Outcomes after extrahepatic portosystemic shunt ligation in 49 dogs.

Department of Veterinary Clinical Sciences, University of Sydney, New South Wales.
Australian Veterinary Journal (Impact Factor: 0.92). 06/1999; 77(5):303-7. DOI: 10.1111/j.1751-0813.1999.tb10268.x
Source: PubMed

ABSTRACT To evaluate outcomes after attenuation of extrahepatic portosystemic shunts in dogs using surgical silk.
Retrospective study.
Case records were reviewed for degree of surgical attenuation, experience of the primary surgeon, perioperative mortality and problems related to persistent portosystemic shunting or shunt ligation. Presence of portosystemic shunting after surgery was evaluated by ammonia tolerance testing, measurement of postprandial serum bile acid, plasma urea and cholesterol concentrations and liver enzyme activity. The influence of age, postocclusion portal pressure, primary surgeon, degree of attenuation and postoperative biochemical findings on the occurrence of postoperative problems was assessed.
The mortality rate was 2.1%. Shunt attenuation was complete in 34% and partial in 66% of dogs. Portal hypertension necessitating ligature removal was encountered in only one dog. Five dogs experienced neurological abnormalities (seizures or ataxia), possibly as a manifestation of 'postligation seizure syndrome'. Postoperative liver function was normal in 78% of dogs, including 70% with partial shunt attenuation. Experience of the surgeon was related positively to outcome after partial attenuation (P = 0.002). Postoperative biochemical evidence of abnormal liver function was the most sensitive predictor of recurrence of clinical signs referable to persistent portosystemic shunting.
In the hands of an experienced surgeon, surgical attenuation of single extrahepatic shunts was safe and effective, even in animals with partial attenuation. Most dogs with biochemical evidence of persistent shunting suffer relapse of clinical signs within 18 months of surgery. Postligation neurological syndromes of variable intensity may be more common than previously thought.

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    ABSTRACT: To determine if there were significant changes in prothrombin time (PT), partial thromboplastin time (PTT), and fibrinogen levels in dogs with naturally occurring congenital portosystemic shunts (CPSS) and to determine if there was any association between these values, serum albumin concentration, and the ability to attenuate the shunt vessel. Retrospective clinical study. Thirty-nine client-owned dogs. Medical records of 60 dogs with confirmed CPSS were retrospectively evaluated. Hemostatic profiles had been performed before surgery in 39 cases. Dogs with CPSS had significantly higher values for PTT (P < .001) when compared with normal dogs. Of the total number of dogs, 64.1% had a PTT greater than 16 seconds (25/39). PTT was prolonged by 25% or more in 51.3% of dogs (20/39). PT tended to be higher in dogs with CPSS (P = .036), although only 7.7% (3/39) of dogs had a PT greater than 12 seconds (the maximum reference value). Dogs with CPSS had significantly lower values for albumin and fibrinogen (P < .001). Platelet numbers were within the normal range in 87.2% of cases (34/39). Of the 5 dogs with platelet numbers outside the normal range, 3 were mildly thrombocytopenic. Fibrin degradation product concentrations were not elevated in any dogs tested (N = 22). There was no significant difference in any of the measured variables between dogs with extrahepatic shunts and those with intrahepatic shunts (P > .1). For PT, PTT, albumin, and fibrinogen, there was no significant difference between dogs that underwent total, partial, or no attenuation (P > .3). Dogs with CPSS have a tendency to have a prolonged PTT. There was no significant difference in hemostatic profile results between dogs with intrahepatic shunts versus extrahepatic shunts. Preoperative hemostatic profile abnormalities were not useful as predictors of ability to attenuate CPSS. Prolonged PTT was not associated with bleeding tendencies in any of the dogs. Assays of individual clotting factors may help to further characterize the abnormalities present in animals with CPSS and may identify specific factor deficiencies. This might enable identification of a noninvasive diagnostic or prognostic indicator.
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