Surgical Attenuation Of Congenital Portosystemic Shunts Research Articles

Congenital Portosystemic Shunts in Dogs and Cats: Treatment, Complications and Prognosis.

Congenital portosystemic shunts (CPSS) are a common vascular anomaly of the liver in dogs and cats. Clinical signs of CPSS are non-specific and may wax and wane, while laboratory findings can raise the clinical suspicion for CPSS, but they are also not specific. Definitive diagnosis will be established by evaluation of liver function tests and diagnostic imaging. The aim of this article is to review the management, both medical and surgical, complications, and prognosis of CPSS in dogs and cats. Attenuation of the CPSS is the treatment of choice and may be performed by open surgical intervention using ameroid ring constrictors, thin film banding, and partial or complete suture ligation or by percutaneous transvenous coil embolization. There is no strong evidence to recommend one surgical technique over another. Medical treatment strategies include administration of non-absorbable disaccharides (i.e., lactulose), antibiotics, and dietary changes, and are indicated for pre-surgical stabilization or when surgical intervention is not feasible. After CPSS attenuation, short- and long-term post-surgical complications may be seen, such as post-operative seizures and recurrence of clinical signs, respectively. Prognosis after surgical attenuation of CPSS is generally favorable for dogs and fair for cats.

Incidence and risk factors for neurological signs after attenuation of a single congenital portosystemic shunt in 50 cats.

To determine the incidence, outcome, and risk factors for postattenuation neurological signs (PANS) in cats treated for single congenital portosystemic shunts (CPSS). Retrospective cohort study. Cats (n = 50) with a single CPSS. Medical records of cats treated by surgical attenuation of a single CPSS between 2003 and 2017 were reviewed for signalment, surgical technique, preoperative management and postoperative clinical outcomes. Binary logistic regression was performed to investigate risk factors for occurrence of PANS and seizures. Congenital portosystemic shunts in 50 cats included 40 extrahepatic and 10 intrahepatic shunts. Postattenuation neurological signs were recorded in 31 (62%) cats and graded as 1 in 10 cats, 2 in nine cats, and 3 in 12 cats. Postattenuation neurological signs included seizures in 11 cats. Five of 31 cats with PANS did not survive to discharge. No association was detected between PANS or seizures and the type of CPSS (intrahepatic or extrahepatic), degree of attenuation, age, or the use of perioperative levetiracetam or hepatic encephalopathy immediately preoperatively. Osmolality at a median 24 hours postoperatively was lower in cats with PANS (P < .049, Wald 3.867, odds ratio [Exp(B)] 0.855, CI 0.732-0.999). Postattenuation neurological signs are common complications in cats treated for CPSS. Preoperative levetiracetam did not prevent the occurrence of PANS or seizures. The only risk factor for PANS detected was lower postoperative Osmolality in cats with PANS at 24 hours. Postattenuation neurological signs including seizures occur frequently in cats undergoing surgical attenuation of a CPSS. Preoperative levetiracetam did not protect against the development of PANS.

Markers of angiogenesis associated with surgical attenuation of congenital portosystemic shunts in dogs.

BackgroundDogs with congenital portosystemic shunts (CPSS) have hypoplasia of the intrahepatic portal veins. Surgical CPSS attenuation results in the development of the intrahepatic portal vasculature, the precise mechanism for which is unknown, although new vessel formation by angiogenesis is suspected.HypothesisThat the degree of portal vascular development and the increase in portal vascularization after CPSS attenuation is significantly associated with hepatic vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2) gene expression and serum VEGF concentration.AnimalsClient‐owned dogs with CPSS undergoing surgical treatment. Forty‐nine dogs were included in the gene expression data and 35 in the serum VEGF data.Materials and MethodsDogs surgically treated by partial or complete CPSS attenuation were prospectively recruited. Relative gene expression of VEGF and VEGFR2 was measured in liver biopsy samples taken at initial and follow‐up surgery using quantitative polymerase chain reaction. Serum VEGF concentration was measured before and after CPSS attenuation using a canine specific ELISA. Statistical significance was set at the 5% level (P ≤ .05).ResultsThere was a significant increase in the mRNA expression of VEGFR2 after partial attenuation (P = .006). Dogs that could tolerate complete attenuation had significantly greater VEGFR2 mRNA expression than those that only tolerated partial attenuation (P = .037). Serum VEGF concentration was significantly increased at 24 (P < .001) and 48 (P = .003) hours after attenuation.Conclusions and Clinical ImportanceThese findings suggest that intrahepatic angiogenesis is likely to occur after the surgical attenuation of CPSS in dogs, and contributes to the development of the intrahepatic vasculature postoperatively.

Association between hepatic histopathologic lesions and clinical findings in dogs undergoing surgical attenuation of a congenital portosystemic shunt: 38 cases (2000–2004)

To review hepatic histopathologic lesions in dogs undergoing surgical attenuation of a congenital portosystemic shunt (CPSS) in relation to clinical findings and tolerance of complete surgical attenuation. Retrospective case series. 38 dogs that underwent surgical attenuation of a CPSS. Hepatic histologic examination findings and medical records of dogs undergoing surgical attenuation of a single CPSS between August 2000 and July 2004 were reviewed. Liver biopsy specimens were obtained from 38 dogs during surgery prior to complete (n = 16) or partial (22) attenuation of a CPSS and from 13 of the same dogs a median of 3 months following surgical attenuation. Portal tracts were inadequate for interpretation in 2 liver biopsy specimens. Liver biopsy specimens obtained prior to surgical attenuation of a CPSS had a lack of identifiable portal veins (13/36 dogs), hepatic arteriolar proliferation (25/36), ductular reaction (5/36), steatosis (16/38), and iron accumulation (32/38). Lack of identifiable portal veins on histologic examination was associated with increased hepatic arteriolar proliferation, decreased tolerance to complete surgical CPSS attenuation, and decreased opacification of intrahepatic portal vessels on portovenography. Ductular reaction was always associated with failure to tolerate complete surgical attenuation of a CPSS. Surgical CPSS attenuation resulted in significant clinical, serum biochemical, and portovenographic changes indicative of improved liver function, but only subtle changes in hepatic histologic examination findings. Dogs without identifiable intrahepatic portal veins that had a ductular reaction on hepatic histologic examination were less likely to tolerate complete attenuation of a CPSS.