In dogs, protein C may be useful in distinguishing CPSS from portal vein hypoplasia (also known as microvascular dysplasia).11 Dogs with CPSS have significantly lower protein C activities than dogs with portal vein hypoplasia.11 When protein C activity is considered with other laboratory findings, it may be useful to distinguish CPSS from portal vein hypoplasia.
Low protein C activity levels have been reported in people with a variety of liver diseases including inflammatory hepatopathy, cirrhosis, portal vein obstruction, and neoplastic infiltration.9,10 Protein C activity levels may be used to assess hepatic function in a variety of liver diseases. In human patients, measurement of protein C levels has been used to assess liver function. Once activated, protein C works to promote fibrinolysis, modulate inflammation, and inhibit apoptosis. Protein C is a vitamin K–dependent serine protease enzyme that is synthesized by the liver. Along with antithrombin, protein S, and plasminogen, protein C is important for preventing thromboembolic disease. Protein C is a plasma anticoagulation protein. Recently, some veterinarians have begun testing protein C activity. A complete blood count (CBC), serum biochemistry profile, urinalysis, and preprandial and postprandial serum bile acids, and/or ammonia level are recommended. Clinicopathologic Findings Laboratory testing is among the first steps recommended in the diagnostic workup of dogs suspected to have CPSS. Although some aspects of the diagnostic workup and treatment of CPSS have remained similar for several years, other aspects have changed dramatically. 2 Thieman Mankin recently, minimally invasive methods of CPSS occlusion have been described.3–8 Laparoscopic placement of cellophane bands has been described in dogs with extrahepatic CPSS, and endovascular occlusion has been described in dogs with either intrahepatic or extrahepatic CPSS.3 DIAGNOSTICS Diagnosis and treatment of CPSS in dogs has evolved with technology. Department of Small Animal Clinical Sciences, Texas A&M University, College of Veterinary Medicine, 4474 TAMU, College Station, TX 77843-4474, USA E-mail address: Vet Clin Small Anim - (2015) -– 0195-5616/15/$ – see front matter Ó 2015 Elsevier Inc. These surgical procedures should result in CPSS closure over approximately 2 to 5 weeks and good clinical results. This goal is often accomplished through open surgical techniques, including ameroid constrictor or cellophane band placement. Operative intervention is often recommended with the goal being slow closure of the anomalous vessel to gradually accustom the liver to increased blood flow and prevent the development of portal hypertension. Typically, a single CPSS is present, although multiple CPSS have been reported.2 The presence of a CPSS allows portal blood to bypass the liver and enter the systemic circulation. Congenital portosystemic shunts (CPSS) are vascular anomalies that occur secondary to inappropriate closure of different portions of fetal vasculature, resulting in intrahepatic or extrahepatic CPSS. A thorough review of portosystemic vascular anomalies was published in 2009.1 Recent information on portosystemic shunts is presented. INTRODUCTION This article focuses on current concepts in portosystemic shunts. Less invasive options for the treatment of intrahepatic and extrahepatic CPSS include laparoscopic placement of cellophane bands and interventional radiologic techniques such as coil embolization. Commonly performed open surgical procedures for congenital portosystemic shunt (CPSS) include the placement of ameroid constrictors or cellophane bands. Many methods of diagnostic imaging are available, including ultrasonography, nuclear scintigraphy, CT angiography, and MR angiography. Thieman Mankin, DVM, MS, DACVS-SA KEYWORDS Shunt Extrahepatic Intrahepatic Surgical management Embolization KEY POINTS Protein C level testing may be a useful blood test to indicate liver dysfunction. C u r ren t C o n c e p t s i n C o n g e n i t a l Po r t o s y s t e m i c Shunts Kelley M.
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