Portosystemic shunts are abnormal vascular connections between the hepatic portal vein (the blood vessel that connects the gastrointestinal tract with the liver) and the systemic circulation.
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.
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.
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.
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 manage- ment of hepatic encephalopathy, however, mean that conservative treatments offer a reasonable prognosis for dogs that are not suitable for surgery.
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.
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 encephalopathy. Other goals include minimizing lower 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 (Table 4). 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 acidifying 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 im-proves 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 increased 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.
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