LIVER SHUNTS IN DOGS

Article 1
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Letter in from Viewer

 

Firstly there can be a lot of variation of clinical signs depending on the severity of the condition, which could depend on how much blood flow is diverted past the Liver. Some of the clinical signs of portosystemic shunts that might be recognised in a puppy or young adult that have been reported could include:
· Failure for a puppy to grow
· Poor weight gain
· Depression, Listlessness, apathy.
· Weakness
· Seizures
· Salivation, drooling
· Vomiting
· Poor appetite
· Balance problems
· Bladder stones
· Blindness

Portosystemic Shunts
Portosystemic shunts are abnormal vascular connections between the hepatic portal vein [the blood vessel that connects the gastrointestinal tract with the liver] and systemic circulation. Such anomalies cause blood in the gastrointestinal tract to be diverted past the liver, there by limiting the liver's vital functions in metabolism and detoxification of compounds and the body's defences against intestinally derived pathogens. This effectively exposes the body to toxic by products of digestion [toxins and bacteria] and mimics the effects of liver failure.

Portosystemic shunts can be present at birth [i.e. congenital] or acquired as the result of another disease process later on. Congenital shunts are more common, representing approx. 75% of all canine cases, and generally result from anatomic abnormalities of the portal vasculature or fetal vessels. One or occasionally two vessels are involved, and the shunts are classified according to their location as either outside of [extrahepatic] or within [intrahepatic] the liver.

Congenital Shunts
Congenital shunts occur more commonly in pure-bred dogs than in mixed breeds; miniature Schnauzers, Yorkshire Terriers, and Irish Wolfhounds appear to be at increased risk. The prevalence of portosystemic shunts in certain breeds suggests an inherited predisposition. This has only been proven in Irish Wolfhounds, where a number of previously unknown genes appear to be involved.

Extrahepatic shunts are most common, accounting for 61% to 94% of congenital shunts, and are typically seen in small breeds of dogs, such as the Miniature Schnauzer and Yorkshire Terrier. Intrahepatic shunts represent between 6% and 40% of congenital shunts and are more common in large and giant breeds such as Irish Wolfhounds and Golden Retrievers. The majority of intrahepatic shunts are as a result of the embryonic connection between the umbilical vein and the caudal vena cava remaining open; in most dogs this connection closes 3 days after birth but, for unknown reasons, remains open in dogs with intrahepatic congenital shunts.

Hepatic microvascular dysplasia is an unusual form of intrahepatic portosystemic shunting in which no gross vascular abnormality can be identified. This rare condition is associated with somewhat milder clinical signs and appears to be the consequence of a developmental abnormality; it has a higher prevalence in Cairn Terriers, suggesting a hereditary basis.

ACQUIRED SHUNTS
Acquired shunts arise secondary to diffuse liver disease where excessive and sustained pressure at some point within the portal vein causes embryonic, non-functional vascular communications to open. These are generally seen in older dogs with cirrhosis, hepatitis or neoplasia of the liver. In contrast to congenital portosystemic shunts, a number of vessels are usually affected.

What are the signs of Portosystemic shunts?
The clinical signs exhibited by the dogs reflects the failure of the liver to eliminate various toxic matter, drugs and bacteria absorbed from the gastrointestinal tract. Problems increase dramatically after eating. A large percentage may show an intolerance to anaesthetics or tranquillisers, and may show increased recovery times following their use. Other clinical signs arise from the liver being deprived of portal blood flow, which is essential for the normal development of the liver; as a result the liver is underdeveloped and its metabolic, storage and excretory functions are further impaired…

Signalment & History.
Dogs with congenital portosystemic shunts are typically pure bred dogs of less than one year old. Generally the lower the fraction of shunting, the milder and later in onset the clinical signs. Nevertheless the affected are often in poor body condition and of small body stature, especially when compared to their litter mates. Owners may complain that the animal fails to grow and that skin and coat condition are poor.

Gastrointestinal Signs.
Vomiting and Diarrhoea are present in about two thirds of cases. Evidence of lower urinary tract disease is present in approximately one-half of cases and is usually due to ammonium urate crystals, which are formed because of excessive excretion of ammonia and uric acid in urine. Some dogs, particularly those that develop signs later in life, have polydipsia and polyuria ascites, although the latter is generally seen only in dogs with acquired shunts.
Management.
Surgery is possible in some cases but can carry a very high risk factor, and a high cost. Dietery manipulations for its control are designed to limit neurotoxin production, which occurs principally in the large intestine. The major toxins are all derived from nitrogenous materials [protein and urea] and are synthesised by bacteria found within the large intestine. The production of these toxins is reduced by limiting the amount of protein fed and ensuring that the dietary protein is high quality and highly digestible. These steps reduce the amount of protein that reaches the large intestine; further reductions can be attained by feeding smaller meals more frquently to maximise the digestive capacity of the small intestine. Specific diets are commercially produced tp provide a balanced protein-calorie intake including dietary fibre which assists in limiting toxin production. Lactulose, a soluble fibre, is often used as a supplement and can readily be purchased. Supplementation with zinc salts also improves the detoxification of ammonia and the control of hepatic encephalopathy. Antibiotics are used in most cases to reduce the bacteria within the large intestine that are responsible for the production of neurotoxins. Oral administered neomycin is commonly used for this purpose and is often used in combination with lactulose in both short and long term medical management of portosystemic shunts……..

[This material used with kind permission of Jay Bianco,
Author & Creator of the "Maltese only" web site. Copyright 1999]

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

Letter sent in from viewer November 2010

Hi, I lost my rough collie on 8th November last week. He was on steroids and like what I have just read it sounds very much like Bobby. I have enclosed a photo of him taken June 2009 when he was well. I live in the UK and just can't praise vets, companion care enough, for all their help, love and support with Bobby...

The disease finally got worse and the past few weeks we were in and out of the vets where they confirmed he had a liver problem as his bile and liver enzyme readings were through the roof..he was hospitalised from 1 to 5th November came home on the 5 to 7th by which time the disease had progressed further and so we took him back to the vets..hoping for a miracle. He was on a drip but we were loosing with Bobby as his abdomen was swollen and he was in a lot of pain..by last Monday morning he had deteriorated even more and we had to make the very heart wrenching decision of having him pts...not an easy decision..a very upsetting one.

The disease progressed very fast and his Liver enlarged over three times - he was on prednisone to help him but in the end that also affected my boys Liver. Another symptom of this disease is that they fail to use their back legs, it affects their mobility and eventually in Bobby;s case, his appetite. There was nothing we could do but just sit and watch helplessly as our best buddy was lost to this awful debhilitating illness!

Hope my experience helps others
Alison Stavert-Barr