Nearly all patients with SAH present with a sudden, severe headache that is classically described as “the worst headache of my life.” As many as 20% to 50% of patients have a “sentinel” headache within the days to weeks before the SAH.^1,2 The headache is typically diffuse, but is lateralized in approximately a third of patients. Common associated symptoms include nausea, vomiting, and meningismus. Depending on the severity of the SAH, patients may have impairment in consciousness that ranges from drowsiness to coma and occasionally focal neurologic deficits. A diagnosis is most often reached by noncontrast head CT scan (Figures 23-1, 23-2, 23-3), which is 95% sensitive within the first 6 to 12 hours following the onset of symptoms. A negative CT in the presence of strong clinical suspicion, however, warrants a lumbar puncture to directly assess for the presence of blood or blood breakdown products in the cerebrospinal fluid.³

Table 23-1 shows the etiologies of SAH. Aneuryms are responsible for the vast majority of nontraumatic SAHs.

The spontaneous rupture of a cerebral aneurysm that results in SAH is a life-threatening condition with an immediate mortality rate of 10% to 20%.^4,5 Survival through the initial incident provides no guarantee, however, as rebleeds (occurring in 7% to 22% of patients^6,7 and vasospasm (clinical vasospasm in 20%-30% of patients⁸) is largely responsible for a 30-day mortality rate as high as 50%.^9,10 Furthermore, as many as one-third of survivors remain functionally dependent following aneurysmal hemorrhage, and approximately 20% have substantial neurocognitive impairment.^10–12

Following initial stabilization and diagnosis, attention turns toward the prevention of recurrent hemorrhage and vasospasm (delayed cerebral ischemia), which are the main causes of mortality and morbidity in patients who survive the immediate post-bleed period.^8,10 Endovascular therapy can effectively treat both the ruptured aneurysm immediately after admission in order to prevent a rebleed, as well as vasospasm that may occur later in the patient’s clinical course. This may be accomplished by occluding the aneurysm with microcoils and using intraarterial vasodilator therapy or balloon angioplasty to treat vasospasm that is refractory to medical management.

It was shown in the 1960s that using surgically placed clips to secure a ruptured aneurysm not only prevents recurrent hemorrhage, which has a mortality rate of up to 80%, but also lowers morbidity compared with nonsurgical management. Since its approval in the 1990s, however, endovascular coil occlusion of a cerebral aneurysm has become an increasingly popular treatment, which has also been shown to accomplish the same goal: prevention of recurrent hemorrhage (Table 23-2). Compared with surgery, advantages of endovascular treatment include femoral access, which avoids the surgical morbidity of a craniotomy; access to midline aneurysms without brain retraction; improved neurologic outcomes; and a lower incidence of seizures.

Endovascular coiling was directly compared with neurosurgical clipping of ruptured aneurysms in the randomized, multicenter International Subarachnoid Aneurysm Trial (ISAT).¹³ The trial randomized 2143 patients from 1994 to 2002 who presented with aneurysmal SAH deemed suitable to treatment with either endovascular or surgical treatment. The primary endpoint was death or functional dependence at 1 year, with dependence defined as a modified Rankin Scale (mRS) score of 3 to 6. The mRS, which is described in Table 23-3, is a well-validated, widely used measure of functional outcome.¹⁴

Patients in the ISAT who were randomized to endovascular intervention experienced significantly better outcomes. Death or dependence at 1 year in the endovascular group was 23.7% compared with 30.6% in the surgical group, with an absolute risk reduction of 6.9%. The mortality rate remained significantly lower in the endovascular group at 5- and 10-year follow-up, although at both time points there was no significant difference in the rates of dependence (Table 23-2).^15,16 In addition to decreased mortality, endovascular patients also experienced fewer seizures. There is a slightly greater incidence of recurrent SAH following the coil procedure when compared with clipping. However, the rate of use is very low, making analysis for statistical significance difficult.¹⁷

However, after 3258 patient-years of follow-up, there were 7 recurrent hemorrhages in the endovascular group compared with 2 in the 3107 patient-years in the surgical group. The higher incidence of rebleeds in the endovascular group may have been related, at least in part, to the durability of aneurysm occlusion: Although 66% of follow-up angiograms demonstrated complete aneurysm occlusion in the endovascular group, the proportion was higher (82%) in the neurosurgical group.^13,17 Similarly, in the recently published 10-year data, the rate of recurrent hemorrhage remained greater in the endovascular group (21 recurrent hemorrhages; 8531 patient-years) than in the neurosurgical group (12 recurrent hemorrhages; 8228 patients years).¹⁶ In summary, the ISAT results show that endovascular treatment represents a clinically effective treatment for appropriately selected patients with aneurysmal SAH despite lower rates of complete aneurysm occlusion.

ISAT has been criticized for specific limitations in the study design, including imprecise selection criteria, lack of requirement for technical proficiency of surgeons performing the clip procedures, lack of angiographic controls of surgically treated patients, poorly chosen primary endpoints, and certain biased statistical analyses.^18,19 In addition, most patients (88%) were in a favorable neurologic condition (World Federation of Neurological Societies (WFNS) grade I or II) following their hemorrhage, and the vast majority of aneurysms were < 11 mm in diameter, factors that may limit the generalizability of the results considering the highly variable posthemorrhagic neurologic status and the heterogenous morphologies and sizes of aneurysms. Nonetheless, ISAT was a pioneering study and has made endovascular embolization the mainstay of aneurysmal SAH treatment.¹⁹

The more recent Barrow Ruptured Aneurysm Trial (BRAT)²⁰ was another randomized study that compared surgical clipping with endovascular coiling of acutely ruptured aneurysms and sought to overcome some of the major limitations of selection biases in ISAT. In BRAT, 238 patients were randomized to surgical clipping and 233 to endovascular coiling at a single center, and a poor outcome was defined as a mRS of 3 to 6 at 1 year. The results were interpreted via an intention-to-treat analysis (ie, the primary outcome was defined by the assigned treatment, regardless of the actual treatment received) to overcome ISAT limitations. At 1 year, poor outcome was observed in 33.7% of patients assigned to clipping and 23.2% assigned to coiling, which reached statistical significance. At the 3-year follow-up, these proportions were 35.8% and 30.0%, respectively, which did not reach statistical significance.²¹ However, in the crossover analysis, of the patients who actually received surgical clipping (and for whom data were available at year 3 of follow-up) 87/248 (35.1%) had a poor outcome (mRS, 3-6) compared with 28/115 (24.3%) in the coiling group. Aneurysm obliteration after initial treatment and then at the 3-year follow-up was 58% and 52%, respectively, in the coil group, and 85% and 87% in the clipping group.²¹ Unlike ISAT, which enrolled only 22% of patients treated at its centers, BRAT enrolled all patients who were admitted with aneurysmal SAH during the study period.²² BRAT has received criticism, however, for taking place only at a single center (although the investigators state that it was intended to be more of a pilot study) and having an unusual study design.²³

The Cerebral Aneurysm Rerupture After Treatment (CARAT) study sought to compare rehemorrhage and intraprocedural aneurysm rupture—dreaded complications—between coiling and clipping among patients presenting with aneurysmal SAH.²⁴ The principal findings of the trial were a greater rate of intraprocedural rupture in the surgical group (18.6% vs 5.4%), but a higher rate of periprocedural death or disability among patients who suffered intraprocedural rupture in the coiling group (63% vs 31%).^24,25

The goal of both surgery and endovascular treatment is to exclude the lumen of the aneurysm from circulation while preserving cerebral perfusion. Although often controversial, certain factors are used in standard practice to decide the type of treatment (Table 23-4). These include patient demographic and clinical factors, ability to tolerate a craniotomy, aneurysm characteristics (eg, size, location, morphology), and available expertise.²⁶

Endovascular treatment was initially shown to be a safe and effective treatment of aneurysms with the Guglielmi Detachable Coil (Target Therapeutics, Fremont, CA), which received Food and Drug Administration (FDA) approval in 1995. At the time, patients deemed eligible for endovascular treatment were primarily those who were poor surgical candidates (eg, high risk of surgical complications due to comorbidities and the difficulty or plausibility of surgery), had previous failed surgical attempts, or had refused surgery. Among the 408 patient included, complete aneurysm occlusion was accomplished in 70.8% of small (4-10 mm) aneurysms with a small neck (≤ 4 mm), 35% of large (11-25 mm) aneurysms, and 50% of giant (> 25 mm) aneurysms. A total of 1.74% died as a result of procedural complications, and another 4.47% died because of the severity of the initial hemorrhage.²⁷ In another trial of 150 patients with ruptured or unruptured basilar tip aneurysms, occlusion was obtained in 75% of cases. Periprocedural cerebral embolism occurred in 13% of cases, and periprocedural death occurred in 2.7%.²⁸

As is the case with surgical procedures in many specialties, significant medical comorbidities (eg, severe cardiopulmonary disease) and advanced age (> 70 years) may affect the patient’s ability to endure the physiological stress of prolonged intracranial surgery. In addition, patients who have certain coagulopathies or who require chronic anticoagulation may have a higher risk of perioperative hemorrhage. Furthermore, in elderly persons, the issue of long-term durability of the treatment is less important because of a shorter expected life span. These patient populations are prime candidates for choosing endovascular treatment over surgical clipping.²⁹

The clinical severity of the SAH should also be considered when determining the appropriate intervention. Patients with high-grade SAH, defined as grade IV or V on either the Hunt and Hess scale or World Federation of Neurologic Surgeons (WFNS) grading scale, present greater challenges to surgical technique, because an edematous or ischemic brain in the setting of increased intracranial pressure (ICP) is difficult to surgically manipulate. However, endovascular therapies are hindered less by conditions such as swelling.^26,30,31 A study of endovascular treatment in patients with high-grade SAH due to aneurysm rupture resulted in a favorable outcome in 62% of grade IV and 25% of grade V patients or in 52.5% of total included patients.³² A study combining endovascular treatment with aggressive medical management, including hypervolemic hemodilution and hypertensive (known as Triple H) treatment, in WFNS grade V patients produced encouraging results. A majority of patients (55%) experienced a favorable outcome, while the mortality rate was 18%.³³ In addition, similar to elderly patients, the long-term durability of endovascular coiling compared with clipping is less of a concern in patients with high-grade SAH, who have a poorer long-term survival rate. Thus, there exists growing support for endovascular intervention in patients with high-grade SAH, particularly when coupled with aggressive medical management.

Certain complications occurring after the initial hemorrhage may affect the decision to proceed with surgical or endovascular intervention. The development of intracerebral hemorrhage (ICH) following aneurysmal rupture is associated with increased morbidity and mortality compared with SAH alone. Depending on the size, location, and accessibility of the ICH, these patients may require surgical hematoma evacuation and/or decompression, during which clipping of the ruptured aneurysm may be undertaken simultaneously. Despite evacuation of the hemorrhage, particularly in WFNS grades IV and V, mortality in ICH patients remains high, ranging from 21% to 85%.^34,35 Additionally, these patients may have increased risk of intraoperative rerupture.³⁶ Although the benefits of surgery in ICH are uncertain³⁷ and may confer an increased risk of intraoperative rerupture, intervention should be considered in order to reduce hematoma-related mass effect.

For this reason, a sequential approach involving endovascular aneurysm occlusion followed quickly by surgical evacuation of the hematoma has been implemented in some centers.^36,38 One series using this approach in patients with WFNS grade IV or V SAH and ICH due to aneurysm rupture demonstrated favorable outcomes in 48% of patients, with death occurring in 21%.³⁹ This strategy may be particularly useful when ICH develops opposite the side of the ruptured aneurysm. Chung et al reported a series of ruptured anterior communicating artery (AComA) aneurysms complicated by significant ICH, making the ICH difficult to evacuate from the optimal site for aneurysm access. These investigators treated AComA aneurysms using endovascular coil occlusion and then evacuated the ICH through a burr hole craniotomy. They observed no rebleed during follow-up and reported that more than half of the patients experienced moderate to good recovery.⁴⁰ Thus, for aneurysms associated with ICH, the evidence suggests that treatment of the aneurysm by endovascular means followed by surgical evacuation of the hematoma is a safe and effective approach to a common situation associated with very high mortality.

The location and morphology of the aneurysm is another major determinant of suitability for endovascular vs surgical treatment. Posterior circulation aneurysms are typically better candidates for endovascular treatment based on anatomic considerations: In addition to more difficult surgical access, posterior circulation aneurysms are in close proximity to important perforator arteries and cranial nerves, and as a result there is a significant risk of iatrogenic surgical morbidity. Patients with multiple aneurysms, found in approximately 20% of cases,⁴¹ especially those in different vascular distributions, may be well served by endovascular treatment.

Aneurysms with small necks relative to the size of the fundus (dome) are the ideal morphology for endovascular therapy. Coil occlusion of an aneurysm arising from a small opening (neck) in the artery can be accomplished without prolapse of coils into the parent artery (Figure 23-4). In aneurysms with larger necks, however, coils may herniate or prolapse out of the aneurysm lumen and back into the artery. Balloon remodeling and stent-assisted techniques, which will be discussed in greater detail, can overcome these issues with coil stability in aneurysms with a wider neck relative to dome size (ie, low dome to neck ratio). In the setting of acute SAH; however, wide-neck aneurysms remain a relative contraindication to the coil procedure.

To perform the coil procedure, the neurointerventionalist must be able to access the aneurysm with a suitable microcatheter. Therefore, issues with proximal vascular access (eg, internal carotid artery), such as occur with stenosis, excessive tortuosity, or vascular diseases such as fibromuscular dysplasia or atherosclerosis, may prevent safe endovascular aneurysm access. However, if the aneurysm or perianeurysmal parent artery contains significant atherosclerotic calcifications, surgical clips may be more difficult to place across the calcified tissue. Aneurysms arising on distal cortical branches may be challenging to reach with a catheter but are relatively easily accessible via open surgery.⁴² Patients who have giant aneurysms (diameter > 25 mm) or severe vasospasm following SAH are typically treated endovascularly, as the surgical morbidity is very high in these cases. In addition, as discussed later, the neurointerventionalism may treat the severe vasospasm as well as the aneurysm. In effect, in some ways endovascular and open surgical techniques are complementary and must be used to advance in each patient.

Middle cerebral artery (MCA) aneurysms represent one of the most common sites of intracranial aneurysms, accounting for roughly 20%, and are often managed surgically rather than endovascularly for several reasons. In general, MCA aneurysms are easily accessible via craniotomy with a transsylvian approach, which requires minimal brain retraction. Fusiform morphology, in which branch vessels arise from the aneurysm wall, is more readily treated with multiple surgical clips. When 53 patients with 58 bifurcation or trifurcation aneurysms of the MCA were evaluated, 88% had a dome to neck ratio < 2%, and in 40% of cases branch vessels were incorporated into the aneurysm sac.⁴³ However, endovascular therapy is not precluded in the case of MCA aneurysms, and new technologies are meant to address the limitations of existing endovascular techniques. In one study of 16 patients with wide-necked MCA aneurysms (including 10 acutely ruptured aneurysms) who were treated with stent-assisted embolization, there was no recurrence, rebleeding, or neurologic deterioration after an average of 20 months of follow-up.⁴⁴ Endovascular treatment of unruptured MCA aneurysms may have a higher success and lower rate of complications (eg, periprocedural bleed or ischemic event).⁴⁵

Intervention in the care of patients with aneurysmal SAH is primarily undertaken to prevent rehemorrhage, an event that has a mortality rate of up to 80%.⁴⁶ The risk of rebleed is greatest in the first 24 hours, reaching 19%, and by 4 weeks the cumulative risk reaches 40%,⁴⁶ with poor-grade patients being at highest risk.^47,48 Ultra-early treatment (< 24 hours from the ictus) confers a benefit on functional outcome.⁴⁹

Endovascular treatment involves placement of prosthetic materials (generally platinum-based coils) within a patient’s vasculature to induce thrombosis of the ruptured aneurysm, which occludes it from circulation and prevents rehemorrhage (Figure 23-5). Although administering anticoagulants in the setting of hemorrhage may at first seem counterintuitive, endovascularly induced thrombus formation carries a risk of vessel occlusion and ischemic stroke. In fact, up to a quarter of these patients may have changes on diffusion-weighted imagining (DWI) after embolization.⁵⁰ In one large, prospective series, thromboemboli complications were confirmed in 13.3% of cases, and intraoperative re-rupture occurred in 3.7% of cases.²⁶ Excessive clotting is avoided by the routine use of intravenous heparin to maintain an activated clotting time (ACT) during treatment only. Although there is not universal agreement, many operators aim for an ACT 2.5 to 3 times the baseline value. After the procedure, the heparin effect can be reversed or allowed to wear off. Patients with small intraparenchymal hematomas have been heparinized safely; furthermore, prior placement of a ventriculostomy is not an absolute contraindication to heparin administration at the time of aneurysm treatment, although this decision should be made with appropriate caution.⁴² If the cerebral artery is occluded iatrogenically, one possible treatment, under certain circumstances, is placing a stent. Although “rescue stenting” may be an effective treatment, patients may require chronic antiplatelet therapy despite having had SAH, a relative contraindication to their use.^42,51,52 There are also retrospective data to suggest that dual antiplatelet therapy, in addition to anticoagulation, may further reduce thromboembolic complications.

The patient is likely experiencing cerebral vasospasm. Macrovascular vasospasm is demonstrable in up to 70% of SAH patients, with roughly 30% becoming symptomatic and/or having evidence of infarction on imaging, termed delayed cerebral ischemia (DCI).^53,54 Vasospasm is one of the most challenging events to treat following SAH, as it is responsible for up to half of deaths occurring in patients who survive the initial hemorrhage.⁵⁵ Although incidence of vasospasm peaks at post-bleed day 7, it may occur at any time between days 3 and 14.⁵⁶ Digital subtraction angiography is the gold standard for diagnosis; however, transcranial Doppler, CT, magnetic resonance (MR) angiography, and perfusion studies are often used for diagnosis and to guide treatment.⁵³ The medical management of cerebral vasospasm consists of administering nimodipine, a calcium channel blocker that has been shown to improve outcomes, along with inducing hypertension and providing excess volume.⁵⁷

For patients with vasospasm that is refractory to medical treatment, there are two endovascular modalities available for dilatation of the narrowed arteries: intraarterial vasodilator therapy and balloon angioplasty. Intraarterial vasodilator therapy has been performed with a number of agents, including opium alkyoids such as papaverine, a phospodiesterase 3 inhibitor milrenone, and calcium channel blockers such as verapamil and nicardipine, and although retrospective data have shown a benefit, the vasospasm often recurs because of short half-lives of the drugs.^58,59 Similar to the technique used when angioplasty of an atherosclerotic lesion is performed, transluminal balloon angioplasty (TBA) uses microballoons mounted on microcatheters to mechanically dilate the vasospastic segment of an artery. The procedure, which is usually performed under heparin anticoagulation and often is combined with intraarterial infusion of vasodilators, has been supported by a number of studies that demonstrated clinical improvement in 31% to 80% of patients,^58–60 and the effects are longer lasting than intraarterial injection of vasodilators.⁵⁹ In one meta-analysis evaluating combined TBA and intraarterial injection of vasodilators, there was clinical improvement in 62% of patients.⁶¹ Probably the most compelling evidence for the role of endovascular therapy was reported in a large population study by Johnston et al: At 70 university medical centers offering endovascular therapy, including balloon angioplasty for vasospasm, there was a 16% overall improvement in patient survival.⁶² There is currently a multicenter, randomized controlled trial underway that will investigate whether TBA reduces the incidence of DCI (Invasive Diagnostic and Therapeutic Management of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage [IMCVS], NCT01400360). Although TBA achieves a durable reversal of vasospasm in the treated segment, there is a small risk of catastrophic vessel rupture.⁵⁶ As a result, TBA is a technique that is generally limited to the treatment of larger, proximal intracranial vessels (eg, intracranial atherosclerosis [ICA], M1, A1, and the basilar artery). TBA may also potentially reduce the risk of vasospasm when applied prophylactically; in a multicenter clinical trial, TBA significantly reduced the incidence of DCI. However, 4 of 85 patients in the group receiving TBA suffered from vessel rupture.⁶³ For this reason, prophylactic therapy is generally not recommended.

Intracranial aneurysms occur in approximately 2% to 3% of the general population. The prevalence appears higher in populations from Finland and Japan, individuals with a strong family history of unruptured intracranial aneurysms or prior SAH, elderly persons, women, and patients with autosomal dominant polycystic kidney disease (ADPKD), fibromuscular dysplasia, glucocorticoid-remediable aldosteronism, Ehlers-Danlos syndrome, aortic coarctation, and other conditions associated with vessel fragility.^64–70 Additional modifiable risks for aneurysmal development and rupture include smoking, alcohol use, and hypertension.⁷¹

Unruptured aneurysms are usually asymptomatic, and rupture is uncommon. Unfortunately, aneurysm rupture with resulting SAH is often the first presentation; other symptoms may include severe headaches, seizures, cerebral ischemia distal to the aneurysm location due to emboli that form in the aneurysmal sac, and focal neurologic deficits secondary to mass effect.⁶⁶ In particular, the onset of a third-nerve palsy in association with a growing posterior communicating artery aneurysm heralds impending rupture. Because of the significant morbidity and mortality associated with SAH, great efforts have been made to risk-stratify patients with unruptured aneurysms in order to determine who should receive intervention (Table 23-5). Any form of surgical or endovascular intervention, however, carries a risk of iatrogenic hemorrhagic and ischemic complications.

The International Study of Unruptured Intracranial Aneurysms (ISUIA)⁷² prospectively followed 1692 patients (1077 of whom had no history of SAH) with unruptured aneurysms ≥ 2 mm and found an overall rupture rate of 3% (0.7% per year), with an overall mortality rate of 65% in those experiencing hemorrhage. The study established, however, that the rate of rupture varies with size and location of the aneurysm. Over a follow-up period of 5 years, patients with no history of aneurysm rupture and with anterior circulation aneurysms < 7 mm, 7 to 12 mm, 13 to 24 mm, and > 25 mm experienced rupture rates of 0%, 2.6%, 14.5%, and 40%, respectively. For aneurysms in the posterior circulation or the posterior communicating artery, patients had relatively higher rates of rupture: a rate of 2.5% for aneurysms < 7 mm, 14.5% for 7 to 12 mm, 18.4% for 13 to 24 mm, and 50% for those > 25 mm. In addition, those patients who had suffered a ruptured aneurysm in the past proved more likely to suffer rupture of a previously unruptured aneurysm than individuals with no history of rupture. Additional factors increasing the risk of rupture include severe headaches, tobacco use, and a family history of aneurysmal SAH. Age alone did not have a significant effect on rupture risk, even though cerebral aneurysms are more common with advancing age.⁴² In a prospective observational Japanese study of 5720 patients, the annual rate of rupture was 0.95%, with death resulting in 35% of cases.⁷³ The study also found that aneurysms with a daughter sac—an irregular protrusion of the aneurysm wall—had a higher risk of rupture than those with a smooth wall. Many other findings were similar to the ISUIA, although the Japanese study found that there was a greater risk of rupture in patients with small (< 7 mm) aneurysms in the anterior circulation, whereas ISUIA had found this risk to be minimal.⁷² In another Japanese study of 466 patients with small (< 5 mm) aneurysms, it was found that the annual rupture rate was 0.54%.⁷⁴

The ISUIA followed groups of patients undergoing surgical or endovascular intervention, and sought to make comparisons between surgical and endovascular approaches to unruptured aneurysms, even though the numbers were too small to achieve statistical significance. Groups undergoing endovascular intervention generally contained proportionally more patients with larger aneurysms; however, compared with the surgical cohort the endovascular group also included a greater proportion of older patients, giant aneurysms (> 25 mm), and aneurysms of the posterior circulation. The overall morbidity and mortality rate observed 1 year after endovascular procedures was 9.5%, compared with 12.15% observed in the surgical group. The study demonstrated that factors, including large aneurysm size and location within the posterior circulation, associated with a greater risk of rupture in the absence of treatment also increased the risk of procedural morbidity and mortality. Although age was associated with a poorer prognosis in the surgical groups, it had a less notable impact on the prognosis of those patients treated endovascularly. The study concluded that patients with aneurysms < 7 mm and no history of aneurysm rupture had the lowest risk of rupture, whereas patients with anterior circulation aneurysms < 25 mm experienced the lowest rate of morbidity and mortality associated with interventions.⁷² Although aneurysms may affect a large number of individuals, guidelines of the Stroke Council of the American Heart Association do not recommend screening except for those with at least 2 first-degree family members who have been diagnosed with an unruptured aneurysm or have a history of SAH and those with heritable disorders such as autosomal dominant polycystic kidney disease.⁵⁵

The current management of unruptured aneurysms varies widely. Treatment is generally offered to patients with posterior circulation aneurysms and anterior circulation aneurysms ≥ 7 mm, because smaller anterior circulation aneurysms have a lower risk of rupture. However, this should only be considered a guide, and patient factors including age need to be considered individually. There should be a higher threshold for intervention in patients with aneurysms in the cavernous segment of the internal carotid artery because these aneurysms are extra-dural and generally do not carry a risk of SAH. Mass-effect leading to cranial neuropathies, however, is usually considered as an indication for treatment of these aneurysms. Any aneurysm that is found on serial imaging to be growing, as well as the presence of any worsening focal neurologic signs, warrants strong consideration for prompt treatment. Decisions must be made on a case-by-case basis, however, and treatment for a smaller aneurysm may be appropriate for patients with an increased risk of rupture, such as those who smoke, have a family history of aneurysmal SAH, or who have an aneurysm that is symptomatic or demonstrates growth on serial imaging.⁴² All patients with aneurysms should be advised to reduce modifiable risk factors (eg, smoking and hypertension) irrespective of aneurysm management. Patients with a history of SAH and coexisting aneurysms should be considered for treatment regardless of their size because they are thought to represent a greater risk. In those patients opting to forgo treatment or those with small aneurysms, periodic follow-up with magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA) or CT/computed tomographic angiography (CTA) is advised.⁷⁵

Balancing the risk of rupture with the risk of intervention is prudent, and these risk have been described by several large studies over the past decade. In a recent meta-analysis of surgical clipping of unruptured aneurysms in 9845 patients, there was an overall mortality rate of 1.7% and morbidity of 6.7%. A study of patients from the National Inpatient Sample (NIS) database found in-hospital mortality of clipping to be 1.6%, whereas endovascular coiling was 0.57%.⁷⁶ In another meta-analysis of endovascular treatment of unruptured aneurysms, the overall mortality rate was 1.8%, and morbidity was 4.7%.⁷⁷ There have also been prospective data: In the Analysis of Treatment by Endovascular approach of Non-ruptured Aneurysms (ATENA), there was an intraoperative rupture rate of 2.6% in 649 patients, although the majority of ruptures did not result in permanent morbidity or mortality.^78,79 One-month mortality and morbidity rates were 1.7% and 1.4%, respectively. The rate of unfavorable outcomes after endovascular treatment of unruptured aneurysms is lower than in ruptured aneurysms. In one of the best series of prospective data, the Clinical and Anatomic Results in the Treatment of Ruptured Intracranial Aneurysms (CLARITY), 782 patients with ruptured aneurysms underwent endovascular treatment. A higher rate of thromboembolic events were observed in aneurysms > 10 mm compared with < 10 mm (28 vs 10.7%), in smokers, and in patients with wide-necked aneurysms. The CLARITY investigators also found that the rate of intraoperative rupture was greatest in patients with MCA aneurysms, in younger patients, and in those without hypertension.⁸⁰

The mainstay of endovascular intervention is intrasaccular embolization of aneurysms through the use of detachable coils (Figure 23-5). There are currently six vendors of endovascular microcoils for aneurysm treatment, and each boasts specific proprietary advantages, although none has been proven to be superior to the others. After careful angiographic assessment of an aneurysm evaluating size, location, morphology, and relationship to the vessels of origin, a microcatheter is advanced over a microguidewire into the aneurysm lumen under fluoroscopic guidance. Subsequently, coils are introduced into the lumen, with the morphology and size of the initial coil selected to match the aneurysm lumen size and to span the aneurysm neck. Aneurysm occlusion is deemed optimal when there is no contrast opacification of the aneurysm lumen (Figure 23-6). Incomplete aneurysm occlusion may be acceptable if there is concern that the placement of additional coils would lead to aneurysm rupture or cause obstruction of the parent artery. Incomplete aneurysm occlusion is one limitation of endovascular techniques. Surveillance evaluation after endovascular aneurysm occlusion is commonly performed to assess the durability of treatment. There is no set surveillance protocol. Catheter angiography or CT angiography or MRI with MRA is generally performed at first review at 6 to 18 months. Subsequent follow-up is typically performed with noninvasive imaging (CTA or MRI/MRA) at increasing intervals.⁴²

Coil embolization is applicable to many aneurysms, particularly those with a dome-to-neck ratio ≥ 2, but is not ideal for fusiform aneurysms, those with vessels originating from the aneurysm, and those with a wide neck unable to restrain coils from prolapsing into the parent artery without adjunctive devices or techniques.⁴² Coils may be broadly divided into two types: nonmodified (eg, bare platinum coils; Figure 23-4) and modified (eg, with hydrogel in addition to biological and nonbiological coating). In a recent review of 97 studies on the endovascular treatment of unruptured aneurysms, the risk of procedure-related mortality and morbidity was similar between bare platinum coils and those that are hydrogel coated, but significantly higher with liquid embolic agents (eg, Onyx, eV3 Inc, Maple Grove, MN) (4.9% vs 8.1%).⁷⁷ In a recent study on aneurysms of the posterior circulation, coil embolization succeeded in completely occluding the aneurysm in 80% of cases, whereas 20% remained incompletely occluded. Complications occurred in 6% and were limited to thromboembolic events that caused transient symptoms. Intraprocedural aneurysm rupture represents a serious complication, which is infrequent, and was found in a retrospective review of 7 years of endovascular intervention to affect approximately 1% of procedures. There is additionally the risk of aneurysm regrowth or recanalization with the need for additional treatment, which affected 7% of patients in that study.⁴²

Balloon-assisted coiling addresses the technical problem of coil herniation from the lumen of wide-neck aneurysms. A balloon catheter is first positioned in the parent artery with the balloon lumen stationed adjacent to the orifice of the aneurysm. A microcatheter is then maneuvered into the target aneurysm in a coiling position. The balloon is temporarily inflated in the parent artery to occlude the neck of the aneurysm, and coils are sequentially placed into the aneurysm via the microcatheter (Figure 23-7). The balloon provides a temporary barrier until the aggregate coil mass develops a stable configuration within the aneurysm lumen. Because balloon-assisted coiling is typically used for technically challenging, wide-necked aneurysms, comparison with simple coiling is imprecise and potentially misleading. Several studies have demonstrated total occlusion rates in the range of 70% to 90% in these challenging aneurysms with minimal or no increase in morbidity or mortality when compared with simple coiling. In addition to providing a treatment option for wide-necked aneurysms, balloon assistance has been demonstrated to be advantageous in reducing the clinically consequences of intraoperative aneurysm rupture by tamponading any extravasation while additional coils are added into the aneurysm fundus.^81–83

Endovascular coiling may also be performed with simultaneous deployment of a stent, in a technique referred to as stent-assisted coiling (SAC). In SAC, the stent, similar to the balloon technique, serves as a scaffold to prevent coil prolapse into the lumen of the parent artery (Figure 23-8 and 23-9).^84,85 SAC may be accomplished by several different methods. According to most manufacturers, after the stent is placed, the microcatheter is advanced through openings in the stent and then into the aneurysm fundus. Some operators will first place the microcatheter into the aneurysm fundus and then deploy the stent into the artery afterwards, thus pinning the catheter between the stent and the vessel wall. This is often termed “jailing” of the microcatheter, which can easily be removed once the process of introducing coils has been completed.⁸⁶ In a systematic review of 656 patients treated with SAC, of whom a third had SAH, the immediate aneurysm occlusion rate was 46.3%, which increased to 71.9% at angiographic follow-up; complications included thromboembolism in 4.6%, mortality of 1.8%, aneurysm recanalization in 13.2%, and delayed in-stent stenosis in 5.6%. The use of SAC generally requires strong antithrombotic medications to prevent stent thrombosis, and for this reason SAC is most often used to treat unruptured aneurysms. In the setting of SAH, the use of antithrombotic agents to place a cerebral stent can have serious hemorrhagic consequences.⁸⁵