T he literature regarding arteriovenous malformations (AVMs) of the external ear is sparse. Most of the treatment paradigms described in these papers include preoperative angiogram with or without embolization, followed by surgical excision. Here we present a case of a patient clinically diagnosed with an AVM of the external ear that was managed empirically with surgical excision, without recurrence. Our opinion is that these lesions can be excised without preoperative angiogram and/or embolization as long as they are small, well circumscribed and do not have clinical evidence of extensive collaterals. case presentationA 15-year-old male patient was referred for evaluation of an enlarging pulsatile mass of the left pinna. The patient noticed the mass two years before presentation. It was described as slow growing with intermittent pain. The patient denied bleeding or drainage from the mass. On examination, there was a 1.5 cm pulsatile, firm, but compressible mass of the inferior pinna, with an audible bruit. The mass extended from the helical rim inferiorly to the inferior sulcus of the ear (Figure 1). There was no evidence of superficial collaterals, ulcerations or active bleeding. Because of the high clinical suspicion of an AVM, the patient underwent excision of the lesion (Figure 2). Postoperatively, the patient was evaluated in the office at one, two and four weeks following resection without recurrence of a mass, pulsation or bruit. Final pathology revealed a benign AVM. To date there has been no clinical recurrence (Figure 3) DiscussionThe arterial origin of external ear vascular malformations can be from the posterior auricular, occipital, temporal and an occipital branch of the extracranial vertebral artery (2). Enlargement of the AVM may be triggered by trauma, infection or hormonal influences, such as pregnancy and puberty. Clinical manifestations of AVM are related to abnormal perfusion and mass effect.The exact pathogenesis of an AVM has not been clearly defined. One theory states that these malformations arise during fetal development as a result of the failure of regression of arteriovenous channels in the primitive retiform plexus. It has