To start this article, below is a section of a report sent to me from Burns Dog Food, because bitches we bred from completely different lines have died of this condition. We have found that by talking about this condition there have been quite a few other cases.

"It is likely that most dogs with this have no readily apparent clinical signs associated with the micro vascular dysplasia and are diagnosed when bile acid response testing is done to rule out liver disease for some reason. Unfortunately, some dogs with this condition do have clinical signs, which can include seizures or other central nervous system disorders, gastrointestinal problems or urinary tract disease associated with ammonium biurate crystals in the urinary tract, which form due to liver problems.

A reduced protein, low fat diet containing the minimum requirements of all macro and trace elements is recommended for the nutritional management of liver function/chronic liver problems. Burns adult maintenance foods; brown rice with either chicken, fish, lamb, venison or duck are low protein; low fat diets and highly digestible. As Burns is highly digestible the feeding amounts are low therefore the liver will not be overworked.

This all started when a bitch we had bred had been rehomed and was spayed. She was not spayed by our vet, and should not have been spayed, as her pre operation test showed she had abnormal liver enzymes, but the vet ahead anyway. She did not recover well after the operation and stopped eating and was vomiting bile. Her new owners were unhappy with their vet and she was transferred back to our vet for further treatment. Unfortunately she went down hill and eventually had to be put to sleep.

About a year later, her daughter was off her food and had a temperature. She was rushed to the vets and immediately kept on a drip. Again her condition deteriorated. She too had tests done, which showed raised enzyme levels, and her liver was small. Eventually she became jaundiced and to save any further suffering she was put to sleep. Our vet was concerned that her symptoms were so similar to the mother that she took some liver samples and sent them away. The report confirmed that the bitch had Hepatic Micro Vascular Dysplasia.

I had rehomed a bitch of completely different pedigree. She had always been fit and well. After about 2 years with new owner decided to have her spayed, by which time she would have been 4/5 years old. The bitch took a long time to recover. A few months later, she went off her food and became depressed. She was admitted to our vets again. Tests were done and her liver enzyme test results proved to be very high. The vet again kept her in for treatment but she would not eat, was sick and eventually died, as her liver just could not cope. Again samples of her liver were sent away and the lab confirmed Hepatic Micro Vascular Dysplasia.

Some might think that this was just bad luck but in 2005 HMD struck again in the Granddaughter of the bitch above. She had her second litter about 4 months previous and was still passing blood in her urine, so she was taken to our vet who confirmed this condition as Subinvolution of Placental Sites. This condition is not common or life threatening although could leave the bitch open to infection but it will disappear at the next season.

The bitch started to miss meals and she was quiet, but had no raised temperature. The owner took her straight back to the vets and liver enzyme tests were done. Results showed abnormally high levels. The vet decided to operate and take a liver sample, during the operation our vet also noticed that the liver was small in size. The results came back a week later stating that she too had HMD and was immediately put on antibiotics and fluids as she was not eating. This went on for a week with no sign of improvement and our vet decided she must be missing something, so she operated again. She found strange lesions on her internal organs and fat around the lungs, which was starting to decay. Her antibiotics were changed in case she was having a reaction to them and instead of oral antibiotics she was given injections daily, a couple of days later she seemed to pick up and went home. She is still not a well dog and the outcome is 50/50 but due to the vet whose knowledge and awareness of previous problems enabled her to start medication early to prevent the onset of jaundice, although the Vet thinks that there may have been early signs of jaundice, hence the lesions on the internal organs.

Most vets will diagnose this condition as Liver Shunts, as the symptoms are very similar, but the only way to confirm diagnosis of HMD is a liver biopsy. We have since found out that a young puppy of 12 weeks has got this condition but luckily has not been ill, and also another 2 possibly 3 bitches have died of this condition.

This article has been written to hopefully bring awareness of this terrible condition. Unless dogs receive quick veterinary attention, the outcome is unfortunately a sad one.

If enough information is found out about this condition, IT COULD be possible to have the Health Trust look into it but it would need the backing of the Rough/Smooth Collie Breed Club to put it forward to the Breed Council.

Our vet has got all the reports from these bitches and for us it seems proof enough that there is danger of this becoming more prevalent in our lovely breed. We CAN do something about this condition, just as we HAVE done for HD and CEA/PRA although it will take a long time, It would be wonderful if the Breed Council could get the Kennel Club to look into it for the good of our breed.

If you have a collie that is ill with possible Liver problems and it is appropriate, then get your vet to test for HMD,which can only be confirmed by a liver sample. An operation is needed to obtain such a sample.

We would ask anybody who has these kind s of problems or lost a collie to a "LIVER CONDITION" to le us know.

Email on pellismer@hotmail.com or collienet2000@aol.com or copy to both please.

First published Stabal Mail Bugle December 2005

A more detailed description of Liver Shunts can be obtained from www.malteseonly.com/shunt2.html

Follow up - Stabal Mail Bugle December 2006

I write to follow on from that first article. [SMB Dec 05] The bitch sick last year Purdy, has now died from HMD. She was only 4 years old, such a sad thing when any animal dies, but to lose one so young is a real tragedy.

Her year between the two sick periods was a good one, and had I bought her to shows no one would ever have known how sick she had been.

Her final stages resulted in her refusing to eat anything (after normally having a good appetite), and her liver function tests showed her liver to be gradually cirrhosing, she had severe jaundice, ascites (dropsy), which all resulted in complete liver failure.
This is now our fourth rough collie to die from this horrible condition. We also know of others.

I must point out that the animal is born with it, it is not contracted, or induced by drugs or inoculations, as was suggested to me when I rang a breed council member to ask for support to help bring this condition to the surface, so we as a whole breed can work together to try to save our lovely breed. The door, as usual, was closed in my face.

Unless we are prepared to open our eyes, get our heads out of the sand and listen, this already prevalent condition will have a severe affect on the future of our breed.

We still do know of one animal, not bred by us, that is still alive which has proof of having this condition, but is showing no signs of it what so ever, and it was only proven as a liver sample was taken during a routine operation at 14 weeks to repair an umbilical hernia.

This animal is now leading a normal life and could be anyone’s dog, as there is no clinical signs of the condition, so unless the animal is sick for another reason, cuts its foot, or has an anaesthetic for some reason which puts stress on the liver, etc then the liver could start to fail as it is abnormal.( the anaesthetic used for the first operation was one that goes through the kidneys, therefore not taxing the liver).

We could use some blood taken from this dog and use it for tests to help us find a blood marker for future screening.

We will then have to find an animal that does not have HMD, this will be very hard as the ONLY WAY to tell if HMD is present is by liver biopsy. There is no other test that can prove an animal has or does not have HMD. But by working off affected and unaffected blood we COULD find a blood marker that will help us to eradicate it.

I therefore ask the breed clubs and breed council to OPENLY TALK about this now serious problem and come up with a strategy to implement the necessary screening programme, and also ask breeders to talk about it, openly.

I cannot stress enough that an animal with HMD may not show any signs of the problem, therefore could
already be a champion or a top winner and may never show any signs, but will still pass it on to all its offspring, through ANYONE’S breeding programme.

So the sooner we get started on working on a screening programme, the sooner we can stop breeding from affected stock

Update 15th January 2007

Can anyone who has had a dog die of liver related problems please send their collies vetinerary file [with pet name]

to Trevor Turner MRCVS, FRSH, MCIArb, MAE. Mr Turner has offered to lok into this problem.

Trevor works for the KC and writes the column "A Vets View" in Our Dogs..

His email is jean.trevor@virgin.net

Fax 0208 841 7828.

An Article sent in by one of our readers which you may find interesting to read...[22/7/07]
HEPATIC MICROVASCULAR DYSPLASIA OR PORTAL ATRESIA

HEPATIC MICROVASCULAR DYSPLASIA OR PORTAL ATRESIAOverview of the conditionThe liver performs an incredible number of functions to maintain health of animals, including filtering out toxins, storing sugar, and making proteins. Most of the blood that is carried to the liver for these processes arrives via the portal vein, which drains the intestines, stomach, pancreas, and spleen. Within the liver, the portal vein branches into smaller and smaller vessels so that the blood can percolate throughout the tissues to each liver cell. When these microscopic vessels are abnormal on liver biopsy, the condition is called "hepatic microvascular dysplasia (HMD or MVD)" or "portal atresia". When the microscopic vessels within the liver are underdeveloped or absent, the liver becomes small ("atrophied") and the animal can no longer process toxins or make proteins necessary for growth and normal function.

Hepatic microvascular dysplasia (HMD) or portal atresia is a histologic diagnosis, meaning it only describes the biopsy findings. In fact, there are many conditions that can cause these findings, including congenital portosystemic shunts; however, when the diagnosis is made without evidence of a congenital shunt, then the dogs are often given the diagnosis of HMD as a specific disease.

Signs/Clinicalpresentation

Dogs with HMD can present with signs similar to dogs with congenital portosystemic shunts; however, many dogs have no clinical signs at all. Often affected dogs are 3 to 4 years old before they have clinical signs. Some affected dogs are smaller than normal, with poor muscle development. They may seem less intelligent or quieter because of the toxins that depress their brains. They may have a loss of appetite or occasional bouts of vomiting and diarrhea. Some dogs may have a greater risk of infections or develop bladders stones. Severely affected dogs may be wobbly or act drunk or blind and can even seizure. Rarely, dogs will develop fluid filled bellies from liver failure.

Risk Factors

Yorkshire terriers and Cairn terriers are most commonly affected, but the condition is also seen in many other small breeds, including Maltese, dachshund, miniature poodles, Shih tzu, Lhasa apso, cocker spaniel, and West Highland white terriers.

Diagnostic tests

In some dogs, basic biochemical tests are normal. Severely affected dogs may have low blood protein, albumin, glucose, and urea nitrogen levels because their livers are not making enough of these chemicals. Some dogs have increased liver enzymes. Urine is evaluated for evidence of infection and crystals; rarely, dogs with HMD will develop ammonium biurate crystals in the urine that look like spiky balls or starfish.Bile acids are measured after an overnight fast ("preprandial" or fasting) and then 2 hours after eating ("postprandial"). In dogs with HMD, one or both sets of bile acids are increased.
Bile acids can increase with any liver disease, so high bile acids are not specific to congenital portosystemic shunts or HMD.
A definitive diagnosis of HMD is made by proving that the dogs do not have any shunts but that they do have abnormal vessels on their liver biopsies. Dogs with HMD have normal portal blood flow on scintigraphies (nuclear scans of liver blood flow), portograms (x-ray studies of liver blood flow), and CT angiograms (Cat scans of liver blood flow), but they have abnormal microscopic portal blood vessels on liver biopsy. The liver biopsy is usually taken surgically through a belly incision or with a laparoscope so that enough liver tissue can be obtained to evaluate the blood vessels. Needle biopsy using ultrasound may not provide enough tissue to make the diagnosis

Differential diagnoses

HMD must be differentiated from congenital portosystemic shunts; unfortunately some dogs can have both diseases, and this cannot be determined before surgery (Figure 1). If a dog undergoes surgical closure of a congenital portosystemic shunt and its bile acids remain high 3-6 months after surgery, it is quite possible it also had congenital HMD. Dogs with HMD are usually older than dogs with shunts when they are diagnosed (2 to 5 years instead of less than one year), and often their blood work changes are less severe than dogs with shunts. They may even have normal fasting bile acids, but usually their postprandial bile acids are increased

.HMD must also be differentiated from other conditions that cause seizures (epilepsy, hydrocephalus, toxins, etc.) or liver disease (viral or bacterial infections, chronic active hepatitis).

Figure 1.

This Yorkshire terrier had surgery for a congenital portosystemic shunt, but her blood work never returned to normal and she continued to have poor muscle development and dry hair coat and bouts of weakness and confusion. She was eventually diagnosed with hepatic microvascular dysplasia.

Treatment Options

There is no surgical treatment for HMD. Dogs with the condition are managed medically, and treatment is based on the severity of the condition. In some dogs no treatment is needed. The mainstay of medical management is to reduce the amount of protein in the diet. Specific veterinary diets such as Hill's L/d have been formulated for dogs with liver disease. The protein is highly digestible (often milk based or soy) and is only mildly protein restricted. Diets for dogs with HMD should contain about 15-20% protein (roughly 2 g/kg per day of protein), 15-30% fat, and 30-50% highly digestible carbohydrates on a dry matter basis. They should also be high in zinc and Vitamin E and low in manganese. Most dogs with HMD do well on diet change alone.
Changing the type of bacteria that live in the intestines can also decrease toxin production and absorption. This can be accomplished by giving lactulose syrup or yogurt. Some veterinarians may prescribe antibiotics for a short time as well.
Nutriceuticals- compounds that are not considered "drugs"- can also improve liver function. Milk thistle ("silymarin") can help improve liver function and regeneration. Because the government does not regulate over-the-counter compounds, purchase of specially formulated veterinary supplements is recommended. Two veterinary companies that sell milk thistle include Nutrimax ("Marin") and RxVitamins ("Hepatosupport"). Veterinarians may also prescribe Denosyl (SAM-e) to improve liver function.

When to seek referral

Specialized tests that are used to diagnose HMD and rule out portosystemic shunts are often not available in general veterinary practices. Your veterinarian may consider referral for scintigraphy, portography, ultrasonography, or surgical or laparoscopic liver biopsies to rule out other liver diseases. Additionally, dogs that do not improve with dietary management (reduced protein in the diet), particularly dogs with seizures or vomiting and diarrhea, may have other conditions that are actually causing the clinical signs. These veterinarians should be seen by and ACVIM Veterinary Internist or Neurologist for further evaluation

.Prevention and prognosisHepatic microvascular dysplasia or portal atresia is a hereditary condition. Dogs with abnormal bile acids should not be bred, and dogs that come from parents with abnormal bile acids should also not be bred. Prognosis is good for most dogs with HMD. Most dogs are clinically normal with medical management and many have normal life spans. Dogs with gastrointestinal signs or partial or focal seizures, however, may show no improvement, possible because they have other diseases besides HMD. Occasionally dogs with HMD can progress to liver failure, and a few dogs will die within 4-6 months of diagnosis because of the severity of their liver disease.
Milk Thistle dosage: Dried herb: 15-20mg/pound once a day; concentrated or alcohol extract: 2-5 mg/pound every 8-12 hours. See manufacturer recommendations for veterinary-formulated supplements. —
Karen Tobias, DVM, MSDiplomate ACVSPosted 8/23/2006