Complication analysis of 469 brain arteriovenous malformations treated with N-butyl cyanoacrylate

Abstract

We independently assessed the frequency, severity and determinants of neurological deficits after endovascular embolization with NBCA of brain arteriovenous malformations (BAVMs) to have a better basis for making treatment decisions. All the charts of 469 BAVMs patients who underwent embolization with NBCA were reviewed. We analyzed the complications and their relation to angiographic features. The 469 patients were treated with 1108 endovascular procedures. Each met one to eight times, average 2.3 times. Eleven patients showed treatment-related complications, including four haemorrhagic and seven ischemic complications. Of these 11 cases, two died, two had persistent disabling deficits, and another seven suffered transient neurological deficits. Our finding suggests a low rate of disabling treatment complications for embolization of brain AVMs with NBCA in this center. The management of AVM patients who have high risk of embolization therapy should be treated by special strategy.

Figure 1

A,B, Lateral left ICA angiograms before embolization. A) Arterial phase showed a Spetzler grade II AVM in the parietal region. B) Venous phase demonstrated the stenoses of the main draining vein. C,D) Lateral left ICA angiograms after embolization. C) Arterial phase showing the nidus significantly reduced. D) Venous phase demonstrating the main drainage vein is completely occluded (arrow). E) Lateral skull films showed the glue cast after embolization. F) Twenty-four hours later, CT scan revealed intracerebral haematoma in the left parietal lobe.

Figure 1

A,B, Lateral left ICA angiograms before embolization. A) Arterial phase showed a Spetzler grade II AVM in the parietal region. B) Venous phase demonstrated the stenoses of the main draining vein. C,D) Lateral left ICA angiograms after embolization. C) Arterial phase showing the nidus significantly reduced. D) Venous phase demonstrating the main drainage vein is completely occluded (arrow). E) Lateral skull films showed the glue cast after embolization. F) Twenty-four hours later, CT scan revealed intracerebral haematoma in the left parietal lobe.

Figure 2

A) CT scan showed SAH. B) Lateral right ICA angiograms demonstrated an ICA-PcoA aneurysm and a Spetzler grade IV AVM. C) Post-embolization angiograms showed that parts of the nidus were glued, but the ICA-PcoA aneurysm was untreated. DD CT scan revealed severe SAH and intracerebral haematoma.

Figure 3

A) Lateral oblique view of a right ICA angiogram demonstrated an ischemic area in the right frontal lobe. B) Postembolization oblique angiogram showed the callomarginal artery demonstrated in figure A (arrowhead) was occluded. C,D) A day later, CT demonstrated the cast of nidus and the cast of the callomarginal artery. Also the low density infarct lesion was noted in the anterior callosomarginal region of the right frontal lobe.