Treatment of Scalp Arteriovenous Malformation

Abstract

We report seven patients with scalp arteriovenous malformations, including two patients with lesions > 10 cm in diameter, who were successfully treated. The principal complaint of each patient was a deforming mass. Each of four patients had a history of blunt traumatic injury. The lesions, each consisting of the nidus, feeders, and draining veins, evolved in all patients. The nidus consisted of fistulae, which exhibited various angioarchitectures as revealed by angiography. A hemangiomatous component was histologically recognized in one patient. In five patients, in whom the lesions were relatively small and whose nidi included only large fistulae, the malformations were remedied by surgical intervention alone or were cured with embolization alone using liquid adhesives. In the two patients with lesions > 10 cm, the nidi consisted of numerous large fistulae and plexiform fistulae in one patient and plexiform fistulae and a hemangiomatous component in the other patient. These patients were treated with a combination of transarterial embolization and surgical intervention. Preoperative embolization greatly reduced blood loss during resection. Total excision and scalp reconstruction using a soft tissue expander were performed in both patients. The cosmetic results were excellent in all of the patients, and no recurrence has been recognized during the follow-up period, which ranges from 31 to 99 months. The treatment of scalp arteriovenous malformations should strive to improve deforming features and to attain a permanent cure. Because each nidus includes a variety of anomalous angioarchitectural features, there should be different means and a combination of treatments for each patient. Embolization alone could be adequate treatment in relatively small lesions, the nidi of which consist only of several large fistulae. For malformations with more extensive, large fistulae or with anomalous components other than large fistulae, a combined endovascular and surgical approach and scalp reconstruction seems to be the best treatment.

Successful surgical management of post-traumatic cirsoid aneurysm

“…It has been hypothesized that a functionally non-patent fistula may be present before the inciting incident, the abundant scalp collaterals aid in slow growth of the swelling and other associated symptoms once the fistula becomes functional. 3 The main arterial feeders originate in the external carotid, occipital and supraorbital arteries. Superficial temporal artery is found to commonly feed post-traumatic cirsoid aneurysms, this may be accounted to the long and superficial course of the artery on the scalp.…”

Arteriovenous malformation of external ear and temporal region: a case report

“…It is generally thought that AVM arises from multiple developmental defects causing the primitive capillary bed to fail to persist. 3,4 Arteriovenous malformations are rare in the auricular region but are common intracranially. They can be divided into two categories: fast-flowing and slowflowing lesions.…”

Giant scalp arteriovenous malformation

“…Their clinical signs are associated with the size of AVMs. Associated symptoms and signs include pain, throbbing headaches and bruit, 3,8,9 hemorrhage, 8,10 seizures and psychomotor retardation. 11 Large lesions have also been associated with scalp necrosis.…”

“…11 Large lesions have also been associated with scalp necrosis. 8 AVMs cause direct shunting of high-volume arterial blood through low-resistance arteriovenous fistulae, often resulting in venous hypertension, hypoperfusion of vessels and tissue downstream, and reduced cerebral perfusion, known as the steal phenomenon. 12 About 10 to 20% of scalp AVMs develop following penetrating or non-penetrating trauma to the scalp.…”