Page 632 - Small Animal Internal Medicine, 6th Edition
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604    PART IV   Hepatobiliary and Exocrine Pancreatic Disorders





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                         A                                     B

                          FIG 36.10
                          Typical small-breed dogs with congenital extrahepatic portosytemic shunts. (A) Eight-
                          month-old female Border Terrier. (B) Nine-month-old female Miniature Schnauzer.















                           A                                   B

                          FIG 36.11
                          (A) Portovenogram in a 1-year-old Golden Retriever with an intrahepatic portosystemic
                          shunt. This was a central divisional shunt, which had a venous sinus–like structure, as
                          demonstrated well in this radiograph. (B) Normal portovenogram in a dog for comparison
                          with A. (Courtesy Diagnostic Imaging Department, Queen’s Veterinary School Hospital,
                          University of Cambridge, Cambridge, England.)
            Clinical Features                                    Chapter  33). Urate  uroliths are also  common and can  be

            Clinical signs are similar to those in cats; neurologic, GI, and   cystic or renal. Anecdotally, urate renal calculi seem to be
            urinary tract signs predominate (see Chapter 35 for more   more common in terriers, and dogs presenting with calculi
            details). About 75% of dogs present before 1 year of age, but   often do not have prominent neurologic signs. On physical
            some present at an older age, with some as old as 10 years   examination, animals are often but not always smaller than
            before signs are recognized. There is a spectrum of severity   their litter mates and may have nonlocalizing neurologic
            of neurologic signs, ranging from severely affected young   signs and, in some cases, palpable renomegaly. The latter is
            puppies that persistently circle, become centrally blind, and   caused by circulatory changes and is not a reflection of renal
            can even have seizures or become comatose, to very mildly   disease or uroliths; it is of no clinical significance and
            affected or asymptomatic individuals. It is likely that this   regresses after shunt ligation. Other congenital defects may
            variation reflects differences  in shunt fraction and dietary   be apparent, particularly cryptorchidism, which is reported
            and other environmental differences among dogs. Concur-  in up to 50% of male dogs with congenital PSSs.
            rent inflammation is an important trigger for HE in affected
            dogs, so clinicians should look carefully in affected animals   Diagnosis
            for inflammatory disease such as urinary tract infections.   The diagnosis of congenital PSS in dogs is the same as in
            PU-PD  with  hyposthenuric  urine  are  relatively  common;   cats (see  Chapter 35) and relies on visualizing the shunt-
            this is probably multifactorial in etiology and partly caused   ing vessel ultrasonographically, with computed tomogra-
            by reduced renal medullar concentrating gradient (see   phy (CT) angiography or portovenography (Fig. 36.11, or
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