Arterio-venous malformations (AVM) are one of various congenital vascular malformations that result from a failure of orderly resorption of the primitive blood vessels in weeks 4–6 of gestation involving the vessels of both arterial and venous origins and resulting in high-flow direct AV communications between different sized vessels (AVMs), vein malformations, and lymphatic malformations. An AVM is defined as a high flow, low resistance communication between the arterial and venous systems without an intervening normal capillary system. Thus, the pivotal function of the capillary system—which is to maintain the delicate balance between the high-pressure (arterial) and low-pressure (venous) system—is not present, thereby, causing arterialized venous pressure increases secondary to the AV shunts, and the tissue normal venous drainage slows and becomes delayed having difficulty competing with the higher pressure arterialized veins. This leads to tissue edema due to venous hypertension [1]. Peripheral AVMs are the least common type representing 5–20% of all congenital vascular malformations. Most of the current data regarding incidence and prevalence of AVMs are based on cerebrospinal AVMs. They are rare and usually go undetected until clinical symptoms appear in patients aged 20–40 years [2]. AVMs are the most complex type of congenital vascular malformations with significant hemodynamic alterations to both the arterial and venous systems, which if they are large and centrally positioned in the body (eg, shoulder, chest, abdomen, pelvis, buttock) can induce high flow cardiac output failure (right heart volume overload), arterial insufficiency (steal) in the affected tissue, and chronic venous hypertension.