Portosystemic shunts are vascular anomalies that divert portal blood away from the liver and into the systemic circulation.1,2 They may be congenital or acquired.1,2 Congenital, single, extrahepatic portosystemic shunts are the most common category in dogs and cats with a high incidence in certain breeds of dogs.1,2
Up to 68% of dogs with congenital portosystemic shunts will develop portal hypertension when surgically treated with acute shunt ligation.3,4 Gradual occlusion of the aberrant vessel is preferred, thereby allowing the cardiovascular and nervous systems to adapt to changes in portal blood flow. This reduces the risk of developing acute portal hypertension or perioperative seizures.5 Various methods have been described to achieve gradual attenuation and ultimate closure of the shunt vessel.1–7
One of the most commonly used methods for gradual attenuation is the use of an ARC. Ameroid is a casein derivative that undergoes rapid volumetric expansion that plateaus in 60 days.4–11 The ameroid core is surrounded by an outer stainless steel ring. Occlusion likely results from a combination of the following 3 mechanisms: reduction in external vessel diameter caused by centripetal swelling of the ameroid, fibroblastic response within the vascular wall at the site of application, and ultimate formation of intraluminal thrombi arising concentrically from the intima.5,9 Factors including size, shape, encasement of the ameroid ring, and the type and temperature of the surrounding fluid modify the expansion pattern.7 More recently, the rate of constriction has been shown to be influenced by the protein concentration of the surrounding fluid.12 Total luminal obliteration of a portosystemic shunt with these devices takes 4 to 5 weeks.5 This has been documented via measurement of shunt fraction by use of transcolonic portal scintigraphy.5,13
Despite the benefits associated with ARC use, compared with acute, complete ligation, the use of ARCs is not entirely benign. In a retrospective study by Mehl et al,14 80% of owners reported an excellent outcome despite 21% of the dogs being diagnosed with persistent shunting in patients in which an ARC was used for shunt attenuation.14 A mortality rate of 9% was also reported.14 It has been proposed that acute kinking of the shunt vessel after ARC placement could account for increased morbidity and mortality rates in a manner similar to acute suture ligation of the shunt vessel, especially in smaller patients.10,15 Two main theories regarding the cause of vascular kinking are the overzealous perivascular dissection and the effect of the relative high weight of the ARC upon the small and compliant vessel.
The outer stainless steel portion of the ring accounts for a large percentage of the weight of the ARC. Because the vessels are low-velocity and low-pressure vessels, changes in the flow rate and diameter can lead to a loss of normal laminar blood flow. Poiseuille's law states that the laminar flow rate of an incompressible fluid along a cylinder is proportional to the fourth power of the radius of the cylinder. Therefore, temporary kinking or flattening of a shunt vessel can lead to a dramatic change in flow turbulence, which can in turn lead to larger and more abrupt thrombogenesis. These events would ultimately lead to a rapid or acute closure of the shunt vessel rather than the desired gradual and progressive one.
By removing the outer stainless steel ring, the weight of the ARC implant is greatly reduced. In smaller patients, some veterinary surgeons will place the ARC without the outer stainless steel portion in place to reduce the weight of the ring. Theoretically, this may minimize the potential risk of shunt vessel kinking. To our knowledge, the effects of removing the stainless steel ring on ameroid expansion pattern and the weights of the constrictor components have not been reported.
The purpose of the study reported here was to evaluate and quantify dimensional changes of ARCs over time in vitro with and without the outer stainless steel ring in place. We hypothesized that changes in measured dimensional variables would not be different between ARCs with the stainless steel outer ring in place versus those without the stainless steel outer ring.
Ameroid ring constrictor
Research Instruments NW Inc, Lebanon, Ore.
Scientific Products-American Hospital Supply Corp, McGaw Park, Ill.
AE50, Mettler-Toledo Inc, Columbus, Ohio.
DSC-S75, Sony Corp, Tokyo, Japan.
Digimatic caliper, model No. CD-6”CS, Mitutoyo Corp, Aurora, Ill.
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Martin RA. Congenital portosystemic shunts in the dog and cat. Vet Clin North Am Small Anim Pract 1993;23:609–623.
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Lange PE, Seivers HH, Numberg J, et al. A new device for slow progressive narrowing of vessels. Basic Res Cardiol 1985;80:430–435.
Murphy ST, Ellison EW, Long M, et al. A comparison of the ameroid constrictor versus ligation in the surgical management of single extrahepatic portosystemic shunts. J Am Anim Hosp Assoc 2001;37:390–396.
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Sereda CW, Adin CS. Methods of gradual vascular occlusion and their application in treatment of congenital portosystemic shunts in dogs: a review. Vet Surg 2005;34:83–91.
Monnet E, Rosenberg A. Effect of protein concentration on rate of closure of ameroid constrictors in vitro. Am J Vet Res 2005;66:1337–1340.
Van Vechten BJ, Komtebedde J, Koblik PD. Use of transcolonic portal scintigraphy to monitor blood flow and progressive postoperative attenuation of partially ligated single extrahepatic portosystemic shunts in dogs. J Am Vet Med Assoc 1994;204:1770–1774.
Mehl ML, Kyles AE, Hardie EM, et al. Evaluation of ameroid ring constrictors for the treatment for single extrahepatic portosystemic shunts in dogs: 168 cases (1995–2001). J Am Vet Med Assoc 2005;226:2020–2030.
Tisdall PLC, Hunt GB, Youmans KR, et al. Neurological dysfunction in dogs following attenuation of congenital extrahepatic portosystemic shunts. J Small Anim Pract 2000;41:539–546.
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