posted 08-01-2003 09:11 AM         

What are the signs?

There can be a lot of variation of clinical signs depending of 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 recognized in a puppy or young adult Maltese that have been reported could include:

Failure for a puppy to grow
Poor weight gain
Depression, listlessness, apathy
Weakness
Seizures
Salvitation, drooling
Vomiting
Poor appetite
Balance problems
Bladder stones
Blindness
Problems increasing dramatically after eating has also been strongly supported as an indication of a portosystemic shunt. Not all Maltese with the shunt will show this meal associated behavioral change, but in 25% of those affected that do, the diagnosis could become clearer. A high percent of affected Maltese show an intolerance to anesthetics or tranquilizers, & will show increased recovery times following their use. Approximately 75% of those affected will show digestive system symptoms including poor appetite, ascites, vomiting, drooling, diarrhea, or occasionally deranged appetite (eating paper, etc.). Urinary system symptoms may include increased thirst and urination, & in a majority of porto-systemic shunt cases, there will be crystals or stones formed in the urinary tract. These crystals will be either uric acid or ammonium urate (ammonium biurate or thorn-apple crystals.). Most Maltese will be diagnosed with port-systemic shunts under one year of age, but some several years older have been diagnosed with the condition.
How is Liver Shunt diagnosed?

There are a number of possible abnormalities that might point towards a portosystemic shunt on:

Routine Labwork
Routine performed serum chemistries are fairly nonspecific toward confirming the diagnosis of porto-systemic shunts, but there may be a decreased total protein (primarily albumin), decreased blood glucose, decreased cholesterol, & decreased blood urea nitrogen (BUN). The uric acid levels may be elevated in a significant number of those Maltese affected.
Acid levels are extremely important in the diagnostic screening of symptomatic potential shunts. Fasting and a two hour post meal blood samples are evaluated for bile acid levels. In virtually all porto-systemic shunts there will be a significant rise in the bile acid levels over normal. The use of bile acids in screening clinically normal for liver shunts is not currently being advised due to the variation of normal bile acid levels in Maltese, and other breeds as well. Reports of recent vaccination with modified-live vaccines causing high serum bile acid levels in normal animals have not been confirmed as of this time.

Liver function testing with Bromosulfaphthalein (BSP) or ammonia tolerance testing are sensitive and reliable if performed correctly. These tests measure the liver's ability to excrete/detoxify known agents, and thus measure liver function accurately.

Radiography
Radiography is one of the most important methods of establishing a diagnosis of porto-systemic shunt, and is currently the only universally accepted method of confirming a shunt, short of major surgery. Injection of a radiopaque dye into the spleen (Splenoportograpy) will show the shunt on radiographs and allow accurate assessment for surgical correction. But this is a pretty invasive test making it a poor choice for "screening" purposes. Special dyes injected into the liver circulation that show up on X-rays can outline the problem pretty clearly. Most of the time. But this is a pretty invasive test making it a poor choice for "screening" purposes. There are a number of possible abnormalities that might point towards a portosystemic shunt on routine labwork, including low BUN (blood urea nitrogen), low albumin, mild anemia, increases in ALT (serum alanine aminotransferase) or ALKP (serum alkaline phosphatase). If these hints are present, it would be a good idea to test the serum bile acid levels prior to eating and after eating. If this test is supportive of poor liver function then it may be a good idea to consider ultrasonagraphy and dye contrast X-rays.

Radioisotope
This procedure requires expensive equipment and the diagnosis is based on the distribution of the radionuclide in the lung or heart compared to that in the liver. The placement of a radioisotope specific for the liver into the colon for absorption through the mucosa has been gaining favor because of its noninvasive diagnostic value. This procedure also does not identify the exact location of the shunt for surgical correction if required.

Ultrasound
Currently there is research using Color Doppler Ultrasound which could soon be the preferred screening and diagnostic tool. In the past, ultrasound was fairly unreliable for nonsurgical diagnosis of porto-systemic shunts.
How is it treated?

Surgery appears to be the only cure for portosystemic shunts at this time.

Is there a genetic predisposition toward Porto-Systemic shunts?

At the present time, according to the experts, yes, most definitely Hepatic Porto-Systemic shunts are a genetic disorder.

posted 08-01-2003 09:12 AM         

--------------------------------------------------------------------------------

Those who engage in the dog breeding game of genetic wheel of fortune are challenged to arm themselves with information that is complex as well as mysterious. When the idiosyncrasies of breeding dogs confront me, I attack with the fervor possessed only by Jurassic Park's flesh eating dinosaurs. In this way, I attempt to convert road blocks into stepping stones. I believe that knowledge is empowering, and I am accountable to share my knowledge with my peers. This dinosaur recently dined on a strict diet of books and articles regarding canine portal systemic shunt. Therefore, contained in this study with be a brief description of normal liver function, followed by a explanation of liver shunt disease, included will be a discussion of the cause, symptoms and treatments concerning dogs with portal systemic shunts (PSS).

According to Dr. Karen Tobias, a veterinary surgeon at Washington State University, in 1974 an increase of PSS was discovered at California Davis Veterinarian School. At that time it was questioned whether the frequency had increased or if knowledge for identifying the disorder had improved. The portal vein transports blood from the gastro-intestinal system to the liver where it is ''detoxified'' before re-entering the circulatory system "Normally ammonia that has been absorbed through the intestine is carried to the liver by portal circulation, were 81 to 87 percent is converted to urea" (301). "With PSS...ammonia is no longer adequately metabolized and is diverted to systemic circulation" (301). Stephen J. Ettinger (1989) reports, that "no...sex predisposition has been identified for animals with PSS (1499). There is a difference in the type of shunt that develops for large and small dogs. Large dogs tend to have shunts inside the liver (intrahepatic), while small dogs will have them outside (extrahepatic). Shunts develop as small side branches connecting the hepatic portal vein and major gesture-intestinal veins. Blood is divertedaround the liver without undergoing hepatic detoxification. Shunts involve a single large vessel or multiple small veins. The most common are outside of the liver and effect small breeds of dogs such as Yorkshire terrier, schnauzer, poodle, Maltese, Shih Tzu and dachshund" (299).

Maddison (1988) states, "The cause of the development of congenital shunt has not been determined, but the apparent breed predilections may suggest a genetic etiology" (248). Tobias (1993) states "The ductus venosus is the embryonic channel that carries oxygenated placental blood from the umbilical vein to the caudal vena cave" (298). The ductus venous should undergo functional closure within the first three days after birth. Ettinger (1989) believes, the shunt is most often a remnant of the fetal duct system that remains open instead of closing at birth. According to Ettinger, the severity of symptoms will vary according to the volume of blood that bypasses the liver, and clinical signs vary but all result in hepatic encephalopathy (disturbances of consciousness that may progress to deep coma). "In many cases the clinical signs have an episodic nature; they are present for a few hours to a day or two and the animal returns to normal" (1499). A large portion of cases are diagnosed before one year of age and many animals are referred to "chronic poor doers". Many are shunted, thin, depressed and have trouble gaining weight. Nearly all have some type of central nervous system signs that may be the best clue to identify the problem. Particularly bizarre behavioral signs or loss of intellectual function, unpredictable bouts of aggression, staggering, pacing, circling, head pressing, blindness, deafness, tremors, seizures and coma may be seen. Other signs include, pica (bizarre cravings for unnatural foods) and polyphagia (excessive eating). Both are considered distinctly characteristic for PSS. These symptoms are corroborated by Tobias (1993), who reports symptoms such as general poorgrowth rate, weight loss, anesthetic or tranquilizer intolerance, lethargy, depression, ataxia (reduced muscular coordination), behavioral change such as head pressing, circling and the development of a head tilt. According to Ettinger, "Hepatic encephalopathy has been recognized in animals with PSS. Clinical signs include depression, dementia, stupor and coma" (1499). The cause of hepatic encephalopathy is now known, but probably is a result of toxins effecting the brain. Gastro-intestinal abnormalities include: anorexia, vomiting, diarrhea, excess excretion of saliva, difficulty swallowing and excessive ingestion of food may be seen. It appears that as high as 52 percent of dogs with liver-shunt problems will have polydipsia (excessive drinking of water) and plyulia (excessive urination). Ettinger reports, "Recurrent urinary calculi [crystals] is another presenting complaint" (1500). "Normal hepatic function is essential for converting ammonia to urea" and 'a decrease in detoxification and uric acid metabolism result[s] in increased excretion of ammonia and uric acid, with eventual discharge of ammonium biurate crystalluria." Tobias reports, that ammonium crystals are seen in as much as 74 percent of reported cases. A routine urine sediment examination will reveal the crystals and the presence of the crystals is specifically distinctive or characteristic of the disease. These crystals are different form normal urinary crystals which are square or rectangular in shape (Tobias 1994). According to Tobias (1993), "Ammonium biurate crystals have a thornapple shape and golden color" and "Any breed except in Dalmatians ammonium biurate crystalluria is suggestive of PSS'' (300). "In one study 50 percent of affected males were cryptorchid'' (298) indicating that other deformities coexist along with the liver-shunt (298)

It has been suggested that type of shunt may influence the age of onset and severity of clinical signs. "It could be speculated that prior to onset of clinical signs, the majority of portal blood passed through the liver rather than the shunt. With time there may have been an increase in intrahepatic resistance which causes a higher proportion of blood to shunt to the systemic circulation resulting in [late life] clinical signs..." (Laflamme, 1988 136). VanGundy (1988) substantiates this theory by reporting the sufficient blood flow though the portal system may maintain a degree of hepatic function for the first years of life. Perhaps a secondary mild insult [to the liver] resulted in loss of function.

Tobias (1993) reports that while history, physical examination and routine laboratory tests may be helpful in diagnosing PSS, liver function tests such as the plasma clearance of certain dyes (BSP), the ammonia tolerance test (ATT) and evaluation of serum bile acid concentrations are more reliable for identifying liver dysfunction associated with liver shunt. "Angiography provides a definitive diagnosis of PSS and is helpful in determining shunt extent and locations" (302). "Urinalysis abnormalities include low specific gravity and ammonium biurate [crystals]" (303). According to Ettinger (1989), an association between the onset of symptoms and ingestion of high protein meals is helpful diagnostically, and a dog that shows signs of dementia coupled with stunted growth and a profound state of ill health is a strong indication. "Small liver size coupled with bizarre neuralogic signs in a young dog... is strong supportive evidence that shunt exists, and indicates other diagnostic tests are needed" (1502). Maddison (1988) confines, "The presence of a small liver and enlarged kidneys. . . is highly suggestive of the presence of a portal caval shunt" (248).

Therapy can be medical or surgical. Usually medical therapy is used to improve preoperative health, or for owners that are unable to consider surgery (Ettinger, 1989). Medical management of PSS includes the restriction of protein and intestinal antibiotics that are non absorbable are effective against colonic bacteria (Tobias, 1993). The "goal [in dietary management] is to provide sufficient nutrients to allow proper growth and maintenance, without stimulating an increase in toxic metabolites" (Laflamme, 1989 199). Medical therapy helps to maintain a quality of life, but the disease will continue to progress and the animal will succumb to the disease. "Hepatic functional failure tends to progress in most animals that are diagnosed before one year of age...They eventually become refractory to medical management and succumb to their disease" (Ettinger 1503). "They will require medical management for life" (1505).

According to Tobias (1993) the preferred treatment for single congenital PSS is surgical closure or partial closure of the shunt. Successful surgeries can result in complete reversal of symptoms. Surgery is used to ligate the shunt flow that will redirect the blood through the liver. When blood is re-routed though the liver the pressure on the liver must be stable. Death from hypertensive shock will occur within 12-24 hours if the pressure is too high. The surgeon is challenged to find the correct pressure by returning to surgery to loosen or tighten the ligature. This explains the elevated cost and threat to life. "If shock is avoided serious postoperative complications are uncommon" (Ettinger 1989 1504). Successful surgeries are more common in shunts located outside the liver than inside, and it is logical to hypothesize that surgical correction of the shunt would result in a spontaneous dissolution of the uroliths (crystals).

In conclusion the portal systemic shunt appears to be growing in frequency however increased clinician skill at detecting the liver-shunt has grown. Furthermore advances in technological ability to detect a liver-shunt though angiography may also be responsible for increased reports of the disease. While the origin of the disease is obscure the disease is considered to be congenital; however, breed predisposition does exist, indicating an hereditary origin. The shunt most likely develops because a fetal duct fails to close after birth. Symptoms vary but all result in central nervous system disorders called hepatic encephalopathy. Puppies that fail to maintain the same growth rate as their siblings are suspect. Specifically shaped urinary crystals develop due to increased concentrations of ammonium. The degree of vessel occlusion may explain animals that are without symptoms until late in life. Small liver size coupled with bizarre neurological signs in young dogs is highly suggestive of the disease. Medical or surgical treatment isavailable however without corrective surgery an animal will eventually succumb to the disease. If the animal survives surgical intervention complete reversal of the symptoms can be expected.

References

Ettinger S. (1989).Textbook of Veterinary Internal Medicine. Philadelphia: W.B. Saunders Company.

Laflamme D.P. (1989). Hepatoencephaopathy Associated with Multiple Portal Systemic Shunts in a Dog. The Journal of the American Animal Hospital Association, 25 (2) 199-202.

Maddison J.E. (1988). Department Veterinary Clinical Studies, the University of Sydney New South Wales 2006. Australian Veterinary Journal , 65(8) 245-249.

Tobias, K. (1993). Disease mechanisms in Small Animal Surgery: Portosystemic Shunts. Philadelphia: Lea & Febiger

Tobias, K. (1994). Personal Communication.

posted 08-01-2003 09:13 AM         

--------------------------------------------------------------------------------

Introduction
The Scottish Terrier is one of over 74 breeds of purebred dogs reported to produce the genetic defect of congenital portosystemic shunt. Currently our STCA Health Survey reports a carrier frequency of 4.7%. This is a rare condition and not a widespread problem in the Scottish Terrier at this time. Unfortunately genetic disorders in dogs can spread rapidly. Two factors, in particular, influence the spread of a genetic disease: 1.) a lack of understanding about the disease and its symptoms and 2.) the widespread use of carrier dogs or bitches, well respected in the area of conformation, for breeding purposes. Much is still unknown about portosystemic shunt and its mode of inheritance. Because PSS is thought to be a polygenic disease, the parents may not contribute equally to the traits responsible for affected puppies and the carrier offspring may only inherit a piece of the carrier parent's traits. A percentage of puppies produced by carrier parents will also be carriers. The purpose of this article is to deal with factor 1.) - the disease, portosystemic shunt, recognition of its symptoms, methods of arriving at a diagnosis and options for treatment.

[Wanted Scottie DNA -- Learn how you can help]

Back to Top

--------------------------------------------------------------------------------

What is a Portosystemic Shunt?
Portosystemic shunts (PSS) are the result of abnormal vascular connections between the portal vein and the systemic circulation. The portal vein should connect the gastrointestinal tract with the liver. Figure 1. is an illustration of correct anatomy.

Correct or normal placement of the portal vein allows blood from the intestinal tract to flow directly to the liver. The liver then performs its function of metabolism and detoxification. The cleansed blood then returns to the heart and is pumped to the rest of the body.

Figure 1. Correct Portal Vein Anatomy

Shunts can be present at birth or acquired later in life as a result of disease process. Approximately 75% of shunts are present at birth. They are the result of anatomical anomalies or failure of fetal vessels to close after birth. Shunts are classified by their location: the extrahepatic shunt is outside the liver and the intrahepatic shunt is inside the liver.

Figure 2. Extrahepatic Shunt Figure 3. Intrahepatic Shunt

Typically, smaller dogs, such as the Yorkshire Terrier, Maltese, Cairn Terrier and Scottish Terrier have extrahepatic shunts and larger dogs such as Golden Retrievers and Irish Wolfhounds have intrahepatic shunts. Size exceptions have been noted within the intrahepatic classification of shunt. Extrahepatic shunts occur more frequently than intrahepatic shunts. Additionally, another phenomenon called microvascular dysplasia (MVD), a series of small intrahepatic shunts appear to be highly prevalent among Cairn Terriers. Hepatic microvascular dysplasia is thought to be a related disease to PSS that the Cairn Terrier carries. Research scientists are not of one mind about this phenomenon. A Cairn Terrier research project was undertaken by Thomas Schermerhorn, Sharon A. Center, Nathan L. Dykes, Peter H. Rowland, A. E. Yeager, H. N. Erb, Karen Oberhansley and Michael Bonda. They published an article in the Journal of Veterinary Internal Medicine, Vol. 10, No. 4 (July-August) 1996: pp 219-230. The article's title is "Characterization of Hepatoportal Microvascular Dysplasia in a Kindred of Cairn Terriers." This article is more technical than practical for our particular discussion. Within the article is a description of anatomical changes in livers of PSS Cairns and description of anatomical liver changes of MVD Cairns. MVD Cairns can appear to be healthy and they can go undiagnosed throughout their lives. If they are undetected, they often remain in the breeding population. The role of MVD Cairns in the spread of PSS isn't known. At this time we do not know if the MVD phenomenon occurs in our Scottish Terrier population.

Back to Top

--------------------------------------------------------------------------------

Acquired Shunts
The differentiation of congenital and acquired shunts is important to this discussion. Acquired shunts are not hereditary in nature. They are a result of progressive liver disease. Dogs suffering from cirrhosis, hepatitis or congestive heart failure can have increased pressure inside their livers. This pressure causes embryonic vessels that normally have no function after birth to open. Often this involves a number of vessels not the one or two seen in congenital shunts. The presence of shunts in an autopsy of an older dog does not mean this dog carries the genetic traits for portosystemic shunt. It requires further examination of liver tissue. Careful examination of the dog's medical history and a study of liver tissue should reveal the origin of this dog's shunt.

Back to Top

--------------------------------------------------------------------------------

Symptoms of PSS in the Scottish Terrier
There are multiple symptoms associated with this disease and the number and severity of symptoms depends on how much blood bypasses the liver. Symptoms are most often seen at a young age. The typical PSS dog is purebred and under one year of age. Dogs as old as eight and ten years have been discovered to have PSS. Although recorded, this is not the norm. Affected dogs can be small in stature, unthrifty and sometimes anorexic. Coat and skin condition are poor. They develop urinary tract infections at an unusually young age. The cause of the urinary tract infection is ammonium urate crystals. These crystals are formed by excessive ammonia and uric acid in the urine. PSS puppies do not react well to sedatives or anesthesia. The liver cannot metabolize these agents to help eliminate them from the dog's body. The sedatives are shunted back to the heart and returned to the body's circulation. PSS dogs can be subject to bouts of lethargy and depression. Dogs with severe shunts develop additional central nervous system signs like hyperactivity, circling behavior, disorientation, severe aggression, weakness, excessive salivation, staggering, temporary blindness, seizures and even coma. Vomiting and diarrhea are present in 2/3 of the cases of PSS. All of the PSS symptoms are affected by the consumption and digestion of protein rich foods. These foods produce ammonia, gamma-aminobutyric acid, natural benzodiazepines and mercaptains during the process of digestion. These chemicals are potential neurotoxins.

Back to Top

--------------------------------------------------------------------------------

Breeder Observations
As the author of this piece my intention is to present information for other breeders and owners to use if necessary. Opinion and emotion can obstruct this purpose, but observation of fellow breeders can be helpful. During the course of research on this disease I spoke to Yorkshire Terrier breeders, Cairn breeders and Scottie breeders. One scenario was repeated to me several times. It mirrored my personal experience. This narrative is anecdotal and not intended to imply that all cases follow this pattern.

A litter of puppies is born and progresses normally. By six weeks of age the puppies are completely weaned and all appears to be well. During the next four to eight weeks the puppies increase their consumption of protein rich puppy food. At this stage of life the introduction of vaccines becomes the next step in the successful raising of the litter. Between six weeks and fourteen weeks most puppies are given three to four sets of vaccinations. Some are combination vaccines and others are individual vaccines. (As a breeder I have never experienced puppies with a vaccine reaction but, I have read the articles concerning the possibility of adverse vaccine reaction especially with combination shots.)

One night my litter was healthy. The next day one puppy, Holly, was wobbly, disoriented and clearly in distress. The outside pen was checked for leaves or other foreign material the puppy could have ingested. Electric cords were checked in the den. All the cords had been raised out of the puppies' reach. We checked Holly for bites or a possible bee sting. Truthfully, it was too early in the season for bees in Massachusetts. Next her temperature was taken. It was normal. Nothing external appeared to have happened to this nine-week-old puppy. Why was she suddenly so sick? Off we went to the veterinarian.

Dr. Cindy Shaefer had seen Holly and her sisters for a routine vaccination and checkup the week before. Dr. Shaefer ordered blood work on Holly and examined her. Nothing specific was found. Later in the day Holly was almost normal in behavior. Then later at night her behavior was nothing less than bizarre and she staggered like a drunken sailor. By morning she was again nearly normal. The blood chemistry results were all within normal range and the blood count showed no sign of infection. For two days this erratic pattern of close to normal behavior and periodic staggering accompanied by rages or vacant staring persisted. Then Holly had a mild seizure. We consulted a veterinary neurologist. He found her symptoms, at the time of examination, unremarkable. She became worse and the seizures and behavior changes occurred more frequently. At the second visit to the neurologist he stated two possible causes for Holly's illness vaccine reaction or possible brain malformation. Some other breeders have reported the initial concern by veterinarians about vaccines.

Neurological tests like MRI and a spinal tap were discussed as possible options for determining the cause of Holly's illness. The first logical course of action was a bile acid test, a simple inexpensive blood test. The neurologist did not strongly believe that Holly was a PSS puppy; however, the test would rule out shunt and tell us if Holly could tolerate Phenobarbital for her seizures. The bile acid test detects diminished liver function. Dogs on seizure medication and older dogs with liver failure symptoms often require bile acid tests to monitor their health status.

For the young dog high bile acid results indicate a need for a PSS work up. This test is an effective screening test. It does not provide definitive diagnosis. Rather, it tells you if more testing in this area is needed. Breeders in other breeds report spending thousands of dollars on sophisticated neurological tests only to find that the simple fifty dollar test, the bile acid test, provides them with a direction for diagnosis of their sick puppies.

Back to Top

--------------------------------------------------------------------------------

Further Information
The full text of this article contains additional information concerning the diagnosis of PSS in the Scottish Terrier. It also includes information about:
a. Screening test: bile acid test;
b. Diagnostic tests: ultrasound, scintigraphy, surgery and necropsy;
c. Medical treatment;
d. What should Scottie breeders know and
e. References used for this article.

posted 08-01-2003 09:16 AM         

This condition is often referred to as a "liver shunt" but the current favored term appears to be portosystemic shunt. These have also been referred to by more exact terms since there are specific types of shunts that vary slightly. The broad categories are extrahepatic and intrahepatic shunts, depending on whether or not the shunt occurs in the liver or outside of it. Specific types of shunts are patent ductus venosus, portal-azygous, portocaval (portal-abdominal vena cava), atresia (lack o f development) of the portal vein and acquired shunts that occur due to
changes in blood pressure or circulation.

Yorkshire terriers are reported to have a higher than normal incidence of liver shunts. They are reported to be more likely to have extra-hepatic shunts which is good since they are easier to repair.

What are the signs?
Most shunts cause recognizable clinical signs by the time a dog is a young adult but once in a while one is diagnosed at a later time in life. Since the severity of the condition can vary widely depending on how much blood flow is diverted past the liver it is possible for a lot of variation in clinical signs and time of onset of signs to occur. Often, this condition is recognized after a puppy fails to grow, making an early diagnosis pretty common, too.
Signs of portosystemic shunts include poor weight gain, sensitivity to sedatives (especially diazepam), depression, head pressing (pushing the head against a solid object), seizures, weakness, salivation, vomiting, poor appetite, increased drinking and urinating, balance problems and frequent urinary tract disease or early onset of bladder stones. If the signs of problems increase dramatically after eating this is a strong supportive sign of a portosystemic shunt.

How is Liver Shunt diagnosed?
This is frustrating since there is not a test for this condition. there was a "definitive" test and there is almost one - special dyes injected into the liver circulation that show up on X-rays can outline the problem pretty clearly. Most of the time. But this is a pretty invasive test making it a poor choice for "screening" purposes. There are a number of possible abnormalities that might point towards a portosystemic shunt on routine labwork, including low BUN (blood urea nitrogen), low albumin, mild anem ia, increases in ALT (serum alanine aminotransferase) or ALKP (serum alkaline phosphatase). If these hints are present, it would be a good idea to test the serum bile acid levels prior to eating and after eating. If this test is supportive of poor liver function then it may be a good idea to consider ultrasonagraphy and dye contrast X-rays.

How is it treated?

So far in my research I haven't found a cure for Liver shunt besides surgery for portosystemic shunts. As far as I know, dogs with extrahepatic shunts (occuring outside the liver itself) is easier to do than surgery in dogs with intrahepatic (inside the liver) shunts. If you know of a different cure please let me know.

--------------------------------------------------------------------------------

CLINICAL DIAGNOSIS OF HEPATIC PORTO-SYSTEMIC SHUNTS
by Larry Snyder, DVM

Clinical Signs: Most dogs will be diagnosed with port-systemic shunts under one year of age, but dogs as old as eight have been diagnosed with the condition. Animals are usually stunted, thin, depressed, have trouble gaining weight, and are usually characterized by the owners as chronic "poor doers". In most affected dogs there will be some degree of behavioral signs ranging from listlessness, apathy, or depression to more severe signs of circling, head pressing, stupor, drooling, blindness, or convulsio ns, some leading to coma. These behavioral changes are due to an accumulation of toxins (especially ammonia) that affect the brain causing a condition called Hepatic Encephalopathy. These toxins are most abundant in the blood stream following the dog eating, especially a high protein meal, & may remain high for hours afterward. Not all dogs with the shunt will show this meal associated behavioral change, but in 25% of the affected dogs that do, the diagnosis becomes clearer. A high percent of affec ted animals show an intolerance to anesthetics or tranquilizers, & will show increased recovery times following use of these products. Even anti-convulsants used to control seizures may be potentially dangerous if allowed to concentrate in a dog with functional shunt. Approximately 75% of affected individuals will show digestive system symptoms including poor appetite, ascites, vomiting, drooling, diarrhea, or occasionally deranged appetite (eating paper, etc.). Urinary system symptoms may include incre ased thirst and urination, & in a majority of porto-systemic shunt cases, there will be crystals or stones formed in the urinary tract. These crystals will be either uric acid or ammonium urate (ammonium biurate or thorn-apple crystals.). There can be bladder stones formed or crystals may be noted on the hair around the prepuce or vulva.

Laboratory Findings: Routine performed serum chemistries are fairly nonspecific toward confirming the diagnosis of porto-systemic shunts, but there may be a decreased total protein (primarily albumin), decreased blood glucose, decreased cholesterol, & decreased blood urea nitrogen (BUN). The uric acid levels may be elevated in a significant number of affected individuals. Acid levels are extremely important in the diagnostic screening of symptomatic potential shunts. Fasting and 2-hr. post meal blood samples are evaluated for bile acid levels. In virtually all porto-systemic shunts there will be a significant rise in the bile acid levels over normal. The use of bile acids in screening clinically normal dogs for liver shunts is not currently being advised due to the variation of normal bile acid levels in Yorkshire Terriers, & other breeds as well. Reports of recent vaccination with modified-live vaccines causing high serum bile acid levels in normal animals have not been confirmed as of this time. Liver function testing with Bromosulfaphthalein (BSP) or ammonia tolerance testing are sensitive & reliable if performed correctly. These tests measure the liver's ability to excrete/detoxify known agents, and thus measure liver function accurately.

Radiography. Radiography is one of the most important methods of establishing a diagnosis of porto-systemic shunt, & is currently the only universally accepted method of confirming a shunt, short of major surgery. Injection of a radiopaque dye into the spleen (Splenoportograpy) will show the shunt on radiographs & allow accurate assessment for surgical correction.

Nuclear Medicine. The placement of a radiopharmaceutical agent (radioisotope) specific for the liver into the colon for absorption through the mucosa has been gaining favor because of its noninvasive diagnostic value. This procedure requires expensive equipment & the diagnosis is based on the distribution of the radionuclide in the lung or heart compared to that in the liver. This procedure also does not identify the exact location of the shunt for surgical correction if required.

Ultrasound. Until recently, ultrasound was fairly unreliable for nonsurgical diagnosis of porto-systemic shunts. With the advent of Color Flow Ultrasound, there is the potential for diagnosis of this condition on non-anesthetized animals. At the present time, this technology appears to be the diagnostic procedure of choice. If currently undertaken research confirms its value, Color Doppler Ultrasound will soon be the preferred screening and diagnostic tool.

At the present time, Hepatic Porto-Systemic shunts are considered to be UNQUESTIONABLY genetic by some of the leading canine experts, but the mode has not been identified at the present time; research is being conducted at Michigan State University to identify this pattern. Genetic disorders in dogs can spread relatively rapidly if a dog, whether affected or a carrier, is a well-respected animal in either conformation or ability, and is used extensively for breeding. This is especially true in the case o f the male that can produce hundreds of offspring during his breeding life. If the cause of such a condition can be discovered, then a working strategy can be implemented to control and eliminate the disorder.

The Yorkshire Terrier Club of America Foundation, Inc. is currently funding research into both the genetic nature of the problem & into the use of Color Flow Doppler Ultrasound as a diagnostic & screening tool. These steps will hopefully become the basis for setting up an open registry for Yorkshire Terriers & other affected breeds to hopefully eliminate, or at least minimize the problem within each breed.

For More information contact the Y.T.C.A.

posted 08-01-2003 09:38 AM         

Portosystemic shunts are abnormal vascular onnections
between the hepatic portal vein (the blood vessel that
connects the gastrointestinal tract with the liver) and
the systemic circulation(Figure 1). Such anomalies
cause blood in the gastrointestinal track to be diverted
past the liver, there by limiting the liver's vital functions in
metabolism and detoxification of compounds and the
body's defenses 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 in
life. Congenital shunts are more common, representing
approximately 75% of all canine cases, and generally result
from anatomic abnormalities of the portal vasculature or
persistence of 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 purebred 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 been proven
only 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 of dogs such as Irish Wolfhounds and
Golden Retrievers. The majority of intrahepatic shunts are
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, nonfunctional 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 dogs with portosystemic
shunts reflect the failure of the liver to eliminate various
toxic matter, drugs, and bacteria absorbed from the
gastrointestinal tract. Certain materials particularly
those produced from dietary protein, are potential
neurotoxins (e.g., ammonia, gamma-aminobutyric acid,
natural benzodiazepines, and mercaptans), which affect the
function of the central nervous system and produce a
syndrome called hepatic encephalopathy. 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 it's metabolic,
storage, and excretory functions are further impaired.
.
SIGNALMENT AND HISTORY
.
Dogs with congenital portosystemic shunts are typically
purebred dogs less than 1 year old. The severity of clinical
signs varies and is related to the anatomic position of the
shunt and the fraction of portal blood that is shunted past
the liver. Generally, the lower the fraction of shunting, the
milder and later in onset are the clinical signs. Nevertheless,
affected animals are often in poor body condition and of
small body stature, especially when compared to their
littermates. Owners may complain that the animals fail to
thrive or grow and that skin and coat condition are poor.
.
Other clinical signs tend to be intermittent or periodic in
nature and relate to the central nervous system,
gastrointestinal tract, and urinary tract. There may also be
a history of an adverse response to sedation or anesthesia.
.

A significant number of dogs (up to 25% of cases of
portosystemic shunts) may develop signs later in life; this
may be due to an acquired rather than congenital shunt or
because the animal can no longer compensate for a low
grade congenital shunt. dogs with acquired shunts have
signs similar to those with congenital disease, although
the previous history may have been uneventful until the
appearance of weight loss and associated clinical signs.
.
CLINICAL SIGNS

Central nervous system signs are the most common, occurring
in over three-quarters of all cases, and may be vague and
subtle such as anorexia, depression, and lethargy.... More
specific signs include episodes of hyperactivity, head
pressing and circling, disorientation, temporary blindness,
weakness, excess salivation, seizures, and occasionally coma.
These signs tend to wax and wane, and their onset may be
connected with the recent ingestion of a protein-rich meal
that resulted in increased production of neurotoxins within
the large intestine.
.
Gastrointestinal signs (vomiting and/or diarrhea) 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 (excessive drinking and
urination).
.
Other less common signs of portosystemic shunting include
recurrent fevers and ascites, although the latter is generally
seen only in dogs with acquired shunts.
.
DIAGNOSIS
.
Although signalment and clinical signs may strongly suggest
the presence of a portosystemic shunt, a series of investigative
steps... must be taken to:
.
*Identify the anatomic location and severity of the shunt
*Indicate whether the shunt is congenital or acquired
.
The latter two criteria are important when considering
whether the shunt is amenable to surgical correction and
the likely outcome of such surgery.
.
Blood chemistry and hematology panels usually show
characteristic patterns of mild abnormalities that as a group
suggest the presence of a portosystemic shunt. These include
mildly elevated liver enzymes, low blood urea nitrogen and
total plasma protein concentrations, hypogly-cemia (low
blood sugar) and low serum cholesterol. Mild,
nonregenerative anemia and microcytosis (undersized
red blood cells) may also be present in all cases. Blood
ammonia concentrations may also be increased, but samples
must be rapidly analyzed soon after collection to detect such
an increase. Urinalysis may reveal a low specific gravity and
the presence of ammonium blurate crystals. Serum bile acid
concentrations taken either after an overnight fast or 2 hours
after a meal are usually confirmatory.
.
The next step is to identify whether the shunt is intrahepatic,
extrahepatic, or microvascular. This generally requires
specialized imaging techniques, and it is likely that dogs
may need to be referred to appropriate specialists. Survey
radiographs of the type normally taken in veterinary
practices simply indicate the presence of a small liver
.
(Figure 2).
.
Ultrasonography is a useful, noninvasive tool for the
detection of portosystemic shunts. Intrahepatic shunts are
easily visualized: the liver usually appears small in size,
there is reduced visibility of intrahepatic portal vessels,
and an anomalous blood vessel may be obvious (Figure 3).
In dogs with extrahepatic shunts the first two features are
usually present, but the detection of the anomalous vessel
is not so easy. Application of Doppler ultrasound, an
advanced technique, may help in such cases, especially
where there is a small extrahepatic shunt.
.
Contrast radiography, whereby a marker dye is injected
into a vein draining the intestine and radiographs are taken
immediately, allows ready visualization of the portal vein
and shunting. This procedure is usually performed in
combination with surgical correction (so that the dog has
to be anesthetized only once) and is often referred to as
operative mesenteric portography. A loop of small intestine
is exteriorized (brought outside of the body) and a tube is
placed in a jejunal vein. A water-soluble radiopaque
dye is injected via the tube, and lateral and ventrodorsal
radiographs are then taken. Where there is a shunt, the
abnormal vessel is outlined as blood is diverted into the
systemic circulation without appearing in the liver
(Figure 4).
.

.
Portal or transcolonic scintigraphy is an advanced technique
whereby the uptake of radiochemicals from the intestinal
tract is monitored. A radiochemical, usually technetium 99m
pertechnetate, is administered via the rectum and first
accumulates in the liver in normal animals. In dogs
with portosystemic shunts the distribution of activity is
altered as the radiochemical bypasses the liver and reaches
the heart first. Although this does not identify the location
of the shunt, it does provide an extremely accurate estimate
of the degree of shunting, allowing the clinician to
predict the likely success of management options and to
follow up the success of surgical management.
.
Liver biopsy is indicated when there is no obvious shunt or
if multiple extrahepatic shunts are identified (as seen in
acquired portosystemic shunting). This may reveal
hepatocyte atrophy, with small or absent portal vessels,
and will allow histopathologic confirmation of micro-
vascular disease.
.
MANAGEMENT
.
There are two broad management options: surgical ligation
of shunts or medical management of the effects of shunting.
The decision as to which is most appropriate needs to be
made on a case-by-case basis depending on the type and
location of the shunt, the age of the animal, and the
severity of clinical signs. There may also be significant
financial considerations on the part of the owner. Surgery
wherever feasible, is generally believed to be the treatment
of choice as it suggests the promise of normal liver function.
Improvements in dietary and medical management of hepatic
encephalopathy, however, mean that conservative treatments
offer a reasonable prognosis for dogs that are not suitable
for surgery....
.
SURGICAL MANAGEMENT
.
Ligation of shunt vessels is an advanced surgical technique
requiring a suitably experienced surgeon, careful selection
and monitoring of general anesthesia, measurement of blood
pressure in the portal vein and systemic circulation, and
appropriate critical care support facilities. Such requirements
usually necessitate referral to specialist centers, and this is
especially true with intrahepatic shunts.
.
Single extrahepatic shunts are usually identified as tortuous,
abnormal vessels. These are ligated close to the vena cava. A
potential fatal complication is portal hypertension, which
occurs when intrahepatic vessels are unable to cope with the
additional volume of blood that is diverted to the liver after
closure of the shunt vessel. Guarding against this requires
careful monitoring of portal and systemic blood pressures
and inspection of the intestines and pancreas for signs of
cyanosis. Failure to alleviate the hypertension and pain,
bloody diarrhea, and shock leading to death in 2 to 24 hours
after surgery.
.
A 60% to 80% degree of ligation can usually be achieved
without complications and is associated with an increase in
the amount of portal blood that enters the liver and with
improvements in the patient's clinical status. In some cases,
the ligation procedure may be repeated on one or more later
dates to progressively attain complete ligation. This un-
fortunately necessitates additional costs and, with successive
surgeries, increases the risk of perioperative, complications.
On the other hand, repeat surgery may not be necessary as
some partially ligated shunts appear to spontaneously
occlude. The prognosis for dogs with partial ligation is
guarded because approximately 50% show recurrence of
clinical signs at an average of 3 to 4 years after surgery.
.
Ligation of intrahepatic shunts is technically more difficult
and is associated with higher risks of fatal complications.
Such cases may be best managed conservatively.
.
MEDICAL AND DIETARY MANAGEMENT

With better understanding of the pathophysiology of hepatic
encephalopathy, it has become possible to prescribe specific
therapies that provide a reasonable prognosis for those dogs
with portosystemic shunts that are not corrected surgically.
The primary objective of medical management is to
eliminate the clinical signs associated with hepatic
urinary tract disease and reducing the metabolic load on
the liver. The chief components of medical management
strategies are dietary modifications and oral antibiotics.
.
Medical management is indicated for all dogs with acquired
shunts and all dogs with microvascular shunts. It should
also be used for a period in those dogs that are about to
undergo surgical ligation. This will allow the veterinarian
and owner to establish the extent to which the condition can
be managed medically, in case it is not possible to completely
ligate the shunt at surgery. medical management is also
indicated in those dogs whose owners are unable to afford
the cost of referral to a specialist surgical facility or whose
owners are unwilling to accept the significant risk of

,
perioperative mortality. All dogs undergoing surgical
ligation should continue to receive medical therapy for 2
to 4 weeks post-operatively. Finally, some degree of medical
therapy may be required in dogs with partially ligated
shunts.
.
Dietary manipulations for the control of hepatic
encephalopathy are designed to limit neurotoxin production,
which occurs principally in the large intestine, and to reduce
the subsequent absorption of these toxins into the portal
vein....The major toxins are all derived from nitrogenous
materials (protein and urea) and are synthesized 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 very
digestible. These steps reduce the amount of protein that
reaches the large intestine; further reductions can be
attained by feeding smaller meals more frequently to
maximize the digestive capacity of the small intestine.
.
Specific diets with restricted protein contents are available
from veterinarians. These are ideal because they provide a
balanced protein-calorie intake, which is important for the
stable control of hepatic encephalopathy.
.Including dietary fiber in the daily ration assists in acidi-
fying the colonic environment and limiting toxin production
and also acts as a mild laxative to increase the elimination
of toxic factors in feces. Lactulose, a soluble fiber, is often
used as a supplement for this purpose and can be readily
purchased from pharmacists. Supplementation with zinc
salts also improves the detoxification of ammonia and the
control of hepatic encephalopathy. A veterinary diet
specifically designed and tested for the management of liver
disease and portosystemic shunts is available in Europe; it
is unique in combining a restricted protein content with in-
creased zinc and added dietary fiber. Available in America
as Waltham Veterinary Diets Canine Low and Medium
Protein, dry and canned.
.
Antibiotics are used in most cases to reduce the bacteria
within the large intestine that are responsible for the
production of neurotoxins. Orally administered neomycin
is commonly used for this purpose and is often used in
combination with lactulose in both the short and long-term
medical management of portosystemic shunts.
.
SUMMARY
.
Portosystemic shunts are serious conditions in dogs and
require significant efforts to diagnose and treat. Specialized
surgical techniques, in association with advances in medical
and dietary management, allow the condition to be effectively
managed and provide a reasonable quality of life.
.

.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
..
ABOUT THE AUTHOR
Dr. Watson qualified from the Royal (Dick) School of Veterinary Studies at the University of Edinburgh in 1987
and received his PhD from the University of Glasgow in 1992. He joined the Waltham Center in 1994, where he currently holds the position of Research Manager.
You can read more here.... http://www.vet.utk.edu/clinical/sacs/shunts_faq.html
l.
.
.
Back to home page

posted 08-01-2003 09:41 AM         

When a shunt does not disappear, the puppy's system in not able to properly process the toxins that naturally accumulate in blood. The liver's purpose is to filter these toxins out of the system, but in the case of a puppy with a shunt, part or all of the blood bypasses the liver. Over time, toxins may accumulate to a degree which can be fatal. The level of seriousness presented by a shunt depends on the percentage of blood that bypasses the liver. The smaller the percentage, the less serious the problem.

Symptoms and Signs

Symptoms of liver shunt may include excessive drinking, depression, weakness, poor appetite, frequent urination, vomiting, drooling, and a general lack of interest in activities. Puppies with liver shunt are also prone to frequent urinary tract infections. If you suspect that your puppy may have a liver shunt, observe him or her closely after they have eaten. A dramatic increase in the severity of symptoms is a sign of liver shunt. Your puppy may also exhibit unusual behaviors, such as running in circles.

Although less common, you should be aware that liver shunts can develop in older Yorkies. The symptoms are the same as discussed of the case of a puppy.

Treatment

If your Yorkie displays the symptoms discussed above, you should contact your veterinarian immediately. A veterinarian can perform conclusive tests to determine whether your puppy has a liver shunt and recommend an course of treatment.

The treatment required depends on the severity of the liver shunt. All treatments are intended to eliminate the symptoms, as the root cause is untreatable. Treatment may range from restricted diets for mild cases to surgery for more severe cases. Sadly, not all cases of liver shunt are treatable. In these cases, the puppy may be euthanized to avoid extended pain and suffering.

Any reputable breeder will be aware of any cases of liver shunt in their bloodlines and strive to avoid a recurrence. Virtually all reputable breeders guarantee their puppies to be free of genetic defects. If your puppy is diagnosed with liver shunt, contact the breeder immediately. Your guarantee should outline the options available to you. These options typically range from a full refund to getting an additional puppy.

posted 08-01-2003 09:43 AM         

My puppy hasn't eaten and is lethargic. Could it be hypoglycemia?

HYPOGLYCEMIA
Many puppies are lost unnecessarily each year, simply because breeders know too little about hypoglycemia and many veterinarians find it difficult to diagnose. My Vet's opinion is that too few background facts are given to a Vet when the sick puppy is brought in for help. Usually the puppy is comatose the first time a Vet sees him and since he usually responds immediately to intravenous or subcutaneous dextrose injections, the Vet often diagnoses the problem as an acute viral hepatitis or encephalitis, (the reaction is the same in all of these cases).
However, in a young puppy, or a very tiny toy dog, this condition is usually hypoglycemia, brought on by stress or shock in some form. Also, it usually occurs in puppies from 4 to 5 months of age but CAN occur in mature toy breeds when they are subjected to STRESS.
The stress usually causing this condition is:

1- Overhandling young puppies and not letting them get enough rest and sleep.
2- A puppy refuses to eat for over a period of 8 hours due to change of home and/or food.
3- Exposure to low room temperatures for a period of time or sleeping in drafts.

The puppy will appear limp and lifeless with the gums and tongue usually grayish blue in color. Often the eyes are unfocused and barely open. They may appear to be slightly sunken in. Temperature will be sub-normal and the puppy will be shivering and trembling in the early stages. As condition worsens, the puppy either goes into a coma or convulsions. Hypoglycemia is a metabolic disorder and death will result, unless properly DIAGNOSED AND CARED FOR IMMEDIATELY, if the case is severe. The level of the blood sugar must be raised at once and the stress condition treated.
My Vet recommends an injection of 5-10 cc of a five percent solution of dextrose with added B-12. He gives this subcutaneously as it provides a longer lasting action and, also, it is almost impossible to locate a vein in a tiny puppy.
With this dextrose or glucose, my Vet also gives an injection for shock and stress. He says that many Vets use a form of cortosteroid for this stress factor. It is produced under many trade names, but your Vet will be sure to have it on hand. When these injections are given in time, the puppy may regain consciousness promptly. If the seizure is bad or not CARED FOR IN TIME, the puppy may REMAIN IN A COMA FOR DAYS. When this happens, you must feed him, keep him warm and quiet and see that he has proper eliminations.
Usually the bowels will move without help, but an older puppy may struggle to be supported erect on his feet for elimination. Check carefully for urination as the pup is in trouble if the kidneys cease to function. Wash genital area with cotton soaked with warm water if the puppy is comatose. If partially mobile, put his feet on a towel at the edge of a wash basin. Support him with one hand and turn the water on in the basin. Hearing the running water usually makes them urinate.
Also, Mix the Glucose Solution shown in "Whelping Supplies" or Mix Honey, Sugar or Corn Syrup with equal amounts of water and feed with syringe 10cc four times a day.
When hypoglycemia is caught in time, there is no reason why a puppy won't come out of it and never have it again if the stress factor is eliminated.
Even if this never occurs to your puppy, or adult, it is important that you know about this to aid your Vet in diagnosing the problem. This usually affects Tiny Toy Breeds and Most of them outgrow this danger by 6 months of age. However, it can happen to a tiny dog even as an adult and careful attention must be paid to the diet of any TINY TOY DOG.

[ Back to the Questions ] [ Back to Alex's Page ] [ Take me to Shooter's Page ]

--------------------------------------------------------------------------------

My Yorkie needs surgery. What should I know about anesthesia and intubating?
There are a couple of different dangers in surgery for toy dogs and they are not insurmountable, but they are VERY SERIOUS.

1) DON'T ever allow the vet technician to intubate your toy dog. Too many small toy breeds have had TRACHEAL INJURY and suffered and DIED because of collapsing tracheas from injury to the trachea during intubation. Make sure that the vet knows that you expect him/her to use the smallest possible tracheal tube to intubate your toy dog. Speak up! It could mean saving the life of your little dog. If the vet treats you like an "overprotective" Mom, find another vet that will understand.

2) Proper use of Ace Promezaine as a pre-anesthetic injection is ok so that the dog can be intubated.

3) Isoflurane is the anesthetic of choice. Don't use Halothane or any of the barbituates (see number 4, below). Some vets will "mask" a tiny dog with Isoflurane rather than use the injectable and some vets will not intubate at all, but this depends on the type of surgery being performed. This is an excellent method whenever possible.

4) Last but not least, DO NOT ALLOW YOUR VET TO USE ANY KIND OF BARBITUATES TO ANESTHESIZE YOUR TOY DOG. MOST PARTICULARLY NOT PENTABARB. Many toy dogs have died needlessly because of UNINFORMED VETS WHO ARE DECADES BEHIND IN USE OF ANESTHETICS FOR TOY DOGS. If your vet thinks Isoflurane is too expensive and refuses to use it, then FIND ANOTHER VET THAT will use it. It could and probably will save your dog's life.

BUTTONS 10/12/97 - 8/11/98
Buttons was almost 10 months old when his owner took him to their vet, a good family friend for many years. Though she received all the normal "warnings" about barbituate overdosing on toy dogs, she felt a great confidence in her Vet that she had for all these years.
He gave a pre-anesthetic tranquizer for intubating which is normal, but then he gave the little 3 pd dog PENTABARB and the little dog went to sleep forever NEEDLESSLY. Look at this little face, and weep with us for something that did NOT HAVE TO HAPPEN. If your vet will not use Isoflurane or gas anesthesia (because it is expensive).... FIND ANOTHER VET THAT WILL.
Here's some of the comments from veterinarians who have heard of this mishap:
"I can't believe that anyone is still using PENTABARB.... that is only used for severe seizures that NOTHING else will control....a last resort"
"This is unheard of in todays veterinary medicine. This vet is DECADES behind"
This was a fine and healthy, chubby little dog, full of mischief and not at all sickly in any way. An autopsy showed no reason that this dog should have expired other than an overdose. Even the Vet, who is a family friend, feels very badly about this "overdose".
When your breeder preaches ISOFLURANE.....FIND A VET THAT WILL USE IT BEFORE YOU NEUTER OR SPAY YOUR LITTLE TOY DOG.
If you are all shocked and moved by this tragedy, please spread the word and Buttons will not have died in vain.

Thank you,
Terri Shumsky

[ Back to the Questions ] [ Back to Alex's Page ] [ Take me to Shooter's Page ]

--------------------------------------------------------------------------------

What is Liver Shunt?
The symptoms of portacaval liver shunt can start to appear at almost any age. Dogs with a liver shunt are usually very thin dogs who pick at food. They not only have a poor appetite but they can become lethargic, dizzy, and stagger. They may try to climb out of their pen, climb higher on you and cry and throw their head far back after eating, and they may go into convulsions.
This is not a new disease but one which is coming to the attention of all Yorkshire Terrier breeders and other toy breeders in the 80's and 90's and many breeders feel that it is an inherited disease and that the only way to eliminate that disease is to cull those dogs who are affected and producing this disease from their breeding program.
This disease usually goes hand in hand with a kidney disorder and it seems that a special diet can sometimes keep it under control with some dogs for a time. Surgery sometimes works depending on where the "shunt" is. What happens is that the blood by-passes the liver and goes directly to the heart and therefore the liver shrivels up, becomes filled with infection and the dog convulses.
These dogs so affected are unable to cope with barbiturates. We accidentally found this out in '86 when I dosed my dogs with Ace Promazine for travel sickness and one "sickly" girl puppy slept as though she died. She did come around the next day. Later we associated this with her condition when she convulsed and died at 12 weeks. An autopsy revealed an infected and shriveled up liver, the result of a liver shunt.
The Yorkshire Terrier Foundation is in the process of trying to clinically prove that this is an inherited disease, but I have proven to myself that it is because of my own test breeding and eliminating those dogs involved which thereby ended my problems now for many years.
There's always the possibility that this is the first time it happened to a breeder. Hey, there was a first time for me too!! It's not SHAME ON YOU for having the problem, but it is SHAME ON YOU if you, as a breeder, don't take steps to see that it doesn't happen again.
If your dog shows any of these symptoms, the blood tests alone and the bile acid tests are INCONCLUSIVE. If the dog dies, have your veterinarian do a simple autopsy to examine the liver.
Do not just put the dog to sleep because the blood test has an elevated white count and the veterinarian THINKS it may be the liver disease. Unless the dog is extremely debilitated, it may not be the liver disease and you will have put him/her down for no reason.
There are various specialists who *know* how to recognize the disease so that you are certain that you are getting an accurate prognosis. We will add more connections for information on liver shunt as it becomes available.

In the Dallas Ft Worth, Texas area:
Dallas Veterinary Surgical Center. Dr. Robert D. Barstad
Phone: 972-235-2096
Fax: 972-680-0859
He is one of only two in the state of Texas that does this surgery and is reported to have a 95% success rate.

Cornell University - Ithaca, New York
Phone: 607-255-2000

Dr. Susan Center at Cornell has been quite helpful with liver shunt pups. She has at times done surgery free and spayed/neutered, and rehoused donated pups. Her email address is sac6@cornell.edu. She is quite knowledgeable, has kept some in her home, and is currently studying diet along with surgical repairs.

University of California at Davis, California
Dr. Clare Gregory

Dr. Karen Tobias
University of Tennessee College of Veterinary Medicine
PO Box 1071
Knoxville TN 37901-1071
(865-974-8387).

Dr. Tobias is undertaking a genetic evaluation of Yorkies with shunts.

"I have no idea whether we will find that this disease is more prominent in one line, or if it's polygenetic. We would hope that all breeders would be interested in clearing this disease from their lines and would welcome the results. The study has been completed in Australia, where they have shown that breeding 2 Maltese dogs with shunts will result in a 25% incidence of portosystemic shunts. We have not performed any breeding studies of Yorkshire terriers, but will start with the basic genetics, and will give the information to the next group, which is planning on trying to find an actual genetic marker. Imagine that- a blood test to diagnose the propensity for shunts! I am not familiar with what will be involved, but I think the possibilities are incredible. I imagine we could test every Yorkie and selectively breed this disease out of the population."

Dr. Tobias Update

My name is Karen Tobias and I am a veterinary surgeon at the University of Tennessee College of Veterinary Medicine. Recently I received funding from the AKC Canine Health Foundation to study liver shunts (congenital portosystemic shunts) in Yorkshire terriers. Our goal is to determine whether liver shunts are hereditary and whether breeders can avoid having liver shunts in their lines by selective breeding. Eventually this information may be used to develop a genetic test for affected animals.

I have an informational letter about the study and a registration form for participation. I may also be sending this same information to some of you by mail. To provide the most accurate results, we need the widest participation possible. I'd appreciate any help in disseminating this information.

If you would like me to mail these forms to anyone, please send me a postal address, FAX, or e-mail address and I will do so. If you have any questions about the study, please contact me.

I have been studying and treating liver shunt in Yorkshire terriers for 15 years. With your help I hope we will be able to find a way to make this devastating problem a distant memory for the breed.

Thank you for any help.

Karen M. Tobias, DVM, MS, Diplomate ACVS
Associate Professor, Small Animal Surgery
E-mail: ktobias@utk.edu
University of Tennessee
College of Veterinary Medicine, PO
Box 1071, Knoxville TN 37901-1071
(865-974-8387).

Dr. Cynthia M. Smith.
State of Washington
253-588-1851

Washington State University College of Veterinary Medicine.
Anthony J. Cambridge, B.V.M.S.,M.A.C.V.Sc.,M.R.C.V.S Resident of Small Animal Surgery.
E-mail: tc@vetmed.wsu.edu

Liver Shunt Experts experienced at liver shunt surgery:
Auburn University: (334)484-44690
Florida State University: (352)392-4746

Dr. Michael Petranto, Twin Rivers, NJ: 609-426-9625
Dr. Kazmierczak, West Trenton, NJ: 609-771-0995
Hopewell Vet Group, Hopewell, NJ: 609-466-0131

Western Hills Veterinary Hospital
Larry Fischer, DVM
1132 SW Wanamaker
Topeka, Kansas 66604-3889
(785)273-0400, (785)357-5188

MORE INFORMATION ON LIVER SHUNT
Fanny Mae Liver Shunt Fund
Jon-An's Yorkshire Terriers Liver Shunt Information
Lacy's Liver Shunt Information
Meet Star, a Liver Shunt Baby
Meet Rayna, another Liver Shunt Baby

UC DAVIS is working in conjunction with AKC Canine Health Reserach to establish the normal DNA for healthy dogs. You can send for the swabs and help by being a part of this data base collection by going to http://www.vgl.ucdavis.edu/Service/Canine/#kit and applying for the swabs for your dogs. Additional information is at http://www.vgl.ucdavis.edu/research/canine/.

Also Catherine Inverson, Research Vet, is interested in DNA Swabs from the parents of Liver Shunt Victims in an attempt to find the DNA responsible for this problem. She can be reached at healthydog@vetgen.com.

Thank you for your participation.