Click on me for a fanciful Image of a simple extrahepatic shunt
If you have come to this page, it is probably because you veterinarian told you that he/she suspects this could be your dog or cat’s problem. This is quite a complicated article because it deals with a complicated problem. I’ll do my best to keep it as simple as possible. If you want a more detailed, scientific explanation with lots of obscure medical terms, follow the article links that I have added. If its still unclear, let me know and I'll try to answer your questions.
Some health problems your veterinarian deals with are easy to diagnose and easy to fix. Others are easy to diagnose and hard to fix. Hepatic shunts are both hard to diagnose and hard to fix. Diagnosis becomes more obvious when organs start to fail or when the dog or cat’s mental status begins to deteriorate. At that point, the pets are often suffering from some degree of hepatic encephalopathy.
You could roughly compare it to your house’s plumbing system. If a small pipe with a slightly higher pressure jumped from the cold to the hot water system bypassing the hot water heater (think liver) water would still come out of both faucets. In the case of plumbing, the hot water would be cooler than it should be. In the case of blood, a portion of the blood in the veins (portal vein) that carries nutrients from the pet’s intestines would miss a vital step in detoxification in the liver and the liver would be partially starved of nutrients.
That abnormal “pipe” that bypassed your pet’s liver (goes around the liver rather than through it) is called a shunt. Others call it an “anomalous vessel” (ie abnormal, shouldn't be there ) and some call them “aberrant connections” - the same thing. Vets and physicians less inclined to be wordy just call them “liver shunts”.
Most developed while the pet was still in its mother’s womb (congenital portosystemic shunt, CPSS). But higher than normal portal vein pressure due to blood flow obstructions or inflammation in the liver can cause them to form later in life (acquired portosystemic shunts). They can sprout from blood vessels in many locations – both within the liver itself or at many points in the tangle of veins within the pets abdomen. There can be a single one ,but on occasion, several. In smaller dog breeds, the shunt most commonly runs from one of the portal vein branches to the vena cava. In larger breed (eg Irish Wolfhounds) , the shunt is often within the liver itself (ref) You can read more detailed scientific articles on portosystemic shunts here, here and here.
When you feed your pet, good nutrients are not the only thing your pet absorbs. Bacterial fermentation and other processes in your pet’s intestines produce many products that are undesirable or toxic if they enter your pets general blood stream (its general circulation). (ref) One of the main jobs of your pet’s liver is to detoxify those products (clean the blood). So nature designed a special many-branched vein (the portal vein) that drain blood from the pet's stomach wall, intestine, pancreas and spleen (the splanchnic viscera) and sends it to the liver – not to the major vein in your pet’s abdomen (its vena cava). The portal vein eventually routs the blood through the liver and to the vena cava. But only after the liver has processed the nutrients and detoxified the chemicals that are in it.
Your pet’s liver needs plentiful blood flow to develop normally. The rest of your pet’s body relies on arteries to supply that blood. But in the special case of the liver, although some of that blood arrives through arteries, much of it (~80%) arrived through the portal vein. When portal blood does not get there, the liver remains small (hypoplastic) and shriveled. If shunts develop after birth, the liver shrinks (atrophies). (ref)
Congenital shunts are the most common type veterinarians see. Most often, they short circuit the portal vein system somewhere outside of the liver but, as I mentioned, occasionally they are located with the liver itself. Most commonly, there is only one. But occasionally more than one exist in the same dog or cat. Owners of pets with CPSS usually notice that their dog or cat is not growing or behaving normally before the pet reaches a year of age. But a few dogs (and cats) are presented much later in life – often brought in because they have begun to show personality changes. Those changes could be confused with dog or cat “Alzheimer’s” disease (aka canine cognitive dysfunction syndrome or CCDS)
Veterinarians see these shunts most commonly in the toy dog breeds and purebred cats (Shih tzus, West Highlands, Maltese, Yorkies, Persian and Himalayan cats). There is even evidence that specific breeds of dogs have tendencies to breed-specific types of shunts. (ref)
When the shunt is located within the liver itself (intrahepatic shunt) it is more likely to be in a large purebred dog.
When a puppy or kitten is still in the womb, it relies on its mother’s liver to cleanse its blood just as it relies on its mother’s lungs to provide it oxygen. During that fetal period, its blood circulates by a different rout. Natural, normal, shunts short circuit the baby’s lungs (the Ductus arteriosus and Ductus venosus) and its foramen ovale, a hole in the heart wall, shunts blood from the right side of its heart to the left side. There are those that believe that liver shunts at that early age are also normal and that it is only their failure to close at birth as the others do that causes the problem.
When normal blood flow through your pet’s portal vein is restricted by liver disease or widespread inflammation from many causes, the pressure builds up (= portal hypertension). That increased blood pressure in the portal vein is thought to be the reasons shunts form that were not present at birth. These are generally multiple small shunts located within the liver itself. Colangiohepatitis/triad disease is thought to be an underlying cause of such chronic inflammation in cats. In some feline cases, the liver problems were apparently birth defects they were born with, but the shunts formed later after birth due to increased portal vein pressure. (ref)
Unfortunately, as I write this in 2015, veterinarians have no way to fix these acquired shunt problem with surgery. The best they can offer you is to attempt to locate and lessen the underlying causes of inflammation and to place the pets on medications (eg lactulose and antibiotics, etc. ) that might decrease the toxins entering your pets circulation. Special diets can be helpful here too.
Many more publication deal with these type of shunts in dogs than cats. But you can view one specifically on cats here.
These are all locations within your pet’s abdomen. They start at various locations but all end up emptying into the pet’s main abdominal vein, the posterior vena cava (or occasionally into the pet’s azygos or phrenic veins which are alternative routs for blood to get back to the heart). When they begin at the spleen and end at the vena cava, they are called spleno-caval shunts. When they begin at the spleen and end at the azygos vein, they are called spleno-azygos, going to the phrenic vein, spleno-phrenic. When they begin at the stomach, gastro-caval or gastro-azygos etc. etc. (ref1, rptref2)
In cats, shunts beginning at the stomach are the most common.
The azygos vein and phrenic veins are a smaller diameter than the pet's vena cava. That is though to allow for less blood to bypass the pet’s liver. So symptoms of those type of shunts are often less severe than those of shunts that end in the much bigger vena cava. (ref1, ref2)
All dog and cat fetuses have that large shunt I mentioned earlier, their ductus venosus, that carries blood quickly around the baby’s liver to the heart. Since its mother's liver does the work of filtering out toxins, storing sugar, and producing protein for her unborn babies, the fetal baby’s own liver function is not required. This ductus venosus shunt is supposed to close down shortly before or shortly after birth as the baby's liver begins to work on its own. In some youngsters, the shunt doesn't close down; then it is then called a "Patent (open) Ductus Venosus", or an intrahepatic shunt. These intrahepatic shunts are much less common than extrahepatic shunts. They generally occur in larger breeds such as Irish wolfhounds, and Old English Sheepdogs (in which patent ductus venosus is thought to be a common genetic defect) Australian cattle dogs and golden retrievers. An occasional cat will be born with this type of shunt as well.
You can read my more detailed description of this problem here
When blood circulates abnormal through your pet’s liver in the tiny blood chambers (sinusoids) that saturate it, liver cells again loose their ability to cleanse that blood. This inherited problem is most common in toy breeds of dogs (eg Maltese, Yorkies, Cairn terriers, etc.). Veterinarians believe that this problem is considerably more common than the larger shunts (portosystemic) that I discussed up to now. Luckily, this malformation causes less damage than the large shunts. Most of these dogs lead a relatively normal life, the only sign being an increase in their blood bile acid level. Problems can arise, however when dogs with this condition are given drugs that rely on the liver to be cleared from the body. Many suspect that breeding for “tea cup” size cuties increases the risk of breeding for this disease as well.
When this genetic problem causes owner concern, it is generally due to the pet being smaller than its littermates or a finicky eater. Dogs carrying this genetic trait should never be bred. If it has occurred in your breeding stock, it is wise to do a bile acid screen on all the puppies you produce.
Vets often suspect a MVD problem when they find that the pet’s serum bile acid level is abnormally high but other blood test values that would suggest a portohepatic shunt are normal (ie normal red blood cell size, normal BUN and creatinine, normal protein C, normal cholesterol, normal ammonia). (rptref1, ref2)
On rare occasion, dogs will have both MVD and a portohepatic shunt.
Measuring your pet’s blood ammonia level is an unreliable way to diagnose this disease. Measuring its bile acid level is a considerably better way.
When MVD pets have no other health issues, there is no need for them to receive a special diet or other medications.
If you are still worried, have Cornell’s veterinary lab run the protein C test (not c-reactive protein). If its normal, stop worrying.
Hepatic encephalopathy, a problem that affects your pet’s brain, is a condition that is often the end result of liver shunts (but any disease that decreases the ability of your pet’s liver to do its work can cause hepatic encephalopathy as well). I devoted an entire article to that problem. You can read it here.
The symptoms owners report in their pets with PSS are often quite vague and they are extremely variable. These symptoms tend to come and go. The most common is a dog or cat that either started out smaller than the rest of its litter or failed to grow at a normal rate after birth.
Many are picky eaters. Some have intermittent bouts of diarrhea (but in a few, constipation is an issue) and vomiting. Many were initially diagnosed as having inflammatory bowl issues (which they could have as well). Some drink and urinate more than normal and many have more infections and reasons to visit the vet than normal. They many have been put on antibiotics many times in the past and often improved on those antibiotics - even though the underlying shunt problem was missed (because those antibiotics decrease the number of bacteria creating toxic products in their intestine that their weakened liver was responsible to handle). Your pet’s liver is also responsible for storing glycogen, a compound necessary to maintain its blood sugar level. That is why dogs with PSS are more likely to have been diagnosed with hypoglycemia (low blood sugar) than other dogs.
So you can see how the problem can be easily missed or mistakenly attributed to something else.
But bells start to ring in your vet's head when the dog or cat’s mental attitude changes. It might develop seizures or becomes aggressive for no obvious reason. Some just appear spacey, others just too quite. Other dogs and cats are disorientation or demented (walking in circles, getting stuck in corners, etc).
The bells ring particularly loud when owners have noticed that those problems are worse shortly after their pet eats. Those are all signs of hepatic encephalopathy that you can read more about through the link I suggested to you earlier.
The bells also ring when urinary tract stones are found to contain ammonium biurate, a product of the excess ammonia in their system. It was often UTI signs you reported or an abnormal urinalysis that got your vet looking for stones in the first place.
They ring as well when a pet is slow to come out of anesthesia or tranquilization. Its liver isn't up to detoxifying those compounds as well as it should.
Common signs in cats are excessive drooling that is not caused by tooth and gum disease and being runts of the litter. Many are also anemic.
The key diagnostic test for this group of diseases is a measurement of your pet’s blood bile acid level. Not all pets with high bile acid levels have portosystemic shunts or MVD. But almost all pets with portosystemic shunts or MVD have higher than normal blood bile acid levels.
When the bile acid results are not dramatically high, a sample taken before a meal and one a few hours after the meal may help. The level often rises after a meal in PSS pets. But please remember, a variety of liver problems - not just PSS – can cause elevated bile acid readings.
Theoretically, dogs and cats with portosystemic shunts should have higher-than-normal blood ammonia levels too. But an accurate ammonia assay is quite a difficult test to run. Some centers still do it; but the methods and interpretation of the results differ from institution to institution. (ref) Here in Texas, A&M performs a single fasting ammonia level assay as part of their PSS work up. In Australia, some challenge the pet with an oral or rectal dose of ammonium chloride to see if their liver can detoxify it (that test is not without risk). (rptref)
At Utrecht, blood ammonia assays are still an important part of PSS diagnosis and their follow up to judge the success of the surgery. (ref)
But others question if blood ammonia levels correlate directly to the symptoms the pet is experiencing. (ref)
The other blood test results that are often abnormal are not specific for this disease. That is, a lot of other health problems could also be the cause, but here they are :
1) Many of these pets are anemic and the red blood cells they do have are often, but not always, smaller than normal (microcytic anemia). It occurs because these pets become deficient in iron.
2) Many of these pets have lower than normal blood BUN and creatinine levels. Many also have lower than normal blood albumin, glucose and cholesterol levels because producing those compounds was one of their liver’s responsibilities.
3) Finding that a urinary tract stone (calculus) is composed of ammonium biurate makes a PSS diagnosis quite likely. They are most often found in older pets that have dealt with PSS for a long time. (ref1, ref2) Those pets may not have even been suspected of having PSS; but finding these distinctive, spiked crystals should be enough to consider it now.
4) Some of these affected dogs and cats have elevated liver enzyme tests (ALT, Alk Phos) or slowed blood clotting tests – all of which point to a liver problem. But just as many pets with PSS do not show this.
5) When the diagnosis is still in doubt, you can have the veterinary laboratory at Cornell University run a protein-C test to help with the diagnosis. But, ultimately, you will need to rely on the radiology (imaging) department of a major veterinary institution to make the diagnosis certain.
Besides, your veterinary surgeon needs to know more than that your dog or cat has shunts. The veterinary surgeon needs to know exactly where the shunt(s) are located before surgery. Only imaging techniques can do that.
Ordinary x-rays (radiographs) won't do. They do not show hepatic shunts. But they may show that your pet’s liver is smaller than it should be. That, plus symptoms, might even prompt a liver biopsy. But biopsies will not confirm or rule out PSS either. If the pet has developed kidney or bladder stones due to PSS, those might show up on the radiographs too. But one stone looks too much like another on x-rays and many biurate stones are too porous (radiolucent) to show up on x-rays (although they might show up on ultrasound imaging if they are large enough).
Some veterinary institutions find CAT scans, enhanced with an injection of contrast material (“dyes”) that highlight the blood vessel image, a preferable way to locate portosystemic shunts. (ref) Like all forms of imaging, the operator's comfort and perceptiveness - learned painstakingly over time - influence success just as much or more than the procedure used. You can read about CAT scans as they are used to confirm and locate portosystemic shunts here: 1rpt, 2rpt, 3rpt, 4, 5rpt
This technique follows the movement of a radioactive material (radioisotopes), placed in your pet’s colon, through the colon wall, into the pet's blood stream, then through its liver and into its general circulation. That is the rout that 85% of the material goes in normal dogs and cats. When less of it goes through the liver but still ends up in the general circulation (visualized in the heart), we know that there must be an alternate rout (a shunt) through which it got there. However, we do not know where the shunt is and we do not know how many there are. Because the pet is radioactive for a short period after the test, they spend the night in the animal hospital. But the procedure is painless and no sedation is required. You can read about the procedure in detail here.
The standard scintigraphy procedure yields a 2-dimensional (flat) image. If the apparatus gives a 3-D image, a PET scanner was used. If the radioactive material was injected directly into the spleen, the image produced is called a nuclear portogram.
All the scintillation methods have the advantage of telling the operator how much blood is actually going through the pet’s liver normally and how much isn’t. If not much blood is abnormally bypassing your pet's liver, perhaps surgery is unnecessary. If a lot of blood is bypassing the liver, it might not be advisable to close the shunt completely in a single operation and a method that slowly squeezes the shunt closed might be best (cellophane banding or ameroid constrictor that I write about later).
This technique uses a series of ordinary x-rays taken after a iodine-containing dye has been injected into your pet’s portal vein system. This dye shows up on x-rays and, by tracing its flow, you can see how blood is moving around in the body. The problem is, one generally has to open the pet surgically to inject this dye into the portal vein. However some radiologists have had success injecting the dye into the pet’s spleen through the body wall using ultrasound to guide them (the University of Tennessee apparently gets the dye to the correct location through a long catheter placed in the dog or cat’s neck). Like scintigraphy and CAT scans, one can get a rough estimate of the size of the shunt and the advisability of closing it suddenly, by the amount of the dye that goes to the liver versus the amount that goes around it through the shunt(s). As I said before, big shunts are best closed slowly. Others make this decision during the surgery by monitoring pressure in the pet's portal vein. You do not want that pressure to rise too high. High pressure means that the pet’s liver is not capable of suddenly handling the large amount of blood it has suddenly been provided. See some excellent photos of those images here and here.
MRIs can also be used to locate shunts in dogs and cats. It is not commonly the method of choice because of the time involved in performing the procedure and its expense. Read about its use in detecting shunts here and here.
This is the least effective way to confirm that your pet has a portosystemic shunt and to confirm its location. But many pet owners just don’t have the financial means to afford the better options. Others may live far from institutions that have the capability of performing anything else. It is quite easy to miss seeing a shunt during surgery. The only advantage, other than cost, is that the veterinarian can examine all your pets’ abdominal organs and, perhaps, find other things that need correcting.
Yes, In many cases a veterinarian can.
But this is not something you would want a general practice veterinarian to attempt. You want this performed at a large veterinary center by a board certified veterinary surgeon who has done many of the same surgeries in the past. One backed up by a team of seasoned technicians and assisting veterinary internists.
To get around the problem of suddenly overloading your pet’s liver with a new blood supply, veterinarians can do four things: The first, a series of operations, each tightening the suture wrapped around the shunt a little bit more. They can attach a device that measures blood pressure in the portal vein and tighten the suture (often silk) just enough so that the pressure does not rise too high. Or, they can apply a band around the shunt that slowly tightens by itself over time. The first of those used was a band of cellophane tape. Cellophane implants are somewhat irritating to the body. As the pet's immune system destroys it, scarring occurs around it. That scarring eventually squeezes the shunt shut – but slowly enough for the pet’s liver to adjust to the new, increased, blood supply. The second automatic constrictor is the ameroid ring (ameroid constrictor).
That is a titanium or stainless steel ring lined with milk casein protein. The casein slowly swells and squeezes the shunt closed over several weeks. Neither are without their detractors (ref) , but they are replacing the older techniques. (ref1, ref2, rptref)
When the shunt has been determined to be inside of your pet’s liver, surgical treatment much more difficult. These are the shunts that are most common in large dog breeds. Some have been successfully closed with ameroid constrictor rings too – but it is a complicated and difficult surgery. More recently, veterinarians have been closing them successfully using intravenous wire coils that block blood from passing through the shunt. You can view a dramatization of that procedure (as done in humans for other purposes) here. Usually, this apparatus is introduced through a small cut in your dog or cat’s neck (jugular vein) or thigh (femoral vein).
I do not know of any surgery that can correct shunts that your pet was not born with. That is, shunts that it acquired later due to some disease of the liver or other health issue. Those are the acquired hepatic shunts. Some shunts are so large and have deprived the liver of proper blood flow for so long that it would be unadvisable to shut them off completely. But those pets usually improve significantly even if the shunt is only partially closed. Some surgeons suggest a first surgery to constrict the shunt partially and a second or even third to constrict it even more or completely shut it off. (ref1, ref2)
These are the current 2015 costs of these procedures at some of the institutions whose surgeons authored the studies I reference in this article. In most cases, it was the author who furnished me with the information:
At the Veterinary School, University Of California, Davis, the workup required to confirm or rule out a portohepatic shunt often runs about $1,000. When discovered, closure of a typical single shunt often costs $4,600 – $6,800 in addition. The precise cost to operate on your pet can not be determined before hand because it is impossible to anticipate all the testing that might be required or unforeseen obstacles that might be encountered by the surgeon during surgery.
When an operable shunt is discovered to be within your pet's liver itself (intrahepatic shunt), they can attempt to close it with a metal coils advanced into the shunt through a catheter. I put a link to that procedure earlier. ( ReptLink) That procedure often costs $8,600-$12,000 at Davis.
At Michigan State College of Veterinary medicine, the workup required to confirm or rule out a portohepatic shunt and visualize it prior to surgery often runs about $1,650. Typical surgery costs to correct a shunt are $2,500 – more if urinary tract stones (calculi) need to be removed, a bit less if not. $3,500 is not an unusual bill for the total service.
At the Veterinary College, Utrecht, Netherlands, presurgical diagnostic work up for portosystemic shunts often cost $376 (350 €). That is the cost when bile acids, ammonia levels and ultrasound exam are sufficient to be reasonably certain of the diagnosis. If a CAT scan proves necessary, the cost is an additional $752 (= 700 € in Nov.2015). When they feel the surgery can be successfully performed, their cost to do it is about $2,148-$2,686 (2,000-2,500 €).Are There Less Invasive Forms Of Surgery That I Might Consider ? Minimally Invasive Techniques
Several of the surgical procedure I previously mentioned can be accomplished either by threading coils or shunt-blocking agents (vascular plugs) through a large vein of the dog’s neck (jugular vein) or its leg (femoral vein). Bands that constrict and close shunts can also be placed within the body through small incisions and then guided into correct placement with a laparoscope.
Procedures that thread these apparatus up veins are usually done by interventional radiologists within the school’s radiology department. Because those veterinarians can measure blood flow in real time, they may also have the option to place metal frameworks (stents) , similar to those used in the heart, to enlarge blood vessels that are too narrow to accept the additional blood flow when the shunt is closed. These advanced techniques are quite new to veterinary medicine. One might still consider them experimental. Pioneers in these procedures are The Animal Medical Center in New York City and the Veterinary School at Purdue University. (ref1, ref2)
The success rate for this complicated procedure is good. However success is highly dependent on the individual skill of the surgeon, the backup support team and the imaging machines at their disposal. Many facilities claim an 85% success rate in dogs in correcting portosystemic shunts. The success rates claimed in cats are lower (~ 66% in one study ) (ref) and 55% in another (ref)
I suppose I need to tell you something that is not widely discussed. Surgeons tend to overstate their success rates in all fields of medicine. It is not a form of deception, it is just our human nature to want to succeed and maintain an optimistic attitude. Studies in human medicine found overstatement of success as high as 35%. (ref1, ref2) In veterinary medicine a similar bias toward claims of surgical success can also occur (ref1, ref2)
So in many cases, success might be better defined as an improvement in your pet’s condition - not necessarily a complete elimination of the problem. Not all shunts can be completely blocked off safely. (ref) Some suggest that in only about 68% of the cases is that possible. (rptref)
Many pets with portosystemic shunts arrive at an animal hospital only after the shunt(s) are producing pronounced symptoms. Those pets need to be stabilized with appropriate diets and medication before surgery is attempted. Low protein diets can help accomplish that. So can lactulose and antibiotics. Some facilities, such as Texas A&M, make the decision on when it is safe to operate based on the pet’s blood ammonia level. At Bristol, UK dogs typically receive a 4-wk course of oral lactulose, ampicillin, and Royal Canin Hepatic™ dog food. (ref) Pre-op treatment for PSS are quite similar around the world. (rptref) Other commonly used antibiotic options are neomycin and metronidazole.
Many of these surgical patients are immature or thin animals that have a hard time maintaining their body temperature while recovering from anesthesia. The surgical nurses will tend to that. Blood sugar levels will be monitored and appropriate sugar solutions given if required. Dogs with abnormal liver function are prone to hypoglycemia. That is why it is important that these pets resume eating as soon after surgery as possible (many do not fast them until just before surgery for the same reason). A healthy liver is also important for normal blood clotting. So the staff will be on the lookout for abnormal post-surgical bleeding as well.
The nurses will also be on the alert for seizures – they are not that uncommon in pets whose shunts have been closed. Vets do not know why. (ref) Another serious post-surgical complication is abnormally high a blood pressure in the portal vein (portal hypertension) subsequent to shunt closing. Some signs associated with that are bloating (fluid leakage into the abdomen=ascites), low blood pressure in the rest of the body, pale gums, and intestinal bleeding (bloody diarrhea). These usually resolve quickly with supportive care. But in a few cases, the shunt must be loosened sufficiently to stop these side effects.
When the surgery was successful, it should not be too long before your surgeon can confirm (using ultrasound) that the pet’s liver is increasing in volume toward a healthy size. (ref)
Generally, the same lower-protein diets, lactulose and antibiotics given before the surgery are continued after the surgery for a number of weeks. There will be pets that have gone through this surgery that will do best when those hepatic diets, as well as lactulose, are fed indefinitely.
Periodic bile acid measurements are also a great way to gauge the speed of your pet’s recovery. A return to normal blood albumin level and improvement in any other presurgical blood test abnormalities are also excellent signs. Expect that to take 3-6 months.
Cats seem to have more post-surgical complications than dogs. Recovery is also a bit more challenging for older dogs than for those less than a year of age when the surgery is performed. A small portion of the pets will develop new shunts when their livers can not bear the burden of the increased blood supply it now receives.
The presurgical imaging techniques I mentioned earlier are quite important for anticipating post-surgical complications. Dogs and cats with multiple shunts, large shunts, stunted portal veins, intrahepatic shunts, and extremely small liver-to-body mass ratios all need careful watching in the weeks following surgery. As I indicated before, complications are more frequent in cats than dogs - although some surgeons report that this is not so. (rptref) Perhaps it is greater familiarity with performing this procedure in cats that accounts for the difference.
Every published study suggests that the quality of life of dogs and cats that have shunt problem corrected surgically is likely to be better than the quality of life of pets that do not undergo the surgery. (ref1, ref2)
However, those studies may be skewed due to the tendency to study dogs and cats that are already showing severe signs. They are also probably somewhat biased because veterinary centers promoting the surgery generate these articles. No two shunts are exactly alike. When the shunt(s) are small or when the body has successfully adapted to them, some pets can live long lives when managed medically and nutritionally.
A key goal in medical management is to decrease the amount of ammonia that enters your pet’s body through its intestine. That can be accomplished by not overloading the pet with dietary protein (the source of much ammonia), by using antibiotics to reduce the amount of ammonia produced by bacteria in the pet’s gut, by giving the pet products that bind to ammonia and allow it to be expelled in the stool (ie lactulose) , and, perhaps by altering the dogs feeding routine (smaller, more frequent feedings). Some say that egg, dairy or soy protein is less likely to cause high ammonia levels. Others, that increased dietary fiber is helpful. I do not believe that any of that has been proven, but there is no harm in trying. (ref1, ref2) .. I certainly would. I personally prefer it when pet owners make their diets from scratch at home. link But I have no proof that that is preferable to store-bought prescription diets either. Remember, not enough protein in your pets diet to meet its body’s requirements is just as bad or worse than too much protein.
Some, suggest a zinc supplement. Too much zinc is also toxic. Periodic blood bile acid assays and blood albumin levels included in a general blood analysis are the best way to adjust and modify the dietary program as time goes by. If surgery is not an option, you will find some other possible treatment options in my hepatic encephalopathy article.
I have no experience using this medication in pets ; and I know of no veterinarian who has. But it showed positive results in some experiments run in 2016. (ref) Go to my hepatic encephalopathy article and read more about the medication there if you wish. I would appreciate any feed back on that or other bile acid sequestrants that you might provide.
Any medications that require the pet's liver for detoxification or elimination should be avoided.