• Journal of Veterinary Clinics
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• v.41 no.2
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• pp.95-100
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• 2024

A 6-year-old neutered male Poodle with a body weight of 2.7 kg was diagnosed with a congenital extrahepatic portoazygos shunt presented with progressive hepatic encephalopathy. Five days after surgical attenuation, the patient showed post-attenuation neurological signs (PANS) such as generalized tonic-clonic seizure, dull mentation, and tremor. PANS were successfully managed with antiepileptic drugs, but third-space fluid accumulation (ascites and peripheral edema) and phlebectasia were newly identified, suggesting marked portal hypertension (PHT). Telmisartan, spironolactone, carvedilol, and prednisolone were sequentially administered. Three months after surgery, both abnormal clinicopathological values such as anemia and hypoalbuminemia, and clinical signs completely resolved. Herein, we report successful management strategies for PANS and PHT in a dog following surgical attenuation of a congenital portoazygos shunt.

• Journal of Veterinary Clinics
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• v.37 no.2
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• pp.88-90
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• 2020

A one year old spayed female Bichon Frise dog presented with gait abnormalities and seizure. Serum biochemical results showed elevated levels of alkaline phosphatase, alanine aminotransferase, and ammonia. Serum bile acid level was also increased to be over 30 μmol/L on preprandial. Urinalysis identified the presence of ammonium urate crystal. Abdominal ultrasonography and CT revealed aberrant, tortuous, and multiple small vessels connected to the caudal vena cava between left kidney and caudal vena cava. Macroscopic specific findings associated with extrahepatic congenital portosystemic shunts (PSS) or other liver diseases were not identified. Liver biopsy was performed. Histopathologic evaluation revealed hepatic lobular hypoplasia with portal arterial duplication and vascular shunts. Based on these finding, this case was diagnosed as multiple acquired PSS secondary to hepatic microvascular dysplasia (HMD) and hepatic encephalopathy. A liver biopsy is recommended to differentiate HMD from other liver diseases and to confirm HMD when a young dog has multiple acquired PSS.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.308.1-308.1
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• 2003

We underwent this study to know correlation between the amount of portosysternic shunt/hepatic fibrosis and bioavailability parameters such as AUC, Cmax, Tmax and t1 /2 of high extraction ratio drug, propranolol, in CCl4-induced liver cirrhosis model of rats. This study describes the bioavaility study of propranolol(5 mg/kg), Shunt Index using thallium-201 per rectum scintigraphy to to measure the amount of portosystemic shunt indirectly and intrahepatic hydroxyproline content performed in the CCl4-induced liver cirrhosis model of rats. (omitted)

• Journal of Veterinary Clinics
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• v.16 no.2
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• pp.514-518
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• 1999

Portosystemic shunts in 3 Dogs with respiratory sign of cough and with dementia signs characterized by hypersensitivity, salivation, and seizure were diagnosed at veterinary teaching hospital of Seoul National University. In radiographs, microhepatica was observed. In abdominal ultrasonography, abnormal intrahepatic connections between the portal vein and the systemic vessels and tortuous vascularity were found. There was no complication such as ammonium urate urolith in kidney or urinary bladder, These dogs were treated with medicine and protein-restricted diet.

• Journal of Veterinary Clinics
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• v.30 no.4
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• pp.273-277
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• 2013

This study was performed to compare clinical and diagnostic imaging features between asymptomatic and symptomatic extrahepatic portosystemic shunts in dogs. The data of thirty patients diagnosed with extrahepatic PSS by multi-detector CT were reviewed, and the dogs were divided into asymptomatic (9/30) and symptomatic (21/30) groups. Signalments, hematologic results, liver size, morphologic classifications and main portal vein to abdominal aortic ratio (PV/AO) at the porta hepatis level from CT images were evaluated in two groups. Shih-tzu (5/9) was the most frequent breed in asymptomatic group, and various breeds were presented in symptomatic group. Mean age of asymptomatic group ($9.2{\pm}3.2$ years) was significantly higher than that of symptomatic group ($4.5{\pm}3.2$ years). The most morphologic form of shunt vessel was the splenophrenic shunt (16/30). PV/AO of asymptomatic group ($1.1{\pm}0.19$) was significantly higher than the values of symptomatic group ($0.55{\pm}0.19$). Clinical signs, hematologic results and diagnostic imaging findings of asymptomatic PSS are too nonspecific to suspect PSS. Therefore, considering of patient's age and CT examination with application of PV/AO ratio could be useful for the diagnosis of asymptomatic PSS.

• Journal of Veterinary Clinics
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• v.20 no.4
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• pp.508-515
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• 2003

A 4-month-old 5.7 kg male Golden retriever with history of seizure, depression, lethargy and anorexia was referred to Veterinary Medical Teaching Hospital, Chungbuk National University. Hematologic examination revealed microcytosis and nonregenerative anemia. Serum chemical values showed increased serum ammonia (423 $\mu$mol/L), ALP (1101 U/L), r-GTP (13.9 U/L) and CPK (1454 U/L), and decreased total protein (4.9 g/dl) and BUN (1.6 mg/dl). Microhepatia was shown in survey abdominal radiographs. Color doppler ultrasonographic examination revealed dilated tortuous vein with turbulent flow within liver parenchyma. Intraoperative jejunoportography and intraoperative ultrasonography confirmed the location and size of single intrahepatic shunt vessel in the left medial liver lobe. Also, the anomalous vessel entering the caudal vena cava was identified beneath the diaphragm. The shunting vessel was ligated with using an Ameroid constrictor. General conditions, hematologic and serum chemical values resolved gradually after surgery. One month after surgery abdominal radiograph showed normal gastric axis and it was consistent whit the normal size liver. Normal echogenecity of liver and enlargement of portal vein were shown in ultrasonography. It is assumed that survey radiography and ultrasonography are useful for diagnosis of single intrahepatic shunt in a dog and especially jejunoportography vein portography and intraoperative ultrasonography are suitable for confirmation of the anatomic location and size of the shunting vessels.

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2007.05a
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• pp.176-176
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• 2007

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2009.04a
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• pp.308-308
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• 2009

• Korean Journal of Veterinary Research
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• v.59 no.3
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• pp.171-173
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• 2019

Two dogs presented with vomiting and head pressing. In both dogs, a large vessel was revealed in computed tomography (CT) angiography, which was found to leave the portal vein (PV) cranial to the splenomesenteric confluence and enter the pre-hepatic caudal vena cava cranial to the right renal vein. The flow of portal blood to the liver was not identified. Based on CT angiography, the dogs were suspected to have congenital PV aplasia with portocaval shunting. Diagnostic imaging of potential malformations for PV continuation should be conducted before attempting shunt closure.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.11 no.1
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• pp.56-59
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• 2008

Extrahepatic portosystemic shunts, known as Abernethy malformations, were first reported by John Abernethy in 1793. They are classified into two types: Type I refers to a congenital absence of the portal vein and Type II refers to a shunt involving a side-to-side anastomosis with reduced portal blood flow into the liver parenchyma. This malformation is so rare that less than 100 cases have been reported in the medical literature. We report the case of a 13-month-old boy who had a congenital extrahepatic portocaval shunt with a hypoplastic portal vein. This case was complicated with an atrial septal defect and a large hyperplastic nodule in the liver. The patient was diagnosed with a Type II Abernethy malformation. We planned on surgical occlusion of the extrahepatic portocaval shunt. However, six months later, the patient had a sudden onset of a fever of unknown origin and developed hepatic encephalopathy. Although he underwent a liver transplantation, he died of acute hepatic failure.