 Introduction/Background Vascular anomalies encompass a broad range of pathologies histologically composed of vascular type cells. These lesions are most commonly classified by the International Society for the Study of Vascular Anomalies according to their underlying histology as either vascular malformations or vascular tumors. Vascular malformations represent focal structural abnormalities of the vascular tree, typically related to developmental errors during vasculogenesis [1], whereas, vascular tumors are caused by neoplastic cellular proliferation of the endothelium [1]. The extremities are the most common site of these vascular lesions outside of the head and neck [1,2]. Vascular malformations more commonly represent isolated spontaneous lesions yet can be part of one of several syndromes such as Parkes Weber syndrome [1,3]. These typically grow commensurate with patient age, often in conjunction with hormonal changes, such as puberty and pregnancy [3-6]. Therefore, vascular malformations that are present at birth may not present clinically until adolescence or adulthood. These lesions can be broadly divided into high- and low-flow lesions. High-flow malformations include arteriovenous malformations and arteriovenous fistulas, both of which demonstrate arterial flow and arteriovenous shunting. The former tend to be congenital lesions, and the latter are typically acquired as sequela of prior trauma or surgery. High-flow lesions comprise approximately 10% of peripheral vascular malformations and may present with pain, skin discoloration, warmth, or mass with palpable thrill or bruit [6]. Compression neuropathy, soft-tissue ulceration, bleeding, arterial steal phenomenon, and high-output cardiac failure may be seen in extreme cases [4,7]. Low-flow lesions include capillary, venous, and lymphatic malformations and are overall more common than high-flow lesions.
Clinically Suspected Vascular Malformation of the Extremities.  Introduction/Background Vascular anomalies encompass a broad range of pathologies histologically composed of vascular type cells. These lesions are most commonly classified by the International Society for the Study of Vascular Anomalies according to their underlying histology as either vascular malformations or vascular tumors. Vascular malformations represent focal structural abnormalities of the vascular tree, typically related to developmental errors during vasculogenesis [1], whereas, vascular tumors are caused by neoplastic cellular proliferation of the endothelium [1]. The extremities are the most common site of these vascular lesions outside of the head and neck [1,2]. Vascular malformations more commonly represent isolated spontaneous lesions yet can be part of one of several syndromes such as Parkes Weber syndrome [1,3]. These typically grow commensurate with patient age, often in conjunction with hormonal changes, such as puberty and pregnancy [3-6]. Therefore, vascular malformations that are present at birth may not present clinically until adolescence or adulthood. These lesions can be broadly divided into high- and low-flow lesions. High-flow malformations include arteriovenous malformations and arteriovenous fistulas, both of which demonstrate arterial flow and arteriovenous shunting. The former tend to be congenital lesions, and the latter are typically acquired as sequela of prior trauma or surgery. High-flow lesions comprise approximately 10% of peripheral vascular malformations and may present with pain, skin discoloration, warmth, or mass with palpable thrill or bruit [6]. Compression neuropathy, soft-tissue ulceration, bleeding, arterial steal phenomenon, and high-output cardiac failure may be seen in extreme cases [4,7]. Low-flow lesions include capillary, venous, and lymphatic malformations and are overall more common than high-flow lesions.