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Surgical treatment of vascular malformations
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Introduction
The most common vascular malformation diagnosed in small animal patients are congenital and acquired portosystemic shunts. Other visceral vascular malformations include hepatic arterioportal fistulas (APF), arteriportal malformations (APM) and aorticopulmonary malformations. Acquired vascular malformations are also sporadically diagnosed and can arise following trauma or within vascular tumours. In man, visceral vascular anomalies account for only 7.6% of vascular malformations with the remainder being cutaneous lesions on the head/neck, trunk or extremities that are classified as infantile haemagioma, cavernous haemangioma or haemangioendothelioma. This presentation will focus on the surgical management of less common vascular malformations and will ignore the more common congenital portosystemic shunts since they are already well described.
Extracardiac shunt pathophysiology (indirect evidence of malformation)
If sufficient blood is allowed to shunt from a systemic artery into a systemic vein, the portal vein or a pulmonary artery, supraphysiological hydrostatic pressure develops in the non-systemic arterial side of the system. If the communication is directly between a systemic artery and a systemic vein and the venous structure is large enough to accommodate all the additional flow, the pathophysiology is similar to a cardiac shunt such as left to right shunting patent ductus arteriosus, ventricular or atrial septal defect. A recirculation “loop” of blood circulation develops that causes relative overload of each vessel and heart chamber within that “loop”. Using a simple post-traumatic arteriovenous communication between the femoral artery and femoral vein as an example; the circuit includes the entire aorta to the level of the femoral artery, the femoral vein all the way back through the caudal vena cava, the right atrium, right ventricle, pulmonary artery, pulmonary vein and left atrium and left ventricle. In this example, if sufficient flow is present, left and right heart chamber enlargement, atrioventricular valvular incompetence, pulmonary vascular engorgement and caudal caval engorgement should be anticipated because of the volume overload. Signs of heart failure and heart murmur are often evident along with features of generalised volume overload on cardiac echo. In addition to the direct effect of the shunting blood, the increase in hydrostatic pressure in the lower pressure limb of the circuit will cause acquired collateral shunting vessels to develop. This is most pronounced in hepatic arterial to portal vascular communications which typically provoke the development of a myriad of extrahepatic shunting vessels (multiple acquired shunts – MAS). [...]
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