy liver to be effective, because of their sedative qualities(they made the cats dopey) or because their potential side effects were as serious as the disease itself. Mirtazapine (Remeron) is probably the most common ones given today (2015). (ref) Mirtazapine, given at the proper dosage, does not appear to have any of the negative properties of the previous medications used to stimulate appetite. I placed a link at the top of this page to a new appetite stimulant, capromorelin sold as Entyce®. It entered the veterinary market in 2018. It is not yet approved for use in cats but you can read some cat-owner feedback on its use when cats won't eat here.
Appetite stimulation alone is rarely if ever sufficient treatment in itself for serious cases of hepatic lipidosis.
A fairly recent health concept is that oxidative stress in the body liberates dangerous "free radical" compounds and that this occurs in many diseases - liver disease included. (ref) Whether this occurs, and if it is an important feature of hepatic lipidosis in cats remains unknown. Compounds called antioxidants can inhibit free radicals. Some are synthesized naturally in the body, others are obtained through what we eat. Some veterinarians believe that providing the cats with additional glutathione, an antioxidant naturally produced in the liver, may help protect them from oxidative stress. (ref1, ref2)
In an attempt to do that, many vets give cats with hepatic lipidosis oral SAMe (N-acetylcysteine, S-adenosylmethionine). The most common veterinary brand used for this in the USA is Denamarin©. Most of the studies of the effectiveness of SAMe have been conducted in people with alcohol and non-alcohol related liver disease. Some of those results have been positive (ref) and some have not. (ref1, ref2) But I would definitely include it your cat’s medications, based on what us veterinarians know today (9/9/15) and the lack of alternatives. ..................Veterinarians are always searching for new treatment options for cats with this problem. (ref)
Humans also suffer from a number of conditions in which the metabolism of fats within liver cells are altered. The most common one is steatohepatitis (aka NASH) - related to obesity. As you know, that is a growing problem. When folks just can't seem to make the diet changes required to solve this problem, there have been encouraging results administering a synthetic bile acid, obeticholic acid. (ref) I do not know of any reports of it having been used in cats. But veterinarians often come to rely on discoveries that are the offspring of studies designed to help humans. Another compound under study is elafibranor. (ref)
I have my veterinary nurses offer a sniff of canned cat food to hospitalized cats every day, morning and evening, to see if they show any interest in it or just turn their heads away. Any interest is a very good sign - more so than any sophisticated test. But the change back to an oral diet needs to be a gradual one. Veterinarians would not wish to remove an implanted feeding tube only to have to reinstall it. Often the change back to an oral diet goes smoothly. When it doesn’t there are some important things to consider; particularly if the laboratory tests are showing improvement and the cat still won’t eat:
The vast majority of cats dislike change – they are creatures of habit. Perhaps the hospital foods or presentation do not appeal to them. Bring the staff some of the cat’s regular food. See if that is more acceptable to the cat. You know your cat’s likes and dislikes better than anyone. Perhaps a top dressing of meaty broth, salmon or tuna gravy would do the trick. Many cats prefer their food warm. See if that helps. Most medications are bitter – be sure none is or has been in the food container. Do not attempt to get the cat to eat soon after an attempt to give oral medications. Don't be ashamed to tell the staff what you were feeding your cat - eating anything is better than eating nothing. I have had clients that fed their cat a diet of lobster. If that's what it takes to get them eating - let it be lobster.
In my experience, recovering cats are more likely to eat food presented on a small coffee cup saucer than in a deep bowl. Sometimes, touching their nose with a finger that has touched the food gives them incentive, but forcing the food into them is never a good idea. If they do not eat the food readily, don’t let it set there all day. Put it back in the fridge in a sealed container, take it out later, re-warm it.
The amount the cat’s stomach can hold can shrink considerably after a bout of hepatic lipidosis. Do not expect the cat to consume its normal amount of food. Instead, try small, frequent feeding. Allowing a large meal can result in the cat vomiting it all back up.
Some cats are slow to resume eating in a hospital setting. They are very spatial - considerably more so than dogs. They like surroundings they are accustomed to – curling up on their favorite chair or sofa, hiding behind the curtain in a back room when they seek solitude. And they are generally quite hostile to cats that they do not include in their family group. They do their best in the settings they are familiar with - attended to by the people they know. That is not the situation in a hospital. Different odors, sounds, objects and the presence of other cats stress out most cats there. (ref)
The exceptions are generally the cats that are taken out for walks and drives or in other ways accustomed to change. But those are generally not the overweight, inactive cats most likely to develop hepatic lipidosis.
Some say that cats do not form the close owner-bonds that dogs do. An article claiming that was published this year. (ref) But my belief is that their comfort and satisfaction when in the proximity of their owner in a familiar environment is very strong. It is just that using bonding tests and criteria designed for humans give incorrect results when applied to cats. There are better ways to judge anxiety levels in cats when subject to separation from their owners (ref) Anxiety is never good for the liver. (ref)
That is why earlier in this article I mentioned the option of your relying on a house call veterinarian to minimize the stress on your cat. These veterinarians generally maintain an intimate relationship with a local full-service animal hospital that they can utilize to perform complicated procedures when necessary and then return the cat to you. (There are naturally cat-oriented people and naturally dog-oriented people and some of them become cat-oriented veterinarians and some become dog-oriented veterinarians. Be sure the one you select is cat-oriented.)
If the pet's blood tests results are improving and there is no other explanation why your cat continues to refuse oral food, an option is to give it a try at home. You can always return the cat to the hospital if it does no better at home.
Be sure to check your favorite doctor's work schedule and your work schedule for the week that is planned. Mondays and Saturdays can be very busy at animal hospitals. Sometimes, evening and weekend staff will not be familiar with the case. You do not want to end up with your pet at some after-hours emergency clinic if that can be avoided.
Yes, making some healthy lifestyle changes can be quite helpful in preventing a future relapse.
Since I can not tell what specifically causes hepatic lipidosis in your cat, I can’t be very specific in offering you advice. But many vets, including myself, have our strong suspicions. We know what cat lifestyles are associated with developing the disease and the body condition (overweight ,inactivity, high-carb/high additive mass-marketed diet) that the majority of these cats share.
(Beware the "grain free", "organic" "all natural" "cats just crave it !" "feed his instinct " stuff on the label. That's just good public relations; Megapetfood companies do that to divert you from noticing that their carbohydrate level is still unhealthily high.)
I mentioned earlier that hepatic lipidosis is relatively common in cats in North America, Great Britain, Japan, and Western Europe. It was relatively uncommon in Southern European countries, Poland, New Zealand and Israel when I practiced there, until the penetration of commercial cat foods and subsequent epidemics of feline obesity. Cats in low-incidence areas generally eat the meat scraps and offal left over from their owners meals or supply a large portion of their diet through hunting rodents and small birds. They receive few carbohydrates (starches and sugars) just like their wild ancestors.. They are rarely confined and they are lean.
The commercial cat foods we used in America and Western Europe favor the laying down of excessive fat that the cat cannot readily metabolize or deal with during a fasting crises. I believe that the obesity these diets encourage is pro-inflammatory in nature (ref) and, I believe, that they are one of the underlying cause of the many chronic inflammations of the liver, pancreas, gall bladder, intestines and stomach that house cats suffer from - as well as hepatic lipidosis (ref) Their formulas and ingredients are based on economics and the industry-dominated AAFCO's (Association of American Feed Control Officials) historic traditions, not the health, general well-being and longevity of cats. My first suggestion is to prepare your cat’s diet from supplemented meat ingredients at home. Read about that here. I am not a fan of raw diets or meat diets sold for pets through stores. Read about that here. I am not a fan of refrigerated cat and dog diets, purchased at stores either because quality control is less certain and contamination more probable than if you prepare it hygienically at home. If you go with my advice you will need to put cotton in your ears and disregard the complaints and warnings of the Megpetfood Giants (the ones with all the slick TV ads) the AVMA , BVA , AVA, and their institutional supporters who – rightly so - sense potential decreases in their revenue streams. But the association between their prepared diets with their high carbs (carbohydrate glut) , additive and disease is just too great to be ignored. Read about that here.
But not all of us have the time to properly prepare a balanced diet for ones cat at home. We are time-rushed, we lead hectic lives. We get home from work tired. If that just doesn’t work out for you, consider the next best option, feline diets prepared by a veterinarian who understands the nutritional needs of cats. I have never met him, I have no financial connection to him - but I respect his opinions. (ref)
As I mentioned earlier, cats are not dogs. Their needs differ. Many (but not all) dogs experienced genetic changes long ago that allow them to handle starch and sugar carbohydrates better. (ref1, ref2) The authors of ref1 told me that that adaptation appears to be less developed in the "arctic breeds"
I am also not suggesting you let your cat run loose and hunt to shed weight and catch prey. The dangers of accidents and infectious disease in loose cats is far greater than the benefit of the exercise they might receive. But regularly taking your cat outside on a leash and doing all that you can to encourage its activity at home are both quite valid options. Other suggestions for getting your cat back to an optimal body weight are given in an earlier link from this article.
Cats establish the eating habits early – when they are kittens. Fat, cubby kittens are not necessarily healthy kittens. That is the time that their feeding habits and choices become ingrained and the number and distribution of their fat cells are determined. (ref) In later life, that can be hard or impossible to change. In all species of animals, it has been found that a slow, steady gain in body size is considerably more healthy than a rapid rise in body weight. (ref)
Spaying kittens too early in life (before sexual maturity) can also have lifelong negative effects on health – including increased risk of obesity. (ref)