Chapter 18 Cerebral Revascularization for Giant Aneurysms of the Transitional Segment of the Internal Carotid Artery
• Giant transitional internal carotid artery (ICA) aneurysms incorporate the cavernous, clinoidal, and supraclinoidal segments of the ICA in their necks and are more than 2.5 cm in diameter.
• The natural history of intracavernous ICA giant aneurysms is relatively benign, compared to transitional segment giant ICA aneurysms. Unruptured giant aneurysms in this location had a rupture rate of 40% in 5 years, according to the International Study of Unruptured Intracranial Aneurysms.
• Elective occlusion of the ICA for treatment of aneurysms carries a significant stroke risk, even after a successful balloon test occlusion of the ICA.
• These aneurysms can be treated by the performance of a high-flow bypass graft (radial artery or saphenous vein) from the external carotid artery or the internal maxillary artery to the M2 divisions of the middle cerebral artery, with simultaneous proximal occlusion or trapping of the giant aneurysm. The procedure carries low mortality and morbidity rates, as shown in the authors’ series of 55 patients with giant ICA transitional aneurysms.
• Flow diversion stents such as the Pipeline stent are being used for the endovascular treatment of unruptured giant ICA aneurysms. Longer follow-up is needed to evaluate the results and complications.
Pure cavernous ICA aneurysms are a separate category of aneurysms that do not extend beyond the dural ring of the ICA. In the neurosurgical literature these aneurysms are considered benign, even when they are larger.1 However, in our experience it is possible that when these aneurysms get significantly large, they can cause rupture through the middle fossa dura, causing hemorrhage and potentially death (Fig. 18.1).
Natural History
Unruptured giant intracranial aneurysms are being diagnosed more often as a result of the availability of better imaging techniques, and these lesions pose management problems for practitioners. The first series of giant aneurysms was presented in 1969 by Morley and Barr, who described giant aneurysms as greater than 25 mm.2 Giant aneurysms are relatively rare, accounting for between 5% and 7% of aneurysms3 in most series. Giant aneurysms have a female predominance with female:male ratios as high as 3:1 in some series4 and most commonly present in the middle decades of life. Giant aneurysms are most frequently located on the ICA, specifically involving the paraclinoid segment 21% of the time.5
The natural history of giant aneurysms is one of a poor prognosis. Some have compared the fate of unruptured giant aneurysms to that of subarachnoid hemorrhage (SAH).6 Patients often present with symptoms consistent with SAH or mass effect. The Italian cooperative study has shown a 28% mortality rate for untreated giant aneurysms compared to a 14% mortality rate for patients who received treatment.7 In the same series, morbidity was seen in 48% of cases owing to aneurysm expansion. Giant aneurysms, not unlike other aneurysms, continue to enlarge over time. Expansion is thought to be from growth of the lumen or thrombus formation within the sac. This progressive enlargement often causes symptoms of mass effect.8
Historically, it was thought that giant aneurysms were less prone to rupture; however, contemporary evidence suggests that this is inaccurate. Drake found that 62 of 174 cases did rupture.9 Aneurysms that were 25 mm or more had a relative risk of rupture of 59.0 compared to aneurysms less than 10 mm.10 Giant aneurysms had a 6% rupture rate in the first year compared to less than 1% for aneurysms less than 10 mm.10 Patients with a giant aneurysm, but without previous SAH, were at a significantly increased risk for rupture based on size. The rupture rate was not dependent on the location of the aneurysm; all anterior circulation giant aneurysms were at increased risk of rupture.3 Risk factors for aneurysm rupture include hypertension, current or former tobacco use, alcohol use greater than five drinks per day, and oral contraceptives.10 It was thought that partially or completely thrombosed aneurysms would be less likely to rupture, thus not requiring treatment; however, in Drake’s large series this was not the case.9
The International Study of Unruptured Intracranial Aneurysms (ISUIA) trial has shown that unruptured aneurysms overall do not pose as high a risk as once thought; and that treating aneurysms, specifically small ones, puts the patient at greater risk than watchful waiting. However, this advice should not be applied to the special case of giant aneurysms, in which “the natural history is ominous.”6 Morley and Barr’s original series demonstrated similar findings, with an 80% mortality rate for untreated aneurysms. Other studies have also shown high 1-year mortality rates.11 Peerless and associates found that 85% of patients with giant intracranial aneurysms were dead at 5 years.12 Additionally, the ISUIA II trial found that the cumulative rupture rates for anterior circulation giant aneurysms with no previous history of SAH were 40%. Patients who do present with SAH are at increased risk of death compared to patients without SAH.13 Figure 18.2 presents a case of a ruptured giant aneurysm without previous history of SAH 6 months after initial diagnosis.
Deliberate Internal Carotid Artery Occlusion
Traditional neurosurgical literature and practice have held a liberal view of ICA occlusion for the treatment of giant ICA aneurysms. Historically this has been accompanied by a relatively high risk of stroke following ICA occlusion (Table 18.1). With more recent improvements in the balloon test occlusion (BTO) paradigms, the risk is smaller but clearly not trivial.
Patients with giant ICA aneurysms are usually younger and have relatively fewer medical comorbid conditions when compared to patients with cervical carotid occlusive disease, and they face an insignificant risk after planned carotid sacrifice. Long-term effects of deliberate carotid occlusion are not well studied. The risks of forming additional aneurysms, developing hemodynamic ischemic disease, and potential cognitive disorders have to be taken into account when this decision is made. Therefore, it has been the practice of the senior author (SIA) to preserve ipsilateral hemispheric flow in the treatment of giant aneurysms, especially in younger patients, by performing a bypass procedure (Fig. 18.3).
Treatment of Giant Internal Carotid Artery Aneurysms
We performed a retrospective review of 55 consecutive patients treated at Saint Louis University Hospital from June 1999 to June 2007. The objectives of this study were to assess the use of high-flow extracranial-intracranial (EC-IC) bypass for the treatment of giant transitional ICA aneurysms, delineate the surgical mortality and morbidity rates, and determine the long-term efficacy of the treatment and the functional outcomes of these patients. All 55 patients had giant transitional ICA aneurysms. The mean aneurysm size was 34.7 mm (range 25 to 70 mm). The mean age was 46 years (range 30-64 years). The mean follow-up period was 34.7 months (range 1-76 months). The most common presenting symptoms were cranial neuropathy (42%), presence of headaches or incidental finding (40%), and subarachnoid hemorrhage (18%) (Fig. 18.4). The World Federation of Neurosurgical Societies (WFNS) grade was 0 in 81%, 1 in 15%, 2 in 2%, and 3 in 2% (Fig. 18.5). All 55 patients underwent a high-flow EC-IC bypass procedure prior to ICA ligation.
FIGURE 18.4 Percentage of patients initially presenting with headache, cranial neuropathy, and subarachnoid hemorrhage.
Surgical Techniques for Extracranial-Intracranial Bypass Procedure
Minimally Invasive Low-Flow Bypass
We rarely utilize low-flow bypass for giant aneurysms in which primary occlusion of the internal carotid artery is planned. In certain situations, such as elderly patients who pass balloon test occlusion and SPECT (single-photon emission computed tomography) scanning, it may be reasonable to perform low-flow bypass to maximally minimize surgical morbidity.
Using a preoperative computed tomography (CT) angiogram that provides clear visualization of the superficial temporal artery (STA), including its frontal and parietal branches, we measure the diameters of these branches and identify the optimal vessel for use as a donor (Fig. 18.6). This enables us to plan a linear skin incision overlying the chosen donor vessel.
The bur hole/craniotomy can be planned preoperatively with the help of the stereotactically reconstructed model based on the CT angiogram. The recipient vessel is chosen based on its caliber and superficial location in the sylvian fissure (Fig. 18.7). The ideal recipient vessel is identified based on the review of the CT angiogram. Using CT angiography–based neuronavigation, the exact location of the bur hole/craniotomy is planned to overlie the selected recipient vessel and to be in the immediate proximity of the selected donor vessel (Fig. 18.8).
FIGURE 18.7 Intraoperative photograph obtained through the microscope while the bur hole/craniotomy was being performed.
(From Coppens JR, Cantando JD, Abdulrauf SI. Minimally invasive superficial temporal artery to middle cerebral artery bypass through an enlarged bur hole: the use of computed tomography angiography neuronavigation in surgical planning, J Neurosurg 2009;109(3):553-558, used with permission.)
A bur hole is made and enlarged to the size of a very small craniotomy (~ 2-2.5 cm) under the microscope (Figs. 18.9 and 18.10), and the recipient vessel is exposed in the distal sylvian fissure over a length of 1 cm. A rubber dam is applied and the anastomosis is performed with a 9-0 nylon suture in a running fashion. The back wall is anastomosed first, followed by the front wall. Temporary clips are applied on the M4 recipient vessel during the anastomosis. Postoperatively, the patients are followed up with angiography (Fig. 18.11) or CT angiography (Fig. 18.12).18
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