12.1.4\ Aneurysm Clipping

and Hemostatic Ligation Clips

12.1.4.1\ Discussion

Aneurysm clips are used to occlude the neck of aneurysms in order to prevent or cease hemorrhage due to rupture. These devices are available in a variety of shapes and sizes. They consist of a hinged wire with parallel ends that are straight or curved. In the past, aneurysm clips were composed of stainless steel or tungsten. Although these materials are biocompatible, they are not MRI compatible. These clips also produce considerable beam-hardening artifact that can obscure surrounding structures. Newer clips are composed of non-ferromagnetic materials, such as titanium, which are MRI compatible and produce fewer artifacts on CT.

Surgery for aneurysm clipping consists of performing a craniotomy. In addition, variable amounts of the anterior clinoid process may be resected in order to access paraclinoid aneurysms (Fig. 12.11). Deeply positioned aneurysms can be difficult to attain for clipping, which can result in aneurysm remnants. Incomplete clipping can present as increased hemorrhage shortly after clipping of ruptured aneurysms, for example, and can be addressed by endovascular embolization (Fig. 12.12). Although the brain can be retracted in order to maximize the field of view and access for centrally located aneurysms, vascular injury can result. Likewise, vessels adjacent to aneurysms that have poor visibility can be inadver-

tently clipped, such as the recurrent artery of Heubner, which can result in caudate infarcts (Fig. 12.13).

Vasospasm is a significant source of morbidity in patients with ruptured cerebral aneurysms and typically manifests 7–10 days after the episode of subarachnoid hemorrhage. Transcranial Doppler ultrasound is routinely used to assess for cerebral vasospasm, but the modality has limited sensitivity and specificity. CTA is also commonly implemented for the detection of cerebral vasospasm following subarachnoid hemorrhage and may demonstrate multifocal steno-occlusive lesions and areas of hemorrhage (Fig. 12.14). In addition, CT perfusion can be performed ­concurrently to provide insight into the extent of cerebral ischemia resulting from vasospasm. Unfortunately, streak artifact from the aneurysm clip can limit the assessment of the adjacent vasculature. Ultimately, catheter-based angiography has been considered to be the historical gold standard to diagnose vasospasm.

The incidence of recurrent aneurysms after complete clipping is approximately is low, but this complication can lead to subarachnoid hemorrhage and requires repeat clipping or endovascular intervention. It is also important to carefully search for new aneurysms on postoperative scans, since the annual rate of de novo aneurysm formation is about 0.9%. These occur on average at about 10 years after surgery. Thus, long-term angiographic follow-up is warranted in patients with clipped aneurysms.

Fig. 12.12  Incomplete aneurysm clipping. Axial CT image at initial presentation (a) shows hemorrhage into the left frontal lobe (arrow) and in the ventricular system due to aneurysm rupture. Axial CT image obtained shortly after anterior communicating artery aneurysm clipping

(b) shows new hemorrhage in the right frontal lobe. Digital subtraction angiogram (c) shows residual filling of the aneurysm sac (encircled) adjacent to the clip. The residual aneurysm sac was then embolized (d)

Fig. 12.14  Vasospasm. Axial CT image (a) obtained 1 week after clipping of a ruptured cerebral aneurysm shows areas of hypoattenuation in multiple vascular territories and scattered subarachnoid hemorrhage. The MTT (b) and CBF (c) maps show perfusion deficits in the bilateral anterior cerebral artery and right posterior cerebral

artery territories. The CTA (d) and digital subtraction angiography images (e, f) show severe vasospasm in the anterior and posterior cerebral vessels, with relatively less pronounced involvement of the middle cerebral artery territories

12.1.5\ Vascular Malformation

Surgery

When possible, microsurgical resection is the optimal treatment option for arteriovenous malformations and cavernous malformations. While the nidus of the arteriovenous malformation represents the target of resection, the remaining draining vein can be clipped for hemostasis (Fig. 12.15). However, proximal ligation of the supplying arteries alone can make subsequent embolization more difficult and may rapidly lead to revascularization. For inoperable arteriovenous malformations that require treatment, stereotactic radiosurgery is an alternative. This treatment essentially results in thrombosis of the malformation. Further, sometimes radiation necrosis can result, which may appear as a peripherally enhancing lesion with surrounding vasogenic edema (Fig. 12.16).

a

With respect to cavernous malformations, developmental venous anomalies are often incidental findings that are not generally considered targets for treatment. However, seizure outcome after resection of cavernous malformations is better when surrounding hemosiderin-stained brain also is removed, although this can be challenging when critical structures are involved (Fig. 12.17).

Head and neck lymphatic malformations are often transspatial and are often not amenable to complete surgical resection. However, when lymphatic malformations compromise critical structures, such as the airway, partial resection may be performed. MRI is a suitable modality for accurate delineation of the residual tumor, which is useful for planning subsequent additional surgery or sclerotherapy if needed (Fig. 12.18). Obtaining up-to-date imaging is particularly relevant since the lesions often evolve spontaneously, with new and enlarging components.

b

Fig 12.15  Arteriovenous malformation resection. The patient has a history of a right frontal lobe arteriovenous malformation. Preoperative axial post-contrast T1-weighted MRI (a) shows an enlarged draining right

cortical vein (encircled). Postoperative axial CT image (b) shows a Weck clip (arrow) used to ligate the vein during surgery

Fig 12.16  Arteriovenous malformation stereotactic radiosurgery with radiation necrosis. Pretreatment axial FLAIR (a) and post-contrast T1-weighted (b) MR images show a left temporo-occipital nidus. Posttreatment FLAIR (c) and post-contrast T1-weighted (d) MR images show

interval development of extensive vasogenic edema surrounding a peripherally enhancing lesion due to radiation necrosis at the site of the arteriovenous malformation, which is no longer apparent

Fig. 12.17  Residual hemosiderin staining after cavernous malformation surgery. Preoperative SWI MRI (a) shows a large right basal ganglia cavernous malformation. Postoperative SWI MRI (b) shows that the bulk of the

cavernous malformation is no longer present, but there is abundant peripheral hemosiderin staining that remains (arrow)

Fig. 12.18  Partial resection of lymphatic malformation. Preoperative axial T2-weighted MRI (a) shows a transspatial macrocystic lesion with a component that obstructs the upper airway (arrow). Postoperative axial T2-weighted

MRI (b) shows successful resection of the component of the lymphatic malformation that compromised the airway but interval appearance of an adjacent cystic component

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