Congenital Extrahepatic Portosystemic Deviation of Gastric Vein with Azygos in a Bitch

Background: Portosystemic shunt (PSS), an alteration commonly found in toy dogs, is caused by an anastomosis between the systemic and portal circulation, interfering with the metabolism of several toxins. It can be of congenital or acquired origin and is classified as intra- or extrahepatic. Clinical signs include the gastrointestinal tract, nervous system, and urinary system according to the fraction of the shunt. It is diagnosed by several imaging tests and exploratory laparotomy. Therapy involves drug therapy and/or surgical correction of the anomalous vessels. Thus, the aim is to present an unusual case of extrahepatic cPSS originating from the left gastric vein and insertion into the azygos vein. Case: A 2-year-old female toy poodle, spayed, weighing 2.7 kg was treated with a history of recurrent cystitis and neurological signs such as focal seizures, ataxia, tremors, blindness, lethargy, head pressing, and compulsive gait. Complementary tests revealed normochromic microcytic anemia, neutrophilia-induced leukocytosis, monocytosis, and lymphopenia. Biochemical analysis revealed hypoproteinemia due to hypoglobulinemia, an increase in alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase, and a decrease in urea. In the urinalysis, ammonium biurate crystals were detected, and Doppler ultrasound revealed microhepathy and the presence of an anomalous gastrosplenic vein inserted into the azygos vein, a finding compatible with the congenital extrahepatic PSS. Abdominal tomography confirmed vascular deviation with a sinuous path originating from the left gastric and splenic veins, inserting into the azygos vein, measuring approximately 5.95 cm in length. Cranial tomography revealed changes consistent with hepatic encephalopathy. Drug therapy was performed with hydration, liver chow, lactulose, probiotics, metronidazole, S-adenosyl-L-methionine, and ursodeoxycholic acid, and after 15 days, surgery was performed to place a 3.5 mm ameroid constrictor ring for gradual occlusion of the anomalous vessel. The animal recovered well, and a control abdominal ultrasound was repeated 30 days after the procedure, noting that the constrictor had not yet fully occluded the deviation. Doppler imaging revealed a favorable evolution with an increase in the diameter of the portal vein in the hepatopetal direction. The patient was followed-up for a year and had a normal and healthy life. Discussion: Extrahepatic PSS is frequently diagnosed in purebred and toy dogs, commonly occurring between the portal vein and one of its tributaries, with a lower frequency of anomalous vessels between the azygos veins, as in the present report. The patient's age and clinical signs were compatible with the disease, in addition to ammonia biurate crystals and hematological and biochemical alterations. The neurological clinical signs observed were compatible with hepatic encephalopathy secondary to congenital PSS. The imaging examinations facilitated the identification of the extrahepatic vascular anomaly, with the tomography being more accurate and helping in proper surgical planning. Clinical treatment should be performed for presurgical stabilization, and occlusion can be performed by placing cellophane bands or an ameroid constrictor, which is the technique of choice for congenital PSS, as it allows for slow constriction to avoid acute portal hypertension, as in this case, emphasizing that anesthesia in animals with portosystemic shunts must be performed with care.