A few days ago I received the following email....
My sister lives in Italy and has just had to put her beloved female cat down of 12 years due to a bad case of hepatic lipidosis. They were moving house, the cat was stressed and feeling out of sorts, and had lost weight. The problem was they have two cats and my sister in all the stress of moving wasn’t aware that she had stopped eating as the other cat was obviously eating for both. I live in Australia and when I first heard that her cat was sick and a trip to her vet with blood tests came back normal, except for an elevated liver result, I immediately started to research this exact thing. ‘Excessive weight loss, no interest in eating, blood tests normal except for high liver result, ultrasound normal showing no mass, but slight inflammation of liver’… It told me a number of things but kept flagging lipidosis as primary or secondary outcome. In any case, I sent my sister this information and she discussed with her vet.
The vet kept the cat in for a few days and immediately rehydrated her via a drip and gave her AB’s, a shot of Vitamin K but at no point did she suggest an entero tube for feeding, instead she allowed my sister to take the cat home (understandably my sister felt that the cat would respond better with people she knows around her) and for my sister to force feed her via syringe a special supplemental food to get her back on track. Of course, my sister did that but noticed not much of an improvement in her cat. She was walking albeit wobbly, rapid, at times laboured breathing and was very emaciated. However, with the force feeding she had started to gain weight. My sister took her back after a week for a check up and they vet gave her a shot of anti-inflammatory medication and then a course of anti-inflammatory pills if she wasn’t vomiting. My sister noticed the next day the cat had really come alive (wanting to go outside for a walk, drinking water and using litter box as normal) but still no interest in eating on her own. Still, there was no mention of putting the cat on a gastro feeding tube via the stomach (which I read is less invasive to the cat and can be administered at home by the owner) which I know my sister would have happily done. In direct contraction now I read that giving an anti-inflammatory medication can make a cat with a liver issue much worse, so I have no idea why this was given when the blood test and ultrasound originally showed pointers to the liver being affected.
To cut a long story short nearly 2 weeks passed of my sister force feeding her cat, the continued laboured breathing got worse, she started vomiting a bit and wetting herself, then her ears became tinged yellow, a clear sign of jaundice related only to the lipidosis. She had to take her back to the vet when it was clear that she was suffering. Two days ago they had to put her down and my sister is blaming herself for a( not noticing her initial lack of appetite amidst all the stress of moving, and not knowing that a cat not eating for a certain period can affect the liver so seriously. What I cannot understand is the vet not immediately putting the cat on a gastro feeding tube, instead allowing her to go home to be force fed and ultimately allow the lipidosis to take a hold where it got beyond manageable. I feel she could have been saved 2 weeks ago and I’m so upset at what has happened.
I guess what I’m asking is do you think there’s a reason it wouldn’t have been offered? Perhaps a cat that is under so much stress from moving house, even with the feeding tube and recovery (and from what I’ve read 80% of cats can recover after a bout of lipidosis) perhaps if the initial stressor remains i.e moving house the cat will still refuse to eat on her own and continue to go down hill?
Maybe I’m clutching at straws, but both of us are feeling incredibly upset, guilty and frustrated that we didn’t do all we could to save Kity.
I would appreciate and be very grateful for any input/insight you have regarding a situation like this.
I definitely don't want to second-guess the vet in charge of this case, or say that they were wrong. I wasn't there and don't have access to the medical notes, so I'm not going to assume that I know better. That's not ethical for me to do as a veterinarian, and it would be the height of hubris for me to assume that I know better than the doctor who is directly involved with the case. So I'm going to take this from a perspective of what I would do, as well as explain a few things about some of the points.
Let's start with the question of elevated liver enzymes. Typically we look at two main values: alanine transferase (ALT) and alkaline phosphatase (ALKP). ALT is more specific to the liver as it is found exclusively in liver cells, while ALKP can be found in a few other tissues. There are also several non-liver conditions that can cause ALKP to become elevated, including steroid use and laboratory artifact. The is always a baseline level of these chemicals in the body, which is why we have a normal range for them. When we see elevations in these values, especially when ALT increases, we generally assume that there is a problem with the liver. However, these values don't give us the specific disorder, and only indicate liver damage with increased destruction of liver cells. The cause for this damage can be from dozens of reasons, including toxins, infection, cancer, trauma, abnormal blood circulation, and many, many other things. Elevation does not necessarily mean liver "failure", as the liver can still be functioning completely normally even while there is damage. So when we see abnormalities in these values, we need to try and do further testing to determine the cause so we can focus treatment on the appropriate disease process.
Hepatic lipidosis, more commonly called fatty liver syndrome, is a condition that in veterinary medicine we see almost exclusively in cats. This happens when abnormal fat metabolism results in infiltration of fat into the liver, causing abnormal liver function and possible liver failure. Overweight or obese cats are far more likely to develop this condition than normal weight cats, and in my personal clinical experience I've never seen a normal weight cat develop fatty liver syndrome. A key thing to keep in mind is that rarely is this a primary condition. In almost every case lipidosis is secondary to another disorder. That primary disease causes the cat to stop eating, and when that goes on for long enough the liver becomes infiltrated with fat. So really it is a cessation of eating that leads to hepatic lipidosis.
Remembering this underlying cause is important for two reasons. First, we need to find out why the cat is no longer eating. We can possibly treat the fatty liver, but that doesn't tell us why the cat stopped eating in the first place. The reason for the anorexia could have nothing whatsoever to do with the liver, and sometimes can be difficult to determine. Second, the primary way to treat fatty liver syndrome is to get food in the cat. And that's not easy.
If a cat won't eat on their own, you have to force food into them. This is rarely done intravenously because the IV feeding solutions carry a significant risk of systemic infection if not handled properly, so they are not done outside of critical care hospital situations. That leaves having to somehow get food into the stomach.
The least complicated but often most difficult method of force-feeding is simply to use a critical care food and give it with a syringe by mouth. Cats hate having anything forced into their mouth, and a cat that is nauseous or sick will typically resist having this done. You also end up wasting some food as it dribbles out of the mouth, you miss with the syringe as the cat pushes away, or they push it back out with their tongue.
Another option is a nasoesophageal tube. This is a small, soft rubber tube that is passed through the nasal passage into the esophagus. It's relatively easy to perform and usually doesn't require any form of sedation. The external part of the tube is taped or sutured to the top of the cat's head. A syringe can be attached to the end of the tube and liquified food be fed through the tube directly into the esophagus. This is a relatively short-term option and is usually used for only a few days. A longer-term option is to perform minor surgery, making a small incision through the skin and esophagus to place a tube directly into the esophagus through the side of the neck. While this second procedure allows longer feeding through the tube it also requires anesthesia and a higher level of skill to perform.
There is a downside and a risk to either nasoesophageal or esophageal tubes. If the cat vomits, the end of the tube can turn back on itself, and the vet or pet owner can't always tell that this happens. The end of the tube can advance back up towards the mouth, and when food is placed into it there is a risk that it can be forced up towards the trachea, resulting in aspiration of the food into the lungs. This is a very bad situation and will result in a form of pneumonia. While the risk of this happening to the tube is low, it is definitely a risk and something to watch for.
A more permanent option is a full stomach tube, often called a PEG tube. This is performed under general anesthesia and usually with an endoscope. A probe is placed into the stomach and pushed up against the stomach wall. A small incision is made through the stomach and abdominal wall, enabling the placement of a small device that goes through the skin and into the stomach. This device has a cap on the outside to allow closure between feedings. The wound quickly seals around the PEG device, giving a long-term way to place food and liquid directly into the stomach, bypassing the esophagus and mouth. These devices can be used long-term, and I've known cats to have them for up to a year. Because of the equipment and expertise needed, PEG tubes are usually placed by a specialist.
As you can see, putting a tube in a cat isn't always simple, and each method carries various degrees of risk and cost. Some vets don't do it because they don't feel comfortable with the procedure or worry about the secondary risks. But if you're trying to treat fatty liver syndrome you absolutely HAVE to get food in the cat. With proper feeding the fat will eventually come out of the liver and the liver has a great ability to regenerate.
Now let's get to some specifics of this particular case.
I've seen a lot of cats get stressed from a move, but I've never seen one completely stop eating. Yes, it's possible, but not common. Most of the time when a cat is stressed from a move it will have other behavioral changes, such as inappropriate urinating and defecating, marking behavior, hiding, and so on. So in this case I would look for other causes of the sudden decrease in appetite, and come back to stress only if other problems have been eliminated.
The vet in this case did what I would have done as the next step after blood tests and performed an ultrasound. It sounds like there was no evidence of a tumor, and apparently the imaging showed "inflammation". Unfortunately this is a very non-specific term, and doesn't indicate lipidosis or any other specific disease. I would also want to know if the inflammation was diffuse throughout the liver or if it was in focal areas. Fatty liver tends to be more diffuse.
A yellowing, or jaundice, is specific to diseases of the liver or gall bladder, but is not specific to fatty liver syndrome. Any advanced liver disorder can lead to this discoloration of tissues
If this had been my case, I would have likely done a trial of antibiotics, low-dose prednisolone, and a liver supplement to improve function. At the same time I would have used an anti-nausea medicaiton and an appetite stimulant to help the cat eat better. If it still wasn't eating I'd recommend at-home syringe feeding of a critical care diet. A recheck would have been scheduled for one week when I would have repeated the blood tests to see if there was any improvement in the lab values, as well as looked for improvement in clinical symptoms. Steroids can be indicated in many cases of liver disease as they do decrease inflammation. However, I feel that oral medication should be used instead of injections because the pill or liquid can be more precisely dosed up or down and gets out fo the system faster.
If the cat wasn't improved I would next recommend a liver biopsy. If someone has the right skills this can be done with a special needle guided by ultrasound, and doesn't always require surgery. The biopsy should be able to tell us more specifically what is happening with the liver. In fact, you can't accurately diagnosis lipidosis without a biopsy.
Yes, that's correct. We can strongly suspect hepatic lipidosis based on clinical signs and the cat's weight but you can only truly diagnosis it by documenting excessive fat within the liver tissue on a biopsy. So "inflammation" on an ultrasound may or may not indicate a fatty liver.
All of these steps and tests are to get down to the bottom of what is causing the lipidosis. Remember that this is typically a secondary condition and we always need to find out why the cat stopped eating. If we don't address that primary problem we'll never get the cat better.
Your sister shouldn't feel guilt. I've moved many times and it's always stressful. You have so many things going on that it's really hard to keep track of it all. Also, the vast majority of cats go through a move with minimal stress, and if there is stress it rarely causes them to stop eating. If her cat became so stressed that it wouldn't eat and that led to a fatty liver, this is an extremely rare situation that she couldn't have predicted.
Since fatty liver syndrome can only be properly diagnosed with a biopsy the vet probably had no reason to immediately suspect this as the main problem. I probably wouldn't have. Most vets probably would have proceeded similarly, with the potential exception of recommending a liver biopsy earlier in the process. Again, I'm not going to completely second-guess that vet since I wasn't involved with the case. But there are many reasons I can see for why they made those decisions. Honestly, the best thing to do is ask that vet these questions, and see why they proceeded as they did.