| 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. |
| . |
You can read more here....
http://www.vet.utk.edu/clinical/sacs/shunts_faq.html
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