Chapter 68 - Endovascular treatment of arteriovenous malformations

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Abstract

Cerebral arteriovenous malformations (AVM) are tangles of blood vessels that permit shunting of blood from the arterial to venous phase without intervening capillaries. The malformation’s arterialization of a low-pressure system creates a risk of rupture that is substantially higher when associated with an aneurysm. The annual hemorrhage rate is 2.2% per year as reported in the randomized trial of unruptured brain AVMs (ARUBA; rupture risk is increased after the first event. Ruptured AVMs have a 10% mortality rate and 20%–30% morbidity rate. The treatment of choice for AVMs is microvascular resection with or without preoperative embolization. Surgical risk can be stratified based on the Spetzler-Martin grading system. Liquid embolic material and coils may be used for the treatment of AVM associated aneurysms, especially in the setting of acute rupture as a bridge to delayed surgical resection. There is some limited reported success in total endovascular treatment of AVMs, but this is not considered standard therapy at this time. Stereotactic radiosurgery (SRS) has been recently described but mainly limited to AMVs deemed too risky to approach in an open fashion and limited to 2.5 cm–3 cm in size. The delayed protection from hemorrhage (approximately 2–3 years) and high marginal failure/recurrence rate are the greatest concerns.

Introduction

McCormick's classic histopathologic classification of cerebral vascular malformations defined arteriovenous malformations (AVM) as a tangle of blood vessels permitting the shunting of blood from the arterial to venous phase without intervening capillaries (McCormick, 1966, McCormick and Nofzinger, 1966, Morris, 2013). AVMs are often intermingled with gliotic brain parenchyma (Decker et al., 2010). The primary treatment is microsurgical resection of the AVM, relegating endovascular approaches to largely diagnostic or as an adjunct. Significant improvements in endovascular technology since the first description of cranial AVM embolization by Luessenhop and Spence (1960) have increased the role of embolization to include: palliative, adjunct to microsurgical resection, adjunct to stereotactic radiosurgery (SRS), or, in some cases, curative.

The majority of AVMs are sporadic and thought to be congenital, though the precise etiology is unknown (Van der Eecken and Adams, 1953, Alexander, 1988, Mullan et al., 1996, Lasjaunias, 2001, Novakovic et al., 2013, Robert et al., 2014). Posttraumatic and other de novo AVMs have been reported, challenging the classic school of thought (Gonzalez et al., 2005, Mahajan et al., 2009, Miller et al., 2014). Rarely, AVMs may be associated with genetic disorders such as Osler–Weber–Rendu and Wyburn–Mayson syndrome (Thomas-Sohl et al., 2004, Leblanc et al., 2009, McDonald et al., 2011).

Epidemiologic estimates are difficult given the rarity of cerebral AVMs; the occurrence rate for symptomatic disease is estimated at 0.94 per 100 000 person-years with a prevalence of less than 10.3 per 100 000 (Berman et al., 2000). Hemorrhage is the most common clinical presentation of AVMs, followed by seizure (Fults and Kelly, 1984, Jane et al., 1985, Itoyama et al., 1989, Turjman et al., 1995, Mohr et al., 2014). The hemorrhage rate of AVMs is reported to be between 1% and 4% (Ondra et al., 1990, Halim et al., 2004, Stapf et al., 2006). Prospective data from a randomized trial of unruptured brain AVMs (ARUBA) report a rate of 2.2% per year (Mohr et al., 2014). After rupture, the hemorrhage risk increases to 6–18% for the first year, then 2–4% per year thereafter (Graf et al., 1983, Nishioka et al., 1984, Jane et al., 1985, Mast et al., 1999). Ruptured AVMs have around 10% mortality rate and 20–30% morbidity rate, less than aneurysmal rupture (Graf et al., 1983, Itoyama et al., 1989). Infratentorial AVMs deserve special mention, as the mortality rate after hemorrhage approaches 50% and patients have a poorer acute and long-term prognosis than supratentorial AVMs (Graf et al., 1983, Wilkins, 1985, Ondra et al., 1990, Abla et al., 2014).

Section snippets

Anatomy and classification

Cerebral AVMs have three components: arterial feeder(s), nidus, and venous drainage (Fig. 68.1). They cause neurologic injury through two mechanisms: hemorrhage (from flow-related aneurysms, weakened arterial walls, the nidus, or the venous drainage) and vascular steal from the high-flow state, leading to ischemia or seizure. Aneurysms are associated with cerebral AVMs, have a 7% rate of hemorrhage, and should be obliterated when possible whether the goal is palliative, curative, or in

Microsurgical resection

Microsurgical resection is the historic gold standard for AVM treatment but requires careful planning and patient selection, and not all patients are candidates. Spetzler–Martin grades I and II (class A) are ideal for microsurgical resection and many grade III (class B) AVMs can be considered as well. Operator experience and center volume should be taken into account, as not all surgical series results are generalizable and patients should be referred to a more experienced operator if

Endovascular treatment

Endovascular treatment of AVMs is most often performed with liquid embolic material such as Onyx or N-butyl cyanoacrylate (NBCA) to occlude the nidus while avoiding migration or extravasation into the draining veins (Fig. 68.2). Total endovascular treatment is achieved in approximately 20% of cases; reports range from 10% to 58% (Roberts et al., 1998, Yu et al., 2004, Song et al., 2005, Katsaridis et al., 2008, Levy et al., 2015). Embolization complication rates range from 9% to 30% and the

Stereotactic radiosurgery

SRS for the treatment of cerebral AVMs began as early as 1972, with much improvement since (Steiner et al., 1972). Modalities commonly employed in SRS include Gamma Knife, proton bean radiosurgery, and linear particle accelerators. SRS can be used as a primary modality or an adjunct to embolization or microsurgical resection. AVM obliteration rates after single treatment SRS vary from 70% to 90% after 3 years (Lunsford et al., 1991, Friedman and Bova, 1992, Flickinger et al., 1996, Kano et al.,

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