Ebook Decision making in neurovascular disease: Part 2

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32 Fusiform Aneurysms of the Anterior Circulation
Leonardo B.C. Brasiliense, Pedro Aguilar-Salinas, Douglas Gonsales, Andrey Lima, Eric Sauvageau, and Ricardo A. Hanel

Abstract The estimated prevalence of intracranial aneurysms (IA) in
the general population ranges between 2 and 4%. Although fusiform
aneurysms are more commonly found in the vertebrobasilar circulation,
these challenging lesions can occur in the anterior circulation with a
prevalence ranging from 0.1 to 0.3%. Fusiform aneurysms are complex
lesions that involve more than 50% of the arterial circumference and are
typically characterized by a lack of discernible neck. In general, this subset of lesions is associated with worse outcomes, higher rates of complications, and death. In this chapter, we discuss their anatomical features
and explore pathophysiological mechanisms as well as current evidence
in surgical and endovascular options. Microsurgery remains an adequate
treatment option and some of the vascular reconstructions include
trapping, wrapping, bypass, and excision and induction of aneurysm
thrombosis by proximal clipping. Endovascular options for fusiform aneurysms are typically associated with the use of stents or flow diverters
with or without the use of adjuvant coiling. Overall, these procedures
have demonstrated a safe and effective profile favoring this option over
microsurgery. However, in some instances, a combined approach can
be done. Although there is no consensus for the optimal management
of fusiform aneurysms in the anterior circulation, the decision is made
on a case-by-case basis assessing the patient’s hemorrhagic risk over an
estimated life span in contrast to neurosurgeon’s perceptions of potential complications, particularly major neurological morbidity and loss of
functional independence.
Keywords: intracranial aneurysm, fusiform aneurysm, surgery, endovascular

Introduction
Intracranial aneurysms are estimated to occur in approximately 2.8% of
the general population and giant aneurysms (≥25 mm in largest diameter) represent an infrequent subset of lesions representing only 3 to 5%
of intracranial aneurysms. These lesions are often also categorized into
saccular and fusiform based on their morphology and appearance on
imaging studies. Saccular aneurysm implies that a discernible neck is

present, which typically occurs following a localized defect in the arterial wall.
In contrast, fusiform aneurysms are complex lesions involving more
than 50% of the arterial circumference and typically characterized by no
discernible neck, which has important treatment implications. Although
fusiform aneurysms are more commonly found in the vertebrobasilar
circulation, these challenging lesions also occur in the anterior circulation with an estimated prevalence ranging from 0.1 to 0.3%. Within
the anterior circulation, the majority of fusiform aneurysms occur in the
internal carotid artery (ICA). Fusiform aneurysms involving the anterior
cerebral arteries (ACAs) and middle cerebral arteries (MCAs) are rarely
seen. Fusiform aneurysms in the supraclinoid segment of the ICA have
a higher rate of rupture (~40–50% over 5 years) compared to aneurysms
located in the cavernous segment (10% over the same period). The former lesions are also associated with worse outcomes, higher rates of
complications, recanalization, and death.
In the past, some authors have suggested that fusiform aneurysms
may have an atherosclerotic component in their etiology. However,
other pathogenic factors unrelated to atherosclerosis have been previously demonstrated to increase the risk of aneurysm enlargement
over time and bleeding. Age of the patient is a very good indicator of
lesion pathogenesis. Young patients often develop these aneurysms in
the context of vessel dissection or underlying vasculopathy, while older
patients (older than 45 years) are more likely to develop these lesions in
association with vessel atherosclerosis.

Major controversies in decision making addressed in this chapter
include:
1. Imaging surveillance versus treatment.
2. Microsurgical treatment versus endovascular techniques.
3. Long-term durability of current treatment strategies.
4. State-of-the-art endovascular devices.

Whether to Treat

Compared to saccular aneurysms, the natural history and risk of rupture for fusiform aneurysms in the anterior circulation remains a topic
only marginally understood and an area that would benefit greatly from
further studies. As with other intracranial aneurysms, factors to aid in
the treatment algorithm include (1) aneurysm size, (2) recent growth
on imaging studies, (3) previous subarachnoid hemorrhage (SAH), and
(4) patient preference. Smaller asymptomatic lesions can be safely monitored with serial imaging and rarely demonstrate further growth (1 in
algorithm). The decision to treat should always take in consideration the
estimated risks associated with treatment weighted against the natural
history.

Anatomical Considerations
Intracranial aneurysms are more likely to occur in certain segments of
the artery, which has generally been based on regional differences in
blood flow. Similarly, fusiform aneurysms tend to occur between areas
of vessel bifurcation in both proximal and distal segments of major
intracranial arteries. The majority of fusiform aneurysms in the anterior circulation are found in the cavernous segment of the ICA (~42%),
followed by the remaining ICA (23–39%), MCA bifurcation (32–41%), and
rarely ACA (0.2–1.0%). Fusiform aneurysms involving the ACA are usually
restricted to the A1 segment and similarly, these lesions are more likely
to occur at the M1 segment when the MCA is involved.

Pathophysiology
The events leading to the development of fusiform aneurysms are often
unknown; atherosclerosis has been postulated as a potential mechanism
due to disruption of the internal elastic lamina (IEL). It has also been
hypothesized that these lesions may arise from arterial microdissections
with intramural hemorrhage between the intima and the media leading to progressive dilatation and tortuosity. As previously mentioned,
dissection or nonatherosclerotic vasculopathy is more likely to occur
in younger patients, and atherosclerosis occurs more often in older
patients. In addition, turbulent flow within the aneurysm lumen has

been shown to create nonphysiological transmural pressures and shear
stress on the vessel wall, which may induce changes in smooth muscle
cell homeostasis and loss of endothelial integrity. Fusiform aneurysms
often have unique underlying pathological features on autopsy including
calcified walls, onion skin pattern in the vessel wall, partial aneurysm
thrombosis, and absence of aneurysm neck. Although uncommon, infection involving the vessel has been found to predispose the arterial wall
to fusiform dilation, which has been correlated with medial fibrosis, loss
of smooth muscle layer, destruction of the IEL, and intimal hyperplasia.
Tumor cell infiltration of intracranial vessels via the vasa vasorum has
also been associated with pseudoaneurysm formation and fusiform dilatations with partial destruction of the vessel wall, microvascular occlusion by the tumor, and direct invasion of the arterial wall. Rare cases
of fusiform aneurysm formation have been reported in patients with
X-linked lymphoproliferative (XLP) syndrome in which the immune
system is unable to mount an adequate response to viral infections,

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32

Fusiform Aneurysms of the Anterior Circulation

Algorithm 32.1 Decision-making algorithm for fusiform aneurysms in the anterior circulation. SAH, subarachnoid hemorrhage; TIA, transient ischemic attack.

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Aneurysms—Anterior Circulation
particularly by the Epstein–Barr virus, which may result in diffuse necrotizing vasculitis affecting major intracranial arteries. Fibromuscular
dysplasia may also facilitate aneurysm formation by causing various
degrees of collagen hyperplasia, IEL rupture, and disorganization of the
medial layer, which can result in dilatation of the artery.

Classification
From an angiographic and pathological standpoint, these lesions can be
classified into the following:
• Type 1: classic dissecting aneurysms. Angiographic features of a
fusiform aneurysm with irregular wall and irregular stenotic portion near the proximal or distal end. Pathological features include
widespread disruption of the IEL without intimal thickening, and the
presence of a pseudolumen, which is filled with thrombus.
• Type 2: segmental ectasia. Angiographic features of a fusiform
aneurysm with a smooth contour and typically associated with other
cerebrovascular diseases. Pathological features such as stretched or
fragmented IEL, moderately thickened intima, and no evidence of
thrombi.
• Type 3: dolichoectatic dissecting aneurysm. Angiographic features of
tortuous fusiform appearance with irregular contrast opacification
caused by intraluminal thrombus. Pathological features include fragmentation of IEL combined with multiple dissections of thickened
intima, and organized laminar thrombi.
• Type 4: saccular aneurysm arising from arterial trunk. Angiographic
features of saccular aneurysms unrelated to the branching zones.
Pathological features of a mixed type such as IEL pattern resembling
a type 1 lesion without a discernible pseudolumen or organized
thrombus as well as absence of IEL at the dome of the aneurysm with
distended fragile adventitia.

Workup
Clinical Evaluation
Fusiform aneurysms arising in the anterior circulation often present with symptoms of mass effect such as headaches, cranial neuropathy (especially visual symptoms) as well as transient ischemic
attacks (TIAs) or stroke. SAH occurs less often and similar to saccular
aneurysms; the majority of fusiform aneurysms (nearly 60%) are found
incidentally. Visual deficits due to optic nerve compression are more
frequently associated with fusiform aneurysm located in the ACA (2 in
algorithm). Skull base erosion with massive epistaxis has been reported
with these lesions although the true incidence is unknown.

Imaging
Imaging of fusiform aneurysms is similar to its saccular counterpart and
should evaluate the aneurysm wall, lumen, and flow. Magnetic resonance
imaging (MRI) based techniques are clearly the best modality for wall
imaging since these provide important information about wall thickness,
the presence of intramural thrombus, and the extent of mass effect. Lumen
imaging can be assessed with multislice helical computed tomography
angiogram (CTA) and has become the primary modality for noninvasive
imaging. Time-of-flight (TOF) magnetic resonance angiography (MRA) is a
reasonable alternative in patients with severe renal disease or in patients
requiring repeated imaging, with the caveat that MRA TOF can provide
misleading information such as apparent vessel stenosis or occlusion.
However, the “gold standard” modality remains digital subtraction angiography (DSA) because it provides real-time imaging of blood flow inside
the parent vessel and aneurysm as well as accurate vessel measurements,
which are essential for endovascular strategies. Catheter-based imaging
also allows us to perform better assessment of collateral flow, very often
useful for treatment of these lesions. Balloon test occlusion for the carotid
artery or superselective into the MCA and ACA (with newer low-profile
balloons) often provides valuable therapeutic guidance.

Differential Diagnosis
The differential diagnosis of fusiform aneurysms in the anterior circulation is broad and includes nonvascular processes such as intracranial
tumors, demyelinating diseases, intracranial infections, and other vascular events such as acute ischemic stroke, vasculitis, and sinus thrombosis.

Treatment
In general terms, treatment of fusiform aneurysms remains an individualized assessment of patient’s hemorrhage risk over an estimated life
span in contrast to the neurosurgeon’s perceptions of potential complications, particularly major neurological morbidity and loss of functional
independence. As with other intracranial aneurysms, the patient’s age,
pretreatment functional status, aneurysm size, location, and relationship
to arterial branches and perforators are important aspects to be evaluated. Management of fusiform aneurysms in the anterior circulation
remains a formidable challenge and is frequently incompatible with
conventional surgical and/or endovascular techniques. For instance, fusiform cavernous aneurysms with intramural thrombus, highly calcified
aneurysms, dissecting aneurysms, and aneurysms with major branches
originating in the dome are often not amenable to conventional microsurgical techniques. Treatment of fusiform ICA aneurysms frequently
requires cerebral revascularization of the distal territory with aneurysmal and/or parent artery occlusion through direct surgical or endovascular approaches. Goals of treatment include preservation of emerging
perforator arteries and the parent vessel. Partial occlusion may result in
complete thrombosis of the aneurysm, but recanalization is not a rare
event.
Endovascular options for fusiform aneurysms are typically associated
with the use of stents or flow diverters with or without use of adjuvant
coiling. Unless therapeutic sacrifice is the goal, simple coiling of fusiform
aneurysms is usually unfeasible or unsafe and may place the parent vessel at unnecessary risks. Stent-assisted coiling as a primary treatment
for fusiform aneurysms has been reported to have high rates of recanalization, ranging from 19 to 50%. Constructs overlapping multiple stents
have also been used with variable success rates.
Flow diverters represent a landmark in the management of fusiform
aneurysms because these stentlike devices are the first stand-alone
option to reconstruct the disease segment of the parent vessel by redirecting blood flow away from the aneurysm (4 in algorithm). Increased
experience with these devices has expanded their use to include complex anterior circulation aneurysms such as fusiform lesions in the ICA
and MCA. It has been demonstrated that aneurysm thrombosis following

placement of flow diverters is a dynamic process that can be manipulated
with different techniques of device placement including telescoping or
deployment of loose coils inside the aneurysm prior to device placement.
Overall, flow diverters could be considered the first-line endovascular
treatment for fusiform aneurysms following several studies that demonstrated their safety, effectiveness, and durability (4 in algorithm).
Microsurgery remains an adequate treatment option for fusiform
aneurysms involving the ICA or its branches with the caveat that it
requires complex techniques for vascular reconstruction. Some of the
goals of the vascular reconstruction are trapping, excision, and induction
of aneurysm thrombosis by proximal clipping. Aneurysm trapping and
resection are usually unfeasible in the distal anterior circulation due to
perforators originating from the aneurysmal segment. Aneurysm wrapping has fallen out of favor, especially with refinements in microsurgical
techniques and endovascular devices. Bypass surgery either in situ or with
extracranial anastomosis continues to be an important surgical option in
the neurosurgeon’s armamentarium. Depending on flow patterns in the
donor vessel, these reconstructive procedures may be divided into lowflow and high-flow bypasses. High-flow bypass is usually performed for
fusiform aneurysms in the ICA where a saphenous vein or radial artery
must be harvested to provide approximately 50 mL/min of blood flow
for adequate distal perfusion. In situ bypass is an elegant solution that

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32
may be performed for MCA or ACA aneurysms after careful assessment
for size match and length between vessels. Interposition grafts may also
be employed in these lesions prior to parent vessel occlusion or surgical

trapping. Although recent innovations in aneurysm treatment have limited the indications for bypass surgery, it remains an essential skill for
cerebrovascular neurosurgeons who intend to treat these lesions.

Conservative Management
When a decision is made for aneurysm observation, aspirin therapy is
generally recommended, although it lacks the support of clinical studies. The anti-inflammatory properties of aspirin can potentially decrease
the risk of progression and hemorrhage. It is prudent to maintain close
surveillance of these lesions with the first repeat imaging at 6 months
to document aneurysm stability (3 in algorithm). As previously mentioned, other aspects to consider prior to treatment include age, baseline
functional status, severity of symptoms, and comorbid conditions.

Cerebrovascular Management—Operative
Nuances
In preparation for open reconstructive procedures, patients typically
undergo ICA balloon test occlusion to assess collateral flow and tolerance
to proximal occlusion.
Hunterian ligation remains a viable option for giant fusiform aneurysms with a relatively simple surgical technique that has been used to
divert flow away from the aneurysm and induce aneurysm thrombosis. Of note, fusiform aneurysm proximal to the anterior clinoid may be
amenable to proximal occlusion alone, whereas supraclinoid aneurysms
are generally better managed with trapping techniques, especially to
alleviate symptoms of mass effect.
When considering microanastomotic techniques, the superficial temporal artery (STA) is a very versatile donor for these lesions, allowing for
simple or double barrel, or in association with a high-flow graft. For in
situ grafts, the internal maxillary artery (IMA) is also a useful alternative.
For ICA lesions, high-flow revascularization with the radial artery or
saphenous vein (~18–20 cm of graft) is necessary. The cervical ICA is
exposed using a standard anterior approach and a pterional or orbitozygomatic craniotomy for intracranial exposure. Exposure of the external
carotid artery for an extracranial–intracranial (EC–IC) bypass, end-toend, or end-to-side anastomosis is performed between the graft and the
ECA distal to the lingual artery. Clip application is performed parallel to
the branch vessels to avoid narrowing of the parent artery. Perforating

or branch arteries emerging from the fusiform aneurysm of the anterior circulation are important determinants of the timing and degree
of occlusion after revascularization as hemodynamic alteration by flow
diversion and acute thrombosis may result in serious adverse effects.
Postoperatively, the pulsations of the graft in the subcutaneous tunnel
are monitored with palpation and Doppler for the first 24 hours. Graft
occlusion within the first 24 hours should prompt immediate bypass
surgery with a new graft. Heparin (5.000 units) is administered every
8 hours for 3 days in addition to 81 mg of aspirin daily for approximately
1 year. MR perfusion and CTA are performed on postoperative day 1 to
confirm revascularization and graft patency. Follow-up MRA or CTA are
recommended at 3 months and then annually. ►Figs. 32.1 and ►32.2
illustrate the management of complex fusiform aneurysms.

Endovascular Management—Operative
Nuances
Patients are preloaded with dual-antiplatelet therapy, aspirin (325 mg
daily), and clopidogrel (75 mg daily) or ticagrelor (90 mg twice a day)
1 week prior to the intervention. Steroids (dexamethasone 10 mg
bolus or 4 mg every 6 hours) are used for giant fusiform aneurysms
and patients with symptoms of mass effect and continued for approximately 10 days.

Fusiform Aneurysms of the Anterior Circulation

A 6 French (6F) or 8F-long sheath is placed using a standard femoral
access and a guide catheter with an intermediate catheter (e.g., Navien;
058 Navien; ev3, Irvine, CA) is navigated to the cervical ICA. A microcatheter and microwire are maneuvered under road–map guidance proximal to the aneurysm in preparation for a device to be deployed.
A number of intracranial stents are currently available, for example,
Neuroform or Atlas Neuroform (Stryker Neurovascular, Fremont, CA), LVIS
or LVIS Jr. (Microvention, Tustin, CA). Multiple flow diverters are currently
available or under development, but we typically prefer to use the pipeline embolization device (PED) or PED FLEX (PED; ev3-Covidien, Irvine,

CA) due to increased experience and positive evidence in the literature.
In general, flow diverters are considered excellent treatment options for
fusiform aneurysms, especially in the anterior circulation where their use
appears to be associated with fewer number of thromboembolic events.
In brief, arterial access is obtained (more often femoral, occasionally
radial/brachial/axillary) with a 6F- or 8F-long sheath and the intermediate catheter (058 Navien; ev3) is navigated selectively in the distal ICA
under road-map guidance. A Marksman (ev3), Phenom 27 (Phenom), or
an XT-27 (Stryker Neurovascular) microcatheter is advanced distal to the
landing zone and the device is deployed across the neck of the aneurysm.
Expansion of the PED is closely monitored with fluoroscopy and Xpert CT
angiography after final deployment (►Fig. 32.3). When the device seems
inadequately opposed to the vessel wall, it can be manipulated with a
wire and catheter or balloon angioplasty (Hyperglide or Hyperform; ev3
Neurovascular, Irvine, CA) can be performed.

Complication Avoidance
Complications of open revascularization include occlusion of the graft,
which can best be prevented by meticulous surgical techniques and
adequate sizing prior to implantation. Stroke may occur after inadvertent placement of the aneurysm clip over adjacent perforators, which
has been greatly reduced with routine use of intraoperative indocyanine
green (ICG) angiography. Other complications include intraoperative
aneurysm rupture and SAH, injury to cranial nerves, and chemical meningitis from intradural drilling of the anterior clinoid and sphenoid bone.
Ischemic events are one of the most frequent complications with endovascular procedures. With flow diverters, the rate of ischemic events
ranges from 4 to 8%, most likely because these devices have a higher metal
density compared to intracranial stents and the procedures require more
extensive catheter manipulation. Other uncommon complications include
acute device thrombosis, vessel dissection, vasospasm, and delayed aneurysm rupture. Long-term complications include device stenosis, spontaneous bleeding from dual-antiplatelet therapy, and stent migration.

Outcome
As mentioned in the earlier sections, the choice of treatment should be

made on a case-by-case basis. The available data on outcomes are lacking
and have been obtained mostly from retrospective case series partially
due to the low prevalence of anterior fusiform aneurysms, which makes
it difficult to compare outcomes between microsurgical and endovascular techniques. In general, microsurgical strategies have estimated rates of
clinical improvement between 58 and 84% (modified Rankin Scale [mRS]
score 0–3) but rates of mortality ranging from 14 to 22%. In contrast, endovascular strategies such as flow diverters have shown excellent outcomes
with rates of clinical improvement in up to 90% (mRS 0–2) of patients and
acceptable rates of aneurysm occlusion ranging from 60 to 78% (supports
algorithm step 4).
A recently published series of 323 intracranial dissecting and/or fusiform aneurysms were classified based on a modified imaging classification in dissecting (type I), segmental ectasia (type II), dolichoectatic
dissecting aneurysm (type III), and large bleeding mural ectasia (type IV).
A logistic regression was done to find predictors of outcome. Of the 323,
66.8% was treated with stent-assisted coiling, 14.5% with internal trapping, and 18.6% with sole stenting. Clinical follow-up was available for
309 patients with a mean of 10.4 months (range 3–60 months). Imaging

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Aneurysms—Anterior Circulation

Fig. 32.1 Case illustration 1. A 48-year-old female patient with previous subarachnoid hemorrhage presenting with enlarging complex fusiform dilatation of the left middle
cerebral artery (MCA) aneurysm demonstrated on computed tomography angiography (CTA; a,b). Cerebral angiogram showed a complex fusiform aneurysm extending
from M1 to superior M2 division (c,d). Note areas of stenosis at the origin of the inferior division on three-dimensional (3D) reconstruction (e). Our initial plan consisted
in performing a superficial temporal artery–middle cerebral artery (STA–MCA) bypass to the superior division with clipping of the M1-inferior division lesion. Prior to
treatment, the stenotic segment of the M1–M2 inferior division was stented (f,g). The STA–MCA bypass was performed 30 days later (h). A remnant M1-inferior division
aneurysm could not be clipped (i). The patient was later treated with coiling of the remaining aneurysm sac (j) and persistent aneurysm occlusion at 5-year follow-up.

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Fusiform Aneurysms of the Anterior Circulation

Fig. 32.2 Case illustration 2. A 34-year-old male patient presented with seizures. Brain magnetic resonance imaging (MRI; a,b) demonstrated a giant thrombosed aneurysm of the anterior cerebral artery (ACA). Cerebral angiogram with anteroposterior (c–e) and lateral (f–h) views showed a giant serpentine aneurysm on the left ACA with
delayed transit time compared to middle cerebral artery (MCA) territory. Balloon test occlusion performed under local anesthesia with balloon placed at distal left A2 (i)
demonstrated adequate A3–A4 collaterals from posterior circulation branches (j). The patient underwent a craniotomy for clip trapping of the lesion and a possible A3–A3
bypass. Intraoperative angiography posttrapping confirmed presence of collaterals (k) and a decision was made for trapping only with evacuation of the aneurysm content.
The patient was seizure free with persisted aneurysm occlusion at 6-month follow-up (l,m).

follow-up was available for 262 patients only; there was a recurrence
rate of 9.16%. The only independent predictor factor was aneurysm type;
types III and IV had a significant unfavorable outcome. Reconstructive
endovascular treatment using conventional stents did not resolve the
mass effect and had a higher recurrence rate compared to the cases that
had reconstruction using flow diverter stents (supports algorithm step 4).

Clinical and Radiographic Follow-Up
Following treatment of fusiform aneurysms, patients are best managed
with clinical evaluation at 1 month to identify early signs of open or
endovascular complications such as TIAs and worsening cranial neuropathy. Vascular imaging is usually obtained at 3 months using noninvasive
tests and at 6 months with DSA, followed by yearly thereafter following
endovascular procedures. A DSA-based scale is used to determine aneurysm occlusion (Raymond–Roy).

Expert Commentary
Fusiform aneurysms of the anterior circulation are some of the most
challenging lesions we face in cerebrovascular surgery. The natural
history for these lesions remains less defined compared to saccular
ones. A thorough risk-versus-benefit analysis should be made prior
to making a decision to treat. Careful analysis with MRI-based images
and catheter-based angiography, including balloon test occlusion, and
collateral flow assessment are paramount. The advent of improved
stent technology, especially flow diverters, has provided a significant
upgrade to endovascular tools. The decision for endovascular versus
microsurgical or combined approaches should be done on a case-bycase basis.
Ricardo A. Hanel, MD
Baptist Neurological Institute, Jacksonville, FL

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Aneurysms—Anterior Circulation

Fig. 32.3 Case illustration 3. A 55-year-old female patient with previous history of subarachnoid hemorrhage and clipped right middle cerebral artery aneurysm. She
presented with headaches and workup demonstrated a fusiform aneurysm in the right M1 trunk (a,b). We decided to treat it with a flow diverter. A single pipeline embolization device (PED; 5 × 35 mm) was used, oversized to decrease mesh density over the M1 perforators covered with the PED (c). Contrast stasis in the aneurysm was
noticed after device placement (d). Intraoperative cone beam computed tomography (CT) demonstrates device in adequate position (e). A 6-month follow-up angiogram
demonstrates complete aneurysm occlusion and preservation of perforators (f,g).

Editor Commentary
Fusiform aneurysms come in many varieties, and each demands its own
solution. These lesions are almost certainly the result of earlier dissection and can be found incidentally or can become symptomatic from

thrombus formation, mass effect, or SAH.
Asymptomatic lesions may best be treated with continued observation, while those that present symptomatically may require the entire
endovascular and surgical armamentarium. Flow diverters, vessel occlusion, bypass, clip reconstruction, and circumferential wrapping are all
options depending on the specific lesion.

Peter Nakaji, MD and Robert F. Spetzler, MD
Barrow Neurological Institute, Phoenix, AZ

Suggested Reading
Anson JA, Lawton MT, Spetzler RF. Characteristics and surgical treatment of dolichoectatic and fusiform aneurysms. J Neurosurg 1996;84(2):185–193
Darsaut TE, Darsaut NM, Chang SD, et al. Predictors of clinical and angiographic outcome after surgical or endovascular therapy of very large and giant intracranial aneurysms. Neurosurgery 2011;68(4):903–915, discussion 915
Drake CG, Peerless SJ, Ferguson GG. Hunterian proximal arterial occlusion for giant
aneurysms of the carotid circulation. J Neurosurg 1994;81(5):656–665

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Kashimura H, Mase T, Ogasawara K, Ogawa A, Endo H. Trapping and vascular reconstruction for ruptured fusiform aneurysm in the proximal A1 segment of the
anterior cerebral artery. Neurol Med Chir (Tokyo) 2006;46(7):340–343
Mizutani T, Miki Y, Kojima H, Suzuki H. Proposed classification of nonatherosclerotic cerebral fusiform and dissecting aneurysms. Neurosurgery 1999;45(2):
253–259, discussion 259–260
Monteith SJ, Tsimpas A, Dumont AS, et al. Endovascular treatment of fusiform
cerebral aneurysms with the pipeline embolization device. J Neurosurg
2014;120(4):945–954
Nurminen V, Lehecka M, Chakrabarty A, et al. Anatomy and morphology of giant
aneurysms—angiographic study of 125 consecutive cases. Acta Neurochir (Wien) 2014;156(1):1–10

Fusiform Aneurysms of the Anterior Circulation

Shokunbi MT, Vinters HV, Kaufmann JC. Fusiform intracranial aneurysms. Clinicopathologic features. Surg Neurol 1988;29(4):263–270
Spetzler RF, Selman W, Carter LP. Elective EC-IC bypass for unclippable intracranial
aneurysms. Neurol Res 1984;6(1–2):64–68
Thompson BG, Brown RD Jr, Amin-Hanjani S, et al; American Heart Association
Stroke Council, Council on Cardiovascular and Stroke Nursing, and Council
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Stroke Association. Guidelines for the management of patients with unruptured intracranial aneurysms: a guideline for healthcare professionals
from the American Heart Association/American Stroke Association. Stroke
2015;46(8):2368–2400

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33 Dissecting Intracranial Aneurysms of the Anterior
Circulation

Stephen R. Lowe, Jan Vargas, Alejandro Spiotta, and Raymond D. Turner, IV

Abstract Dissecting intracranial aneurysms are anatomically unique
and thus are not easy to classify in the same way that saccular aneurysms
have been in the neurosurgical literature. These lesions are dynamic and
may present with both hemorrhagic (i.e., subarachnoid hemorrhage)
and ischemic symptoms. These are complex anatomical lesions and generally require some form of neurosurgical intervention. Neurosurgical
intervention may be both an open surgical procedure or endovascular

vessel reconstruction, or vessel sacrifice. In cases where endovascular
reconstruction is feasible, it is generally preferred. However, given the
variability in location and morphology of these lesions, treatment must
be individualized as much as possible. In this chapter, we present the
relevant natural history, prognosis, anatomy, pathophysiology, workup,
and management of dissecting intracranial aneurysms of the anterior
circulation. We will also discuss blister-type aneurysms, a special subset
of dissecting aneurysms with a unique physiology, natural history, and
treatment algorithm
Keywords: dissecting intracranial aneurysm, dissecting pseudoaneurysm, blister-type aneurysm, subarachnoid hemorrhage, clip reconstruction, flow diversion

Introduction
Dissecting intracranial aneurysms (DIAs) represent a unique challenge
to the cerebrovascular surgeon. These rare lesions must be addressed
carefully and thoughtfully to ensure a safe and durable treatment for
the patient. Their friable anatomy makes them technically complex
lesions to treat, either by open or by endovascular techniques. More
significantly, these are lesions that do not conform to the typical saccular morphology seen with aneurysms described in the large International Subarachnoid Aneurysm Trial (ISAT) and International Study of
Unruptured Intracranial Aneurysms (ISUA) series. Due to this lack of
high-quality randomized and observational data, and due to the relative paucity of reports in the literature regarding the natural history,
prognosis, and treatment of these lesions, developing a well-validated
treatment algorithm for these lesions is challenging. We aim to describe
the classification, natural history, pathogenesis, and treatment considerations for DIA of the anterior circulation.
For the purposes of this chapter, we will consider dissecting pseudoaneurysms (i.e., those that arise either spontaneously or secondary to trauma or
iatrogenic causes), which we will term DPA, separately from a unique group
of dissecting aneurysms, which we will term blister-type aneurysms (BTAs).
The abbreviation “DIA” will refer to DPAs and BTAs collectively.
Major controversies in decision making addressed in this chapter
include:
1. Whether or not treatment is indicated.

2. Open versus endovascular management for DIAs.
3. Advanced strategies for open reconstruction of DIAs.
4. Advanced strategies for endovascular reconstruction of DIAs.

Whether to Treat
DIAs are uncommon lesions with an ill-defined incidence in the literature. While BTAs are reported to represent 0.3 to 2% of all intracranial
aneurysms, DPAs of the anterior circulation are even more unusual, with
less than 100 reports of spontaneous DPAs in the literature and less than
50 reports of DIA secondary to trauma reported in the literature. Unlike
the more common saccular or “berry” aneurysm, where long-term rates
of rupture are well defined, the natural history of DIAs is not well defined

due to their infrequent presentation and lack of observational studies.
The large majority of these lesions in the literature are described in the
setting of subarachnoid hemorrhage (SAH), suggesting a malignant natural history (1, 2, 3 in algorithm). Additionally, many retrospective studies have shown these lesions to be dynamic in nature (particularly for
BTAs), demonstrating rapid growth and rapid change in the conformation of the aneurysm, even in short intervals of follow-up. Rapid growth
and change in these lesions is even observed after attempted treatment,
particularly with BTAs. In the setting of SAH, patients with DIAs tend
to have worse outcomes than those with a ruptured saccular aneurysm
history (2 in algorithm).
As noted earlier, the natural history of these lesions is not well documented. BTAs are almost always described in the ruptured setting, and
short-interval follow-up vascular imaging suggests that these lesions
are dynamic, demonstrating rapid conformational change suggestive of
instability and a malignant natural history. DPAs were historically implicated as a rare cause of ischemic symptoms in young patients; however,
recent reports suggest that they are more commonly associated with
SAH. When presenting with SAH, DIAs have been reported to have a
higher rate of rebleeding (44%) compared to saccular aneurysms (14%),
and as such the prognosis is worse in these patients. As such, when a DIA
is diagnosed in the setting of SAH, it should be treated aggressively and
promptly (1, 2, 3 in algorithm).

DPAs with ischemic symptoms, on the other hand, can have a more
benign course. Compared to dissecting aneurysms of the vertebral
artery, DPAs of the internal carotid artery (ICA) tend to persist longer,
but carry little risk of recurrent ischemic events. Patients with recurrent ischemic symptoms may warrant definitive treatment, but in the
light of the good prognosis of these lesions, medical management to
prevent thromboemboli is usually first-line treatment before subjecting a patient to invasive treatments (4, 12 in algorithm). Despite the
associated higher risk of treatment, the aggressive course of DIA seen in
the literature suggests that these lesions should be treated aggressively
when presenting with SAH. Treatment should be offered to all patients
with evidence of a ruptured DIA.
In patients with an incidentally discovered DPA with ischemic symptoms, conservative management is appropriate, unless the patient suffers recurrent ischemic events. DIA secondary to trauma should be given
strong consideration for treatment in the unruptured setting given they
likely have an aggressive natural history. The natural history of incidentally discovered BTAs is not well documented, but the malignant natural
history of these lesions suggests that conservative management is not
appropriate and these lesions must be treated aggressively despite clear
risks of treatment.

Anatomical Considerations
Dissecting Pseudoaneurysms
The majority of dissections occur in the extracranial ICA, and most spontaneous DPA arise in the same location. DPAs that originate at the skull
base, however, are more challenging to access and treat, both with open
microsurgery and endovascular techniques. These lesions tend to have
large, irregular domes with irregular and variable neck segments, and
generally arise from nonbranching segments of their parent vessel.
DPAs secondary to trauma are generally seen arising from distal
branches of the anterior cerebral artery. However, traumatic dissections
can be seen in any location involved with a penetrating trauma or iatrogenic injury, including in association with malpositioned ventriculostomy catheters or intracranial pressure monitors. Traumatic DPA can

220

Due to the paucity of literature regarding anterior circulation DIA, much
of the proposed pathophysiology has been adapted from histopathological studies of vertebrobasilar DIA.

Dissecting Pseudoaneurysms
Primary DPAs arise from a dissection of the parent vessel, and as such the
natural history of these lesions is linked to that of cerebral artery dissections (►Fig. 33.1). Most dissections of the anterior circulation present
spontaneously. Connective tissue disorders, dissections of multiple vessels and redundancies of vessels, and a history of migraines and tobacco
use have been identified as risk factors for the formation of DPAs after
an intracranial dissection. A subset of these lesions will be secondary to
trauma or to iatrogenic causes. Aneurysms secondary to trauma can be
either penetrating or blunt, but those arising secondary to blunt trauma
are extremely rate, accounting for approximately 0.5% of all intracranial
aneurysms. The pathophysiological mechanism of the classic type of
traumatic DIA arising from the anterior cerebral artery (ACA) is felt to be
related to injury to the vessel arising from contact with the falx cerebri.
Iatrogenic causes are generally a result of complications from surgical or
endovascular manipulation of the intracranial vasculature.
In cases of DPA that present with SAH, a dissection plane is generally seen confined to the subadventitia, whereas ischemic strokes

are generally associated with dissection planes seen in subintimal
layer. Hirao et al classified DPA of the ACA into types I, II, and III. Type
I originates at the ICA and extends into the ACA and middle cerebral
artery (MCA). Type II often occurs at the A1 segment of the ACA, and type
III generally involves the distal ACA branches. There are no classification
schemes described for DPA secondary to trauma or iatrogenic causes and
the exact pathophysiology is not well delineated owing to the paucity of
reports and lack of anatomical studies. Indeed, these aneurysms tend to
be unique to the process that created them, and as such each aneurysm
is slightly different.

Blister-Type Aneurysms
BTAs of the anterior circulation are manifested by a disruption of the
normal internal elastic lamina and media with normal adventitia covering the defect. Sim et al noted an interesting corollary between the BTAs
seen classically on the supraclinoid ICA and Mizutani type IV dissections
of the vertebral artery, suggesting a focal dissecting process is responsible for the unique morphology of this lesion. While generally the causative factor is thought to be shear stress on the arterial wall caused by
the unique flow dynamics of the supraclinoid ICA, other rare causes of
BTA, such as Ehlers–Danlos syndrome and invasive Aspergillosis have
also been described, generally in conjunction with BTAs in locations outside of the supraclinoid ICA.
There are no widely accepted classification schemes for BTAs of the
supraclinoid ICA. Bojanowksi et al proposed a four-tiered classification
scheme, with type I dissections representing a small bulge in the arterial wall without an appreciable neck segment (►Figs. 33.1, ►33.2, and
►33.3). Type II BTAs are larger, with a defined neck that is not greater
in size than the diameter of the ICA. Type III has a neck segment that
is longer in the longitudinal plane than the diameter of the ICA. Type
IV represents circumferential disease of the carotid at the diseased segment, with or without a focal outpouching. The authors recommend
simple clip reconstruction for types I and II, a multiclip reconstruction
for type III lesions owing to their large size, and a clip-over-wrapping
technique for type IV lesions. They note that these lesions may not be
separate, but may in fact represent different stages of the same disease
process. This survey included only 10 patients, which underscores the
paucity of literature on the topic.

Workup
Clinical Evaluation
Generally, patients present with signs and symptoms of aneurysmal
SAH. Many of the patients without SAH may also present with headache (►Figs. 33.2 and ►33.3). Clinical evaluation and management
should proceed according to the standard of care for patients with this
life-threatening condition.
Patients can also present with a wide range of ischemic symptoms
such as massive cerebral infarction, transient hemiparesis, loss of vision,

or headaches. These symptoms are almost exclusively seen in patients
with DPA and never in patients with BTA.

Imaging

Fig. 33.1 Artist’s illustration demonstrating the pathophysiology of a dissecting
aneurysm.

In patients presenting with clinical suspicion of SAH, a computed tomography (CT) and CT angiography (CTA) should be obtained. For patients
with ischemic symptoms, CTA has been used to definitively diagnose an
intimal flap and subsequent aneurysm, and in patients in which radiation or contrast loads prohibit CTA, magnetic resonance angiography (MRA) has been equally helpful in diagnosing DIAs. Additionally, for unruptured DPAs, diffusion-weighted magnetic resonance
imaging (MRI) is critical for the diagnosis of ischemia. Formal digital
subtraction angiography (DSA) is usually undertaken next for definitive
diagnosis and to prepare for treatment (►Figs. 33.2 and ►33.3). If catheter angiography including three-dimensional (3D) reconstructions

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33 Dissecting Intracranial Aneurysms of the Anterior Circulation

Fig. 33.2 Internal carotid artery (ICA) dissecting aneurysm. (a) A 65-year-old female patient presented with
acute subarachnoid hemorrhage (Hunt and Hess 2 and
Fisher 2). (b,c) Digital subtraction angiography revealed
dissecting aneurysms of the right ICA. Notice the
blister (arrow) component of the dissection. (e,f) The
dissecting ICA aneurysm was successfully treated with a
flow-diverting stent. The patient did not require any further interventions and recovered successfully. (Images

provided courtesy of Leonardo Rangel-Castilla, MD,
Mayo Clinic, Rochester, MN.)

Fig. 33.3 Anterior cerebral artery (ACA) dissecting aneurysm. (a) A 49-year-old female patient presented with acute subarachnoid hemorrhage (Hunt and Hess 4 and
Fisher 3). (b,c) Digital subtraction angiography revealed a dissecting aneurysm of the left ACA. Notice the blister (arrow) component of the dissection. Patient underwent
a microsurgical exploration with the intention of primary clipping. During the procedure, the parent vessel (ACA) was found to be very fragile and had to be sacrificed.
(d,e) Intraoperative images of the left ACA blister aneurysm (arrow heads) treated with complete parent vessel occlusion (e). (f,g) Postparent vessel occlusion angiography
demonstrating complete occlusion of the dissected left ACA with preservation of both ACAs (A1 and A2) and left Heubner artery. The patient recovered successfully. Her
modified Rankin Scale (mRS) score at the last visit was 0. (Images provided courtesy of Leonardo Rangel-Castilla, MD, Mayo Clinic, Rochester, MN.)

is unrevealing, a short-interval follow-up DSA is warranted as a rapidly evolving lesion such as a DIA can be identified in this setting. It
is important to ensure a complete and adequate image of the lesion is
obtained as angiographic appearance will guide treatment.

Treatment
Conservative Management
In the setting of a DPA presenting with ischemic symptoms, conservative management and clinical follow-up is warranted. Patients should
be placed on antiplatelet therapy; however, due to the rarity of these
lesions, there are currently no recommendations for duration of antiplatelet therapy. Conservative management should never be attempted
in the setting of SAH for any DIA, nor should it be attempted for an incidentally discovered BTA.

Cerebrovascular Management—Operative
Nuances
Open cerebrovascular management options are well documented in the
literature, and include parent vessel sacrifice, trapping with or without
bypass, clip occlusion of the lesion by any number of techniques, or
wrapping techniques with or without clip application. Open cerebrovascular management can be challenging due to friability of the aneurysm
dome, adhesion of the dome to the surrounding parenchyma, difficulty
in reconstruction of the diseased vessel via clip application techniques,
and potential rerupture due to incomplete occlusion of the diseased

vessel segment.
Definitive management of DIAs involves sacrifice of the parent vessel with complete removal of the lesion from circulation (►Fig. 33.3; 7
in algorithm). However, in many cases parent vessel sacrifice is not a
feasible option due to a high resultant neurological morbidity for the

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Aneurysms—Anterior Circulation
patient. Additionally, DPAs that originate at the skull base are difficult to
access and occlude. Trapping the diseased segment between clips with
or without bypass represents an alternative option for definitive treatment of the diseased segment, and can achieve a permanent occlusion
from the circulation similar to vessel sacrifice. Bypass is not ideal in the
setting of acute SAH for a variety of reasons; it could be technically challenging due to cerebral edema and cisternal blood inherent to the postSAH state. Also, even “high-flow” bypass techniques ultimately provide
lower flow than the carotid itself, which can be deleterious in a patient
who may develop vasospasm as a sequela of SAH. Despite these obvious drawbacks, these techniques represent the only definitive way of
permanently occluding the aneurysm itself and thus obviating the risk
of rerupture, and should be considered if felt to be technically safe and
with low risk of neurological morbidity in all patients. Indeed, Kamijo
and Matsui reported a 100% occlusion and long-term patency rate in four
patients treated with trapping and extracranial–intracranial (EC–IC) bypass
in the setting of acute SAH. However, given success of other, lower risk
strategies, the above options should only be considered in the hands
of an experienced and high-volume surgeon who has a high preoperative certainty of success with minimal neurological morbidity for the
patient (9 in algorithm).
If parent vessel sacrifice and/or trapping are not possibilities, then
more traditional methods of clip reconstruction remain a viable option.

An open clipping procedure in a patient with DIA is fraught with risk and
should be undertaken only with the most meticulous of preoperative
preparation and care. As these patients have a high risk of intraoperative
rupture, the surgeon should make all preparations to manage intraoperative rupture or avulsion of the aneurysm dome during clip application.
One particular clip application technique specific to the clipping of BTAs
worth highlighting involves a parallel clipping of the aneurysm along the
length of the vessel (almost always the supraclinoid ICA), incorporating
a portion of the healthy vessel wall into the clip tines in order to provide
a better stability for the clip and minimize risk of recurrence. This does
result in some degree of stenosis of the ICA, so careful assessment of the
patient’s preoperative angiography is important in determining what
degree (if any) of iatrogenic stenosis the ICA is able to tolerate prior to
this type of clipping.
If the above are not options, clipping-and-wrapping techniques or
wrapping techniques alone remain fallback options. These are associated
with high rates of recurrence and should never be first-line therapies;
rather, they should be reserved for lesions that either fail a first-line
clipping (or endovascular) procedure or are not deemed suitable for
such an approach due to complicated morphology (9 in algorithm).

Endovascular Management—Operative
Nuances
Endovascular treatment of DIA with traditional coil embolization techniques have been associated with high recurrence rates. Introduction
of a coil mass into dissecting aneurysms can lead to rupture given the
fragility of the aneurysm walls; similarly, manipulation with a microcatheter may also result in intraprocedural rupture. In cases where the
aneurysm is broad based, care must be taken to prevent coil loop herniation into the parent vessel. In many cases, this would require balloon- or
stent-assisted coiling. The use of such adjuvant techniques may lead to a
more satisfactory initial result but ultimately still have an unacceptably
high recurrence and rebleed rate. Another strategy that was developed
and has proven to be more effective and durable is the use of multiple

overlapping stents to preferentially shunt flow down the parent artery
and disrupt the inflow at the neck of the aneurysm (8 in algorithm).
Such early “flow-diverting” techniques promoted aneurysm thrombosis over time and, as they did not involve manipulation of the fragile
aneurysm itself, were associated with lower rates of intraprocedural
rehemorrhage. The downside of this strategy is that it requires dualantiplatelet therapy. As the next-generation strategy to the use of multiple overlapping stents, the development of novel, flow-diverting stents

has allowed for the treatment of dissecting aneurysms without vessel
sacrifice or coil packing into a friable aneurysm (►Fig. 33.2). When associated with a dissection, flow diverters can be used to treat the underlying injury and remodel the vessel (8 in algorithm).
Some limitations to flow diversion include the need for dual-antiplatelet therapy for 3 to 6 months to minimize the risk of thromboembolic complications. This requirement can be a large deterrent in the
setting of SAH. Conversely, patients with ischemic symptoms from a
DIA may benefit from antiplatelet therapy to prevent recurrent ischemic
symptoms. Additionally, while these devices immediately divert blood
flow away from the aneurysm lumen, it can take several weeks for
endothelial and neointimal tissue to form along the scaffolding provided
by the flow diverter.

Complication Avoidance
Complications of treatment for DIAs generally involve aneurysm recurrence and rerupture, or intraprocedural rupture. Careful knowledge
of the type of DIA, cause of DIA, and specific anatomy of the lesion in
question, along with meticulous preoperative planning and preparation, are critical to minimizing the high risk of complication in these
patients. With open neurosurgical clipping, it is important to remember
that larger lesions may adhere to the surrounding parenchyma and put
the patient at higher risk of rupture with aggressive brain retraction.
Iatrogenic carotid stenosis with a direct clip-application technique is a
potential pitfall of open neurosurgical treatment of BTAs. Additionally,
improper selection of patients for parent vessel sacrifice or bypass surgery can lead to devastating neurological morbidity and mortality. In the
two largest meta-analyses of treatment paradigms for BTAs, Gonzalez et
al showed a higher rate of morbidity and mortality in surgical patients
as compared to endovascular patients and recommended an individualized approach to treatment depending on institutional expertise
(supports algorithm step 8).

Endovascular management is not without peril. Aggressive microcatheter practice and/or coiling of aneurysm increase risk of intraprocedural rupture. Use of a multiple-overlapping stent technique or a
flow-diverting stent brings with it the risk of early or delayed in-stent
thrombosis, with potential resultant ischemic complications. The use
of antiplatelet agents after stent placement can also present an issue,
particularly if patients may later warrant further surgical intervention.
While there are no guidelines on use of antiplatelet agents after SAH
specifically in conjunction with a treatment procedure such as intracranial stent placement, rates of hemorrhage with ventriculoperitoneal
shunting in patients on antiplatelet agents range from 32 to 74%.

Outcome
Dissecting Pseudoaneurysms
There have been reports of unruptured DPAs resolving on angiographic
follow-up. In cases where patients present with ischemic symptoms,
the outcome is good once patients are started on antiplatelet therapy,
and most do not exhibit recurrent ischemic events (4 in algorithm). In
contrast, patients presenting with SAH from a ruptured DPA tend to have
a poor prognosis, with a mortality of up to 50%, which given the complexity of these lesions is not unsurprising. In untreated cases, rebleeding has
been reported to occur in 50% of patients within 14 days, highlighting the
need for early intervention (supports algorithm steps 2, 4, 5, 6). Unfortunately, due to the rarity of these lesions, outcome data are available only
through case reports and case series.

Blister-Type Aneurysms
Outcomes for BTAs are invariably poor. Morbidity and mortality rates
range from 20 to 40% in most studies for all patients with BTAs. In
patients with rerupture, mortality rates are high and many survivors
are left permanently disabled. Operative outcomes are similarly worse

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33 Dissecting Intracranial Aneurysms of the Anterior Circulation
for BTAs as well, with up to 25% of patients undergoing any type (i.e.,
open or endovascular) of intervention experiencing an intraprocedural
rupture, as compared with a 2.5% rate of intraprocedural rupture for saccular aneurysms treated via endovascular means and a 6% risk of intraoperative rupture for that same group. Similar to DPAs, outcome data are
limited to small case series and small reviews, and much of the outcome
data are dated and dependent on the type of treatment utilized (which,
in retrospect, may have been suboptimal).

Durability and Rate of Recurrence
Dissecting Pseudoaneurysms
Due to the lack of outcome data, the durability and recurrence rates of
anterior circulation DPAs are limited. No cases of DPA that were treated
with open surgery showed evidence of rerupture or recurrence. There
are also reports of ICA and MCA lesions that were successfully treated
with flow diverters, with no evidence of recurrence or endoleak at follow-up. Thus, newer endovascular techniques represent an attractive
alternative to open surgery. Given paucity of data, we cannot recommend endovascular techniques over open microsurgical reconstruction
(or vice versa) if vessel sacrifice is not an option, although endovascular
therapies with flow diversion appear promising and may in fact represent best practice, depending on the optimal skill set of the treating
physician (5, 6 in algorithm).

Blister-Type Aneurysms
There are few reports that directly compare outcomes of open neurosurgical clipping to endovascular management. Two meta-analyses published in 2013 attempted to draw parallels between the two, albeit with
fundamentally different review and paper inclusion criteria. Szumuda et
al found that all combined types of endovascular therapy had a higher
rate of aneurysm regrowth and rerupture as compared to surgical intervention. Additionally, Gonzalez et al showed a higher rate of retreatment (46–21%) in patients undergoing endovascular reconstruction as
opposed to open clip reconstruction (supports algorithm steps 7 and 9).
Szumuda et al were able to show a very significant increase in rate of

regrowth and recurrence in patients treated with a stent-assisted coiling technique, making this a last-line option in our algorithm. Indeed,
in many of the older series looking at endovascular therapies for BTA,
retreatment rates approached 50%. Efficacy of flow-diversion and overlapping stent techniques appears to be much higher, though because
reports of these techniques are few in number, accurate assessment of
recurrence and retreatment rates are difficult. Yoon et al report a 63%
complete occlusion rate and a 27% complication rate in their series of 11
patients treated via the Pipeline device. Chalouhi et al showed complete
occlusion in five of six patients treated with the Pipeline device who
were available for long-term follow-up. They did not report any procedural complications (supports algorithm step 8). Similar to DPAs, we cannot recommend open microsurgical intervention over flow diversion (or
vice versa) as second-line treatment for BTAs if vessel sacrifice is not an
option. Again, flow diversion may in fact represent best practice as the
overall morbidity is likely lower than with open surgery, but there is no
high-level evidence to support this. The technique that is felt to be safest
in the hands of the treating physician taking into account each unique
clinical scenario should be utilized (supports algorithm steps 5–9).

Clinical and Radiographic Follow-Up
In patients with ruptured DIAs, angiographic follow-up is critical to ensure no signs of recurrence or, in the cases of flow diversion,
endoleaks. Serial angiography and clinic visits help establish a baseline
to which treatments can be compared. There are no consensus guidelines on number and frequency of follow-up imaging studies; however,
given the tendency for early and rapid regrowth of suboptimally treated
DIAs, we would recommend early and aggressive follow-up, preferably
with posttreatment diagnostic angiography prior to hospital discharge.

Expert Commentary
Dissecting or blister-type pseudoaneurysms are a rare and highly challenging subset of intracranial aneurysms. Most frequently identified in
the setting of SAH, these aneurysms have a more sinister clinical course
with higher rates of rerupture and growth, which justifies aggressive
and definitive treatment. Due to the fragility of the aneurysm wall, traditional methods of aneurysm treatment including conventional microsurgical clipping and coil embolization have unacceptably high rates of
intraprocedural rerupture, so treatment modalities have been adjusted

to address these high-risk aneurysms. Surgical treatment has evolved to
include trapping and bypass or intentional “over clipping” and stenosing
of the parent artery. Endovascular methods include flow diversion with
either multiple overlapping stents or newer generation flow-diverting
stents, with the caveat that dual antiplatelet therapy will be required.
However, if the dual antiplatelet therapy can be managed safely, flow
diversion has proven to be effective in reducing the likelihood of
immediate rerupture and delayed growth. These complex, technically
challenging aneurysms are best addressed at centers with high-volume
surgical and endovascular expertise.
Raymond D. Turner, IV, MD, and Alejandro Spiotta, MD
Medical University of South Carolina, Charleston, SC

Editor Commentary
The malignant natural history of atherosclerotic dissecting aneurysms
that present with SAH both justifies an aggressive approach to treatment and should give the microsurgeon pause about the same. These
aneurysms tend to have fairly extensive SAHs at presentation and high
risk for rebleeding. At the same time, they are at higher risk for bleeding
or thrombosing during surgery. Where possible, trapping and bypass or
primary occlusion should be the first choice. Where this is not possible,
clip wrapping is an option. Endovascular deconstruction is an option if
it appears that distal ischemia is not an issue. However, stenting must
be approached with caution as the risk of rehemorrhage is high, and the
use of antiplatelet agents in this setting can therefore pose a problem.
Aggressive isolation of the aneurysm is the best treatment.
Peter Nakaji, MD
Barrow Neurological Institute, Phoenix, AZ

Suggested Reading
Barrow DL, Spetzler RF. Cotton-clipping technique to repair intraoperative aneurysm neck tear: a technical note. Neurosurgery 2011;68(2, Suppl Operative):294–299, discussion 299

Bojanowski MW, Weil AG, McLaughlin N, Chaalala C, Magro E, Fournier JY. Morphological aspects of blister aneurysms and nuances for surgical treatment. J
Neurosurg 2015;123(5):1156–1165
Chalouhi N, Zanaty M, Tjoumakaris S, et al. Treatment of blister-like aneurysms
with the pipeline embolization device. Neurosurgery 2014;74(5):527–532,
discussion 532
Chan RS, Mak CH, Wong AK, Chan KY, Leung KM. Use of the pipeline embolization
device to treat recently ruptured dissecting cerebral aneurysms. Interv Neuroradiol 2014;20(4):436–441
Kamijo K, Matsui T. Acute extracranial-intracranial bypass using a radial artery graft
along with trapping of a ruptured blood blister–like aneurysm of the internal
carotid artery. Clinical article. J Neurosurg 2010;113(4):781–785
Kurino M, Yoshioka S, Ushio Y. Spontaneous dissecting aneurysms of anterior and
middle cerebral artery associated with brain infarction: a case report and
review of the literature. Surg Neurol 2002;57(6):428–436, discussion 436–438
McLaughlin N, Laroche M, Bojanowski MW. Surgical management of blood blister-like aneurysms of the internal carotid artery. World Neurosurg 2010;
74(4-5):483–493
Ohkuma H, Suzuki S, Ogane K; Study Group of the Association of Cerebrovascular
Disease in Tohoku, Japan. Dissecting aneurysms of intracranial carotid circulation. Stroke 2002;33(4):941–947

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Sikkema T, Uyttenboogaart M, Eshghi O, et al. Intracranial artery dissection. Eur J
Neurol 2014;21(6):820–826
Szmuda T, Sloniewski P, Waszak PM, Springer J, Szmuda M. Towards a new treatment
paradigm for ruptured blood blister-like aneurysms of the internal carotid
artery? A rapid systematic review. J Neurointerv Surg 2016;8(5):488–494

Walsh KM, Moskowitz SI, Hui FK, Spiotta AM. Multiple overlapping stents as monotherapy in the treatment of “blister” pseudoaneurysms arising from the

supraclinoid internal carotid artery: a single institution series and review of
the literature. J Neurointerv Surg 2014;6(3):184–194
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copyright © 2018 Thieme Medical Publishers. All rights reserved. Usage subject to terms and conditions of license.

34 Traumatic Intracranial Aneurysms of the Anterior
Circulation

Ben A. Strickland, Joshua Bakhsheshian, and Jonathan J. Russin

Abstract Traumatic intracranial aneurysms (TICAs) are rare lesions that
present diagnostic and operative challenges. TICAs are often present
in delayed fashion following blunt head trauma, most commonly in
the anterior circulation in locations immediately adjacent to the falx
cerebri. TICAs have been noted to have a higher rate of rerupture and
aneurysmal growth as compared to their saccular counterparts. Due
to the high morbidity profile, endovascular or operative intervention
is recommended. Any patient experiencing a traumatic injury with
delayed hemorrhage suspicious for a TICA should have urgent imaging.
Computed tomography angiography (CTA) remains a viable useful initial

screening test; however, in some cases cerebral angiogram is necessary.
There are reports of successful management utilizing a multitude of
strategies including endovascular intervention or microsurgical techniques. When approaching TICAs with an open surgical treatment, it is
important to decide whether parent vessel sacrifice or preservation is
the goal. In cases where the parent vessel requires preservation, multiple strategies should be prepared. Primary clip ligation is the treatment
of choice; however, bypass donors, grafts, and instruments should be
readily available if clip ligation is not possible. Follow-up imaging is indicated in most cases at least up to a year to rule out aneurysmal regrowth
or recurrence. To date, there is no clear consensus on the optimal treatment strategy, and cases should be approached on an individual basis.
Keywords: traumatic intracranial aneurysm, revascularization, EC–IC
bypass, vascular neurosurgery, trauma

Introduction
Traumatic intracranial aneurysms (TICAs) can present with both diagnostic and management challenges. Intracranial aneurysms related
to trauma comprise ≤1% of all cerebral aneurysms and are associated
with morbidity and mortality rates as high as 50%. TICAs are most commonly associated with blunt head trauma and less commonly a result
of penetrating trauma. TICAs are more commonly reported in the
pediatric population rather than adults. The delayed presentation and
difficult diagnosis of TICAs can contribute to the high mortality rates
(1, 2, 3 in algorithm). A male predominance has been described, likely
attributable to the greater frequency of head trauma in young males.
Traumatic aneurysms typically involve vessels in the anterior circulation, likely explained by the arteries’ relationship to the falx cerebri and
skull base, which can result in shearing forces during trauma leading to
arterial wall destruction and aneurysm formation. Traumatic aneurysms
tend to form distal on the anterior cerebral artery (ACA) and are at risk of
being missed on diagnostic testing. This potential for delayed diagnosis
can also help explain the high morbidity and mortality rates observed
in these patients.
Major controversies in decision making addressed in this chapter
include:
1. Which traumatic brain injury patients have a high risk of TICA

and when should they undergo vascular neuroimaging?
2. Open versus endovascular treatment for TICAs.
3. Ideal timing for TICA treatment.

Whether to Treat
Most authors agree that surgical treatment of traumatic aneurysms
is indicated because of their very poor natural history. The morbidity and mortality of untreated ruptured TICAs can be as high as 50 to
70%, whereas the morbidity and mortality with surgical treatment

is 15 to 30%. The common occurrence of these lesions on the cavernous and paraclinoid internal carotid artery (ICA; ►Fig. 34.1) and distal ACAs allows for acceptable surgical exposure through a pterional
or interhemispheric fissure. Distal aneurysms can be challenging for
endovascular access.

Conservative Management
Conservative management of TICAs is associated with high morbidity
and mortality, and is typically not recommended. However, one study
estimated that 20% of all TICAs will spontaneously resolve and proposed that repeat angiography be performed for observation and recommended surgical intervention only in cases with aneurysm enlargement or neurological deterioration. The majority of studies, however,
have consistently demonstrated that spontaneous resolution of TICAs
is improbable with an estimated 40% of TICAs hemorrhaging and 21%
enlarging on follow-up imaging. Ultimately, the large majority of the
published literature supports early and aggressive management of traumatic aneurysms (7 in algorithm).

Anatomical Considerations
Traumatic aneurysms are classically located in regions were subarachnoid arteries are in transition from or in contact with a rigid structure.
The most common locations for TICAs include distal branches of ACA,
pericallosal, callosomarginal, and the proximal ICA. The proximal ICA is
at risk due to it being fixed at the distal dural ring and transitioning at
that point into the subarachnoid space (►Fig. 34.1).
Histologically, traumatic aneurysms can be categorized as true,
false (or pseudoaneurysms), dissecting, or mixed. True TICAs are a dilation of the arterial wall in which only the adventitia is intact, as opposed

to saccular aneurysms that involve both the adventitia and intima. A
rupture of all arterial layers with associated perivascular hematoma
formation describes false TICAs, considered the most common histological subtype. Dissecting TICAs form following a traumatic event
splitting the arterial wall layers with false lumen forming between the
intima and elastica as blood enters through intimal tears. Mixed TICAs
form following the posttraumatic rupture of true aneurysms with false
lumen development and hematoma formation. The histological type is
not clinically relevant as the high risk of hemorrhage warrants intervention regardless, and angiography cannot always reliably differentiate
between subtypes.

Classification/Pathophysiology
In 1988, Buckingham et al reported that TICAs secondary to blunt injury
can be classified as skull base or peripheral. Skull base TICAs are classically associated with shearing forces resulting in arterial injury at
transition points from being fixed in the skull base to being free in the
subarachnoid space (►Fig. 34.1). Shearing forces can also damage distal ACAs when they impact the falx cerebri. More distal, cortical arteries can suffer TICAs when local trauma results in linear skull fractures
that can traumatize underlying arteries. Location of the aneurysm is
strongly indicative to the mechanism of injury. The anterior circulation
is the most frequent location for TICA formation. Up to 90% of reported
TICA following blunt trauma are associated with underlying skull fractures (►Fig. 34.1).
Traumatic aneurysms have been described following iatrogenic
injury and penetrating trauma. Several case reports have detailed

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Aneurysms—Anterior Circulation

Algorithm 34.1 Decision-making algorithm for traumatic intracranial aneurysms of the anterior circulation.

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34

Traumatic Intracranial Aneurysms of the Anterior Circulation

Fig. 34.1 Traumatic internal carotid artery (ICA) aneurysm. This is a 23-year-old male patient who was involved in an autopedestrian accident. (a) Computed tomography (CT) with diffuse traumatic subarachnoid hemorrhage (SAH). (b) Initial CT angiography (CTA) demonstrated a left ICA traumatic aneurysm that enlarged significantly on a repeat CTA 4 days later (c). The patient was not a candidate for endovascular stenting due to the need of dual antiplatelet therapy and multiple systemic
injuries requiring multiple procedures, ICA sacrifice, and high-flow bypass (using radial artery [RA]) was then performed. (d) Intraoperative view of the intracranial
anastomosis (radial artery–middle cerebral artery [RA–MCA]). (e) Intraoperative view of the extracranial anastomosis (ICA–RA). (f) Intraoperative indocyanine green
angiography demonstrating bypass patency.

Fig. 34.2 Traumatic iatrogenic anterior cerebral
artery (ACA). This is a 33-year-old female patient who
developed acute arterial hemorrhage while undergoing
sinus surgery because of which surgery was aborted.
(a) Computed tomography (CT) head demonstrated
intraparenchymal and subarachnoid hemorrhage.
(b) Digital subtraction angiography demonstrated a
distal ACA aneurysm (arrow) successfully treated with
primary coiling (c; arrow).

TICA formation following endoscopic surgery, paranasal sinus surgery (►Fig. 34.2), skull base surgery, and ventriculostomy. Aneurysms
following these procedures are generally the result of injury to the
internal carotid, but less commonly secondary to insult of the ACA, middle cerebral artery (MCA), or basilar artery. The majority of TICAs are

reported following blunt injuries. Of the TICAs following penetrating
injury, it is has been observed that low-velocity injuries are more likely
to lead to TICA formation as compared to high-velocity injuries.

Workup
Clinical Evaluation
The most common presentation of traumatic aneurysms is delayed
hemorrhage. This is typically associated with an acute deterioration
and/or new neurological deficits. Different locations and subtypes of
TICAs can give rise to variable clinical presentations. Infraclinoid TICAs
can present with epistaxis, cranial nerve palsy, diabetes insipidus, or
headaches. Supraclinoid TICAs can present with cranial nerve palsies,
severe headaches, and/or neurological deterioration resulting from
subarachnoid hemorrhage (SAH). The timeline for TICA presentation is
variable; however, the majority of patients will be diagnosed within 2

to 3 weeks of injury. The risk of SAH is significant with morbidity and
mortality estimated as high as 70%, but is lowered to 30% with treatment. Fewer than 20% of TICAs are detected while still asymptomatic;
however, early identification and intervention can significantly reduce
morbidity and mortality.

Imaging
Computed tomography angiography (CTA) is the screening modality of
choice for the initial workup of suspected cerebrovascular injury after
head trauma. However, CTA is sometimes limited by the field of view and
can be further compromised by the initial superimposed brain injury at
time of presentation. Although TICAs are rare, they are associated with a
high morbidity and mortality. Early diagnosis and intervention are crucial in order to provide the patient with the best chance for a functional
recovery. As such, clinical decision makers should hold a high index of
suspicion for patients presenting with traumatic brain injury, particularly

when SAH is present within the interhemispheric or basal cisterns. A negative CTA is generally acceptable to rule out a TICA. However, when there is
a high clinical suspicion, and the patient’s overall status allows, a digital
subtraction angiogram (DSA) can be performed (1, 3, 12 in algorithm).
In most cases, a DSA is an option but is not a recommendation.

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Aneurysms—Anterior Circulation
However, when a patient suffers a delayed SAH after head trauma and a
CTA is negative, a DSA is recommended due to the improved sensitivity.
Additionally, in cases when foreign body or bone artifact interferes with
CTA imaging, a DSA is recommended to allow for adequate visualization
of the intracranial vasculature.
Timing of CTA can be complicated by patients requiring multiple interventions from different services. In general, when evaluating for TICAs
imaging should be obtained as soon as the patient is stable for transport to
radiology. Patients being evaluated in a delayed fashion who present with a
history of brain trauma associated with recurrent epistaxis, blurred vision,
or progressive cranial nerve palsy should undergo a CTA as soon as possible.

Differential Diagnosis
In some cases, history alone cannot determine whether an aneurysm
is traumatic or not. Typical angiographic features of a traumatic aneurysm include its lack of an associated branch point, peripheral location,
delayed filling and/or emptying, and irregular contour. It is important to
differentiate between traumatic aneurysms and preexisting aneurysms
when possible. When an accurate history is unobtainable and a likely
preexisting aneurysm is identified, treatment consideration is warranted, particularly when radiographic evidence raises a concern for a

possible rupture of the preexisting aneurysm that could have preceded
the traumatic event. Traumatic aneurysms of the ICA at the skull base
can obscure the parasellar region. Formal angiography can be helpful to
rule out a carotid-cavernous fistula.

Treatment
Initial treatment of TICAs is dependent on the clinical status of the
patient at the time of diagnosis. There have been reports of both open
surgical and endovascular modalities employed in the management of
these lesions. When associated with intracranial hemorrhage resulting
in elevated intracranial pressure (ICP) that is refractory to medical therapy, emergent open surgical treatment with evacuation of the hemorrhage is recommended (2, 5, 6 in algorithm). However, in less emergent
cases, the consideration of endovascular aneurysm management, followed by surgical decompression is reasonable. When ICP is controlled,
the presence of an intracerebral hematoma is not as critical of a consideration and both open surgical and endovascular management can be
considered (5, 6, 7–11 in algorithm).
Open surgical approaches should be considered when there is an
opportunity to preserve the parent vessel, particularly when eloquent
territory is at risk. Primary clip ligation is the treatment of choice; however, secondary to relatively large aneurysm size when compared to
peripheral vessels and the frequency of pseudoaneurysm formation, it is
not always feasible. In cases when parent vessel preservation is favored,
a backup strategy of aneurysm excision with re-anastomosis or bypass
and trapping of the aneurysm should be prepared. When parent vessel occlusion is an option, endovascular techniques tend to be favored
in this population. Exceptions would be cases when branching arteries
are in close approximation to the segment requiring occlusion. In these
cases, it may be beneficial to perform open trapping of the aneurysm
with direct visualization of the branching arteries. Due to the multiple
comorbidities in polytrauma patients, there is an associated morbidity
and mortality of up to 30% regardless of treatment.
Several authors have begun to report their experience with endovascular treatment for TICAs. A few recent reports have advocated for the
use of liquid embolic polymers, such as Onyx, in the treatment of TICAs.
Unfortunately, the same anatomical nuances that complicate open surgical management also affect endovascular techniques. TICAs are common

in distal vasculature, making the accessibility for endovascular techniques difficult. Coiling of the aneurysm sac without parent vessel sacrifice is associated with a high risk of recurrence and hemorrhage since
pseudoaneurysm formation is common. Coiling can be further complicated by the dome-to-neck ratio. As TICAs do not necessarily form at
bifurcations, the placement of a catheter can prove difficult.

Ultimately the treatment modality employed is determined on a caseby-case basis. Both open and endovascular strategies are complicated
by the frequency of pseudoaneurysm formation, the peripheral location,
and the often poorly defined aneurysm neck. To date, there is yet to be
a method demonstrating superiority as a dominant treatment strategy.

Complication Avoidance
The first step for complication avoidance in TICAs is early diagnosis and
treatment. Any patient experiencing a traumatic injury with delayed
hemorrhage suspicious for a TICA should have urgent imaging. When
CTA is negative, a formal diagnostic angiogram should be obtained. A
delay in diagnosis can have disastrous consequences in this population (1, 2, 3, 4 in algorithm). Delaying treatment is another pitfall to be
avoided when dealing with TICAs. A treatment plan should be established and implemented as soon as possible. Using a wait-and-see policy for these lesions is inviting complications. When approaching TICAs
with an open surgical treatment, it is important to decide whether parent vessel sacrifice or preservation is the goal. In cases where the parent
vessel requires preservation, multiple strategies should be prepared.
Primary clip ligation is the treatment of choice; however, bypass donors,
grafts, and instruments should be readily available if clip ligation is not
possible (►Fig. 34.1). Preparation allows the surgeon flexibility when
dealing with unpredictable pathology and is paramount for complication avoidance when managing TICAs.

Outcome
Because these aneurysms present rarely, there are no large studies
assessing long-term outcomes for TICAs. The current literature is limited
to case reports and small series. Further, outcome will be determined
largely by the inciting traumatic event, neurological status prior to TICA,
timing from diagnosis to treatment, and if rupture occurs. Therefore, it
is difficult to draw conclusions from the existing literature with regard

to long-term outcomes. Of the reported cases, regardless of treatment
modality, there are only a few instances of recurrence. Most recurrences
are associated with initial endovascular management, and such recurrences are subsequently treated with the open surgical technique.
Moon et al presented their results of a small series of patients with
traumatic cerebral pseudoaneurysms. They included eight patients with
a mean age of 25 years. Six of the pseudoaneurysms were located at
the cavernous/ophthalmic segments of the ICA and two located at the
MCA (M2 segment). The causes of the trauma were car accidents in six
patients, penetrating injury thought the orbit in one patient, and slip
down injury in one patient. Massive epistaxis occurred in all patients
with ICA pseudoaneurysms. Treatment included trapping of the ICA
in one patient, balloon ICA occlusion in five patients, and clipping of
both MCA pseudoaneurysms. All patients with ICA pseudoaneurysms
underwent balloon test occlusion and passed. Clinical outcome was
excellent (modified Rankin Scale [mRS]: 0–1) for ICA pseudoaneurysm
patient group and good/fair (mRS: 2–3) for the two patients with MCA
pseudoaneurysms (supports algorithm steps 8–11).
Rangel-Castilla et al reported their experience of a group of patients
with iatrogenic skull base ICA injury. It included eight patients in whom
the injury was related to endoscopic transsphenoidal surgery, endoscopic transfacial–transmaxillary surgery, myringotomy, cavernous
sinus meningioma resection, posterior communicating artery aneurysm
clipping, and cavernous ICA aneurysm coiling. Endovascular management was considered first-line treatment but was not successful. All
the patients underwent high-flow extracranial–intracranial (EC–IC)
bypass with radial artery graft and parent vessel (ICA) sacrifice. At a
mean clinical/radiographic follow-up of 19 months (3–36 months), all
the patients had an mRS score of 0–1. All bypasses remained patent
(supports algorithm steps 8–11).
A single center experience of patients with TICAs from blunt injuries
included 15 patients. Etiology of trauma included motor vehicle accident and falls. The most common clinical presentation was epistaxis

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34
and ophthalmologic symptoms. The anatomical locations were infraclinoid (nine patients), supraclinoid (five patients), and parafalcine (one
patient). Majority of them (11 patients) were treated endovascularly,
bypass surgery and trapping (2 patients), and balloon-assisted transnasal
endoscopic repair (2 patients). At discharge, two (13.3%) patients had poor
clinical outcome, five (33.3%) had fair, and eight (53.3%) had good outcome.

Durability and Rate of Recurrence
TICA have significantly higher rates of rupture when compared to
saccular or nontraumatic aneurysms. Although it is difficult to assess
the true incidence of TICAs, it is estimated that 40% will hemorrhage and
21% will grow in size after initial diagnosis. Most will rupture in the first
2 to 3 weeks after formation with mortality as high as 50%.
Once treated, rarely do TICAs reoccur; however, there has been an
association with initial endovascular management. Coiling of the aneurysm sac without parent vessel sacrifice is associated with a higher risk
of recurrence as pseudoaneurysms are frequent. There are no reported
cases of TICAs reoccurring following open surgical management.

Clinical and Radiographic Follow-Up
There is no clearly defined algorithm for the timing of follow-up imaging. Lack of TICA diagnosis on initial screening does not exclude eventual
TICA formation. Although most institutions will include CTA as part of
the initial trauma screening, it is possible for the TICA to be missed on
initial imaging. Patients that develop new intracranial hemorrhage posttrauma that is not explained by evolving injuries should undergo CTA
and subsequent DSA in the cases in which CTA is negative and there is a

high suspicion. Those patients with both a negative CTA and DSA suspicious of harboring a TICA should have a repeat CTA at 2 weeks. Patients
that undergo treatment for their TICA are typically reimaged at 1 year
to rule out any recurrence. In the case that 1-year follow-up is negative,
typically no further imaging is obtained. These imaging recommendations are made based on the senior author’s experience, given that there
are insufficient data to support a rigid protocol. Individual cases may
require more frequent imaging, or no follow-up imaging based on clinical course and treatment employed.

Editor Commentary
One needs a high index of suspicion and a positive CT scan to diagnose a
TICA. Blunt trauma with a normal CT is likely low yield unless the patient
has neurological findings suspicious of posttraumatic ischemic events. In
nonpenetrating trauma cases, the direct vascular injury source is either a
dural fold or bone. The most common sources include injury to ACA at the
falx or posterior cerebral artery at the tentorium or the M1 segment from
the sphenoid wing or supraclinoid ICA at the clinoidal segment.
In ruptured cases, the safest means for treatment is parent vessel
occlusion, which can usually be performed endovascularly following a
balloon test occlusion. If the patient fails a balloon test occlusion and
vessel deconstruction is going to result in major neurological deficit,
then one can consider clip reconstruction usually using a clip-wrap
approach or possible clip occlusion with bypass. In unruptured cases,
one can consider flow diversion or coiling with stents. My strong preference in sidewall situations is flow diversion alone without coils.
Cases of penetrating injury with associated subarachnoid or intracerebral hemorrhage absolutely need adequate vascular imaging including
CTA and possibly diagnostic angiogram. The penetrating object should
be removed only under direct vision out of the brain. For example,
I recommend performing craniotomy leaving the penetrating object in

Traumatic Intracranial Aneurysms of the Anterior Circulation

situ and then exposing brain area including potentially opening deep

cerebrospinal fluid (CSF) spaces to gain proximal control of closest major
vessel prior to direct extraction of penetrating object from the brain.
Once the object is removed, one should inspect cavity to make sure there
is no concern for residual injury and delayed hemorrhage.
Adnan H. Siddiqui, MD, PhD
University at Buffalo, Buffalo, NY

Editor Commentary
Traumatic ICAs are unusual aneurysms that are true pseudoaneurysms
and have a high risk of rerupture. They vary considerably in their location and morphology, so general rules in their management are hard to
define. For larger ones, bypass and trapping is likely the best strategy.
When multiple branches are involved, strategies can quickly turn complicated. Iatrogenic trauma is often more straightforward, with simple
repair or isolation of the segment and bypass. Those associated with
skull base trauma are less likely to be repairable, and salvage more often
consists of bypass and endovascular or open sacrifice. Furthermore,
these patients are often sicker due to polytrauma or associated brain
injury. Timing of repair therefore needs to be adjusted to the clinical circumstance.
Peter Nakaji, MD
Barrow Neurological Institute, Phoenix, AZ

Suggested Reading
Buckingham MJ, Crone KR, Ball WS, Tomsick TA, Berger TS, Tew JM Jr. Traumatic
intracranial aneurysms in childhood: two cases and a review of the literature.
Neurosurgery 1988;22(2):398–408
Cohen JE, Gomori JM, Segal R, et al. Results of endovascular treatment of traumatic
intracranial aneurysms. Neurosurgery 2008;63(3):476–485, discussion
485–486
Fleischer AS, Patton JM, Tindall GT. Cerebral aneurysms of traumatic origin. Surg
Neurol 1975;4(2):233–239
International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured

intracranial aneurysms—risk of rupture and risks of surgical intervention.
N Engl J Med 1998;339(24):1725–1733
Larson PS, Reisner A, Morassutti DJ, Abdulhadi B, Harpring JE. Traumatic intracranial
aneurysms. Neurosurg Focus 2000;8(1):e4
Lath R, Vaniprasad A, Kat E, Brophy BP. Traumatic aneurysm of the callosomarginal
artery. J Clin Neurosci 2002;9(4):466–468
Mao Z, Wang N, Hussain M, et al. Traumatic intracranial aneurysms due to blunt
brain injury—a single center experience. Acta Neurochir (Wien) 2012;154(12):
2187–2193, discussion 2193
Medel R, Crowley RW, Hamilton DK, Dumont AS. Endovascular obliteration of
an intracranial pseudoaneurysm: the utility of Onyx. J Neurosurg Pediatr
2009;4(5):445–448
Miley JT, Rodriguez GJ, Qureshi AI. Traumatic intracranial aneurysm formation following closed head injury. J Vasc Interv Neurol 2008;1(3):79–82
Moon TH, Kim SH, Lee JW, Huh SK. Clinical analysis of traumatic cerebral pseudoaneurysms. Korean J Neurotrauma 2015;11(2):124–130
Parkinson D, West M. Traumatic intracranial aneurysms. J Neurosurg 1980;52(1):
11–20
Rangel-Castilla L, McDougall CG, Spetzler RF, Nakaji P. Urgent cerebral revascularization bypass surgery for iatrogenic skull base internal carotid artery injury.
Neurosurgery 2014;10(Suppl 4):640–647, discussion 647–648
Wiebers DO, Whisnant JP, Huston J III, et al; International Study of Unruptured Intracranial Aneurysms Investigators. Unruptured intracranial aneurysms: natural
history, clinical outcome, and risks of surgical and endovascular treatment.
Lancet 2003;362(9378):103–110

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35 Previously Coiled Recurrent Aneurysms of the Anterior
Circulation

Ethan A. Winkler, Brian P. Walcott, and Michael T. Lawton

Abstract Multiple large randomized clinical trials have led to the widespread adoption of endovascular treatment of cerebral aneurysms.
Cerebrovascular neurosurgeons are therefore increasingly confronted
with recurrent or residual aneurysms that have been previously treated
with endovascular coiling. Previously treated aneurysms present unique
anatomical and decision-making challenges to open microsurgical or
endovascular retreatment. In this chapter, we discuss several major
controversies complicating clinical decision making when treating previously coiled cerebral aneurysms. Topics addressed include whether
treatment is indicated, selection of treatment modality (microsurgical
vs. endovascular), anatomical considerations that should guide selection of the optimal microsurgical technique (clipping vs. bypass), and
complication avoidance.
Keywords: recurrent aneurysm, residual aneurysm, endovascular coiling, microsurgical clipping, cerebral bypass, prior treatment

Introduction
Multiple large randomized clinical trials—the International Subarachnoid Aneurysm Trial (ISAT) and Barrow Ruptured Aneurysm Trial
(BRAT)—have led to the widespread adoption of endovascular treatment
of cerebral aneurysms. However, many of these techniques are associated with lower rates of complete aneurysm occlusion than microsurgical clipping. Incomplete obliteration and/or compaction of the coil mass
may lead to aneurysm recurrence over time. In the reported literature,
rates of residual and recurrent aneurysms range from 39 to 61% and 13
to 21%, respectively.
Cerebrovascular neurosurgeons are increasingly confronted with
recurrent or residual aneurysms previously treated with endovascular
coiling. At the University of California San Francisco, there was in excess
of a threefold increase in the number of incompletely coiled and recurrent aneurysms requiring microsurgical treatment from 1997 to 2007.
More recent publication has suggested that the incidence of retreatment
has stabilized. Still, retreatment following endovascular coiling represents approximately 2% of all microsurgically treated aneurysms and is
most commonly encountered for aneurysms in the anterior circulation.
Major controversies in decision making addressed in this chapter

include:
1. Whether or not treatment is indicated.
2. Microsurgical versus endovascular treatment of previously coiled
anterior circulation aneurysms.
3. Anatomical guidance of proper selection of microsurgical technique.

remains higher in those treated with endovascular coiling (endovascular: 1.56 per 1,000 patient-years; microsurgical clipping: 0.49 per 1,000
patient-years). Despite this relative infrequency, rerupture of previously
treated aneurysms is frequently neurologically devastating with a mortality rate up to 58% (1, 2 in algorithm).
The identification of clues of looming rupture in the context of previously coiled aneurysms is less well established. Similar to the initial
treatment of cerebral aneurysms, factors to consider are size, location,
and morphology of the recurrent aneurysm and whether it previously
ruptured. Additional factors unique to recurrence should also be considered, including time since initial treatment and degree of aneurysmal
occlusion. In the CARAT study, the risk of rerupture of recurrent aneurysms varied as a function of initial aneurysm occlusion (overall risk:
1.1% for complete occlusion, 2.9% for 91–99% occlusion, 5.9% for 70–90%,
and 17.6% for <70% occlusion). Given the consequences of rerupture, we
favor retreatment when postcoiling residual or recurrence is detected in
our center. However, desires to treat should be tempered by the patient’s
perioperative risk including age and comorbid conditions, patient preference, surgeon or interventionist experience, and likelihood of successful intervention, and clinicians should engage in detailed risk versus
benefit discussions with the patient and/or family to carefully design
the most appropriate treatment plan.

Anatomical Considerations
Recurrence following endovascular coiling presents challenging anatomy not present in an untreated aneurysm. The normal soft, compressible sac is no longer empty, but now filled with a hard coil mass that
prevents collapse or softening of the aneurysmal dome with application
of temporary clips. Coil-induced separation between the aneurysm’s
walls similarly converts the soft, easily closeable neck into a more rigid
wedge. Clip blades are more prone to splaying or sliding down the less
compressible neck and risk occluding the parent vessel, nearby branches,
or adjacent perforating arteries. Protrusion of coils into the aneurysm

neck confounds this issue, and may further interfere with permanent
clip placement and/or oppose closure. In up to 55% of cases, coils extrude
from the aneurysm dome into the subarachnoid space, but coil extrusions are rarely detected on preoperative angiogram (►Figs. 35.2, 35.3).

Whether to Treat
There is an absence of unequivocal clinical evidence to guide decision
making for retreatment of recurrent aneurysms after endovascular
coiling. This leads to substantial variability among experienced clinicians on whether to re-treat. The decision to re-treat and selection of
appropriate technique requires careful clinical judgment on a caseby-case basis (►Fig. 35.1). Risk of rehemorrhage from residual and/or
recurrent aneurysms following endovascular coiling is not trivial. Published studies—including ISAT, BRAT, and Cerebral Aneurysm Rerupture
Treatment (CARAT)—have suggested that the annual risk for rebleeding
after coiling ranges from 0 to 1.3%, but varies with the timing from initial
intervention. For example, in CARAT and ISAT, rates of rerupture in the
first year following treatment occur in 1.7 and 1.8%, respectively, across
treatment modalities, but may be as high as 3.4% in those treated with
endovascular coiling. After the first year, the annual risk declines, but

Fig. 35.1 Factors influencing clinical decision making of microsurgical versus
endovascular management of previously coiled anterior circulation aneurysms.

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35 Previously Coiled Recurrent Aneurysms of the Anterior Circulation

Algorithm 35.1 Decision-making algorithm for previously coiled recurrent aneurysms of the anterior circulation.

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Aneurysms—Anterior Circulation
Several morphological parameters may be measured on preoperative
angiography to facilitate operative planning—including neck width (N),
compaction height (H, which is the distance beneath the compacted
coils to the neck of the aneurysm), and the coil width (C), which is the
widest diameter of the coil mass parallel to the neck but perpendicular
to the direction of anticipated clip application. Prior works have shown
that the ratio of coil width to compaction height (C:H), but not the ratio
of neck width to compaction height (N:H), is predictive of successful
intraoperative clipping.

Workup
Clinical Evaluation
In one clinical series, up to 85% of residual and/or recurrent aneurysms
are detected on surveillance angiography. For those who become symptomatic, attention should be paid to symptoms of mass effect—including
cranial nerve palsies, focal neurological deficits, seizure, and headache—or
symptoms of overt rupture and subarachnoid hemorrhage.

Fig. 35.2 Tandem clipping of a recurrent left posterior communicating artery aneurysm after stent-assisted coiling in a 49-year-old woman. Surveillance digital subtraction
angiography with internal carotid artery injection and lateral (a) and anteroposterior (b) views showing recurrent aneurysm. (c) Intraoperative photograph showing coil extrusion into the subarachnoid space. Note the Neuroform stent is visible through the wall of the internal carotid artery. (d) The aneurysm was clipped with a fenestrated clip on the
proximal neck with a straight clip closing the fenestration distally. (e) Extruded coils were seen to extend into the temporal lobe and were surrounded by hemosiderin from antecedent subarachnoid hemorrhage. (f) Intraoperative indocyanine green angiography showing complete aneurysm occlusion and preservation of the anterior choroidal artery.

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35 Previously Coiled Recurrent Aneurysms of the Anterior Circulation

Fig. 35.3 Clipping of a residual anterior communicating artery (ACoA) aneurysm requiring coil extraction in a 34-year-old man with subarachnoid hemorrhage complicated by aneurysm perforation and hemorrhage during attempted coiling. Lateral view of digital subtraction angiography with left internal carotid injection (a) and threedimensional reconstruction (b) showing residual aneurysm. (c) Intraoperative photograph showing perforation of the aneurysm dome with coil extrusion and intrasaccular
coils filling the neck. (d) The ACoA aneurysm was trapped with temporary clips (gold). The aneurysm was then transected and the coil mass was gently removed. (e,f) The
aneurysm neck was clipped with a straight clip, and the untreated anterior lobe of the residual aneurysm was clipped with four stacked clips. Anteroposterior view of postoperative digital subtraction angiography with left internal carotid injection (g) and three-dimensional reconstruction (h) confirming complete occlusion of the aneurysm.

Imaging
Four-vessel digital subtraction angiography is the preferred modality of
choice and permits detailed analysis of aneurysm and parent vessel morphology. A computed tomography angiography may also provide additional information regarding partially thrombosed and/or calcified vessels.
However, the sensitivity and utility of these techniques may be limited by
artifact from the radiopaque coil mass. A noncontrast computed tomography scan of the head should evaluate for potential subarachnoid hemorrhage in any patient presenting with sudden or severe headache with
known aneurysm previously treated with endovascular coiling.

Differential Diagnosis
The differential diagnosis for a recurrent aneurysm following initial
coiling is limited, but comparison with prior angiograms may help
deduce the etiology—including incomplete initial treatment, regrowth,

and/or compaction of the coil mass—as this may influence selection
of treatment modality. Coil compaction results from a decrease in the
interspaces between adjacent coils, whereas regrowth is an increase in
aneurysm volume without decrease in coil volume.

Treatment
Choice of Treatment and the Influence of
Intracerebral Hematoma

The selection of the appropriate microsurgical or endovascular technique for retreatment of a previously coiled recurrent aneurysm is
heavily governed by aneurysm morphology, likelihood for success and
durability, physician and patient preference, and surgical candidacy.
If the recurrence is small and can be packed densely, coiling may be
preferred. However, a second recurrence may occur in 50% of cases

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copyright © 2018 Thieme Medical Publishers. All rights reserved. Usage subject to terms and conditions of license.

Aneurysms—Anterior Circulation
with repeated coiling. More sophisticated endovascular techniques—
such as stent-assisted coiling and flow diversion with pipeline embolization devices—have shown initial promise, and further work is ongoing to refine their application in previously coiled aneurysms (11 in
algorithm). Microsurgical clipping is favored under the following conditions: when the recurrence is larger in size with sufficient tissue in the
neck for clip placement; when the predominant mechanism of recurrence is regrowth rather than coil compaction as this excludes the dysplastic tissue; or when there is evidence of coil extrusion (►Figs. 35.2,
35.3). Microsurgical clipping offers a more durable solution to available endovascular options (5, 8 in algorithm). A large associated intracerebral hematoma would favor microsurgical treatment—as with
untreated ruptured aneurysms—as this would facilitate securing the
ruptured aneurysm and enable subsequent evacuation of the clot
(5 in algorithm).
The preferred microvascular technique for retreatment of previously coiled residual and/or recurrent aneurysms is direct surgical
clipping. Clips should be placed below or against the coil mass to facilitate complete mechanical closure. This configuration prevents refilling,
excludes dysplastic tissue, and places the healthy arterial wall tissues in
direct apposition to facilitate repair and re-endothelialization (5, 8 in
algorithm; ►Figs. 35.2, 35.3). In our clinical series, ≥80% of previously
coiled aneurysms were successfully treated with microsurgical clipping
alone. To predict successful clipping, preoperative determination of the
coil width and compaction height (C:H, or compaction ratio) is informative. A compaction ratio ≤2.5 correlates with the likelihood of successful
clipping (8 in algorithm). A noncompressible coil mass with a wider coil

width and shorter coil height (compaction ratio >2.5) creates a wedge
to which the clip is applied. An angle greater than 90 degrees opposes
clip closure and increases risk of the downward displacement of the clip
to occlude the parent vessel and/or branches. Roughly 70% of all aneurysms with a C:H ratio greater than 2.5 require complex clip reconstruction after thrombectomy or coil mobilization, bypass, and/or wrapping
(9 in algorithm). Aneurysms with little coil compaction—a compaction
height greater than 2 mm—may not leave enough room to accommodate
placement of a clip across its neck, and delay in surgical treatment may
allow for further compaction and easier operation at a later date.

Cerebrovascular Management—Operative
Nuances
Previously coiled aneurysms of the anterior circulation are surgically
accessed through a standard pterional or modified orbitozygomatic craniotomy—like their untreated counterparts. Subarachnoid dissection,
acquisition of proximal and distal control, adequate visualization and
preparation, and contingency planning (e.g., temporary clip strategy, in
case of intraoperative rupture) are of paramount importance. To date,
the risk of intraoperative rupture appears lower with a previously coiled
aneurysm—none in our experience.
Clipping of a recurrent aneurysm with favorable anatomy is relatively
straightforward. However, less favorable anatomy requires contingency
plans. If the coil mass interferes with aneurysm mobilization and/or clip
placement, opening the aneurysm dome to mobilize and/or extract coils
may convert an unclippable aneurysm into a clippable one. The aneurysm should first be successfully trapped with temporary clips. The
aneurysm dome should be opened by transecting the aneurysm at its
equator to access the coil mass. Coils accessed early after deployment in
the acute period are easily mobilized. With greater time elapsed, intraluminal fibrosis makes the coils more adherent to the aneurysm wall.
Careful dissection at the points of adhesion will release the coils. Excessive and more diffuse force applied to coils runs the risk of tearing the
aneurysm further complicating repair. After mobilization, gentle traction may be applied to extract the coil mass from the opening. Removal
of coils through a small opening is unpredictable. Complete extraction
of coils is rarely required, and should be avoided. The goal of coil extraction is to soften the neck and make room for the clip, and usually only

a portion of the coils need to be removed. This maneuver may be com-

plicated by a multitude of factors, including bleeding from incomplete
proximal and distal control, backbleeding from perforators or branches,
insufficient tissue for reconstruction of the aneurysm neck, extensive
scarring of the coil mass, or distal embolization from the thrombosed
coil mass. These complications may prolong ischemia times.
Bypass is another viable surgical option for recurrent aneurysms that
cannot be clipped (►Fig. 35.4). With bypass, the vascular territory distal
to the aneurysm is first revascularized through a variety of techniques—
including extracranial–intracranial bypasses, in situ bypasses, and radial
artery, or saphenous vein grafts—which are tailored to the anatomy, location, and desired blood flow. The aneurysm is then trapped or proximally
occluded, eliminating or altering blood flow to promote thrombus formation within the aneurysm. Bypass has a number of potential advantages
when confronting a previously coiled aneurysm—most notably avoidance
of direct aneurysm manipulation and predictable ischemia times. Preoperative decision making is important because selection of technique influences patient positioning, draping, and preservation of structures, like the
superficial temporal artery, with initial dissection. We routinely prepare a
bypass contingency plan and prepare the forearm or leg for potential harvest of the radial artery or saphenous vein, should microsurgical clipping
not be possible. Finally, aneurysms not able to be clipped or bypassed may
be wrapped with muslin or cotton to induce scarring of the aneurysm wall.
This should be treatment of last resort (10 in algorithm). With experience,
ingenuity, and technical skill, one can design a strategy to permit more
definitive clipping and/or bypass in the vast majority of clinical scenarios.
In our published clinical series, 81% of previously coiled residual
and recurrent aneurysms were treated with microsurgical clipping—
including 72% in which the clip was placed below the coil mass and 6%
in which clips were placed across coils present in the neck of the aneurysm. Aneurysm transection with mobilization and/or removal of coils
was required in 12% of cases. Bypass was required in 11% of cases. No
aneurysm has required wrapping in the past 10 years.

Endovascular Management—Operative

Nuances
Endovascular options for treatment are either recoiling or flow diversion. Additional adjuvants, such as balloon-assisted coil delivery, double
microcatheter coil delivery, and stent-assisted coiling can be considered
in specific situations.

Balloon-Assisted Coiling
Stand-alone coiling can be challenging with recurrent aneurysms that
have neck-based recurrences, bifurcation aneurysms, and aneurysms
with a branch vessel originating near the neck of the aneurysm. Using
inflatable balloon techniques can remodel the neck and/or protect a parent vessel/side branch. It can also reduce “kickback” during coil deployment, allowing for the maximum number of coils to be deployed.
For patients with subarachnoid hemorrhage, heparinization is initially
held. Once one or two coils are deployed into the aneurysm, systemic
heparin can be administered. The balloon catheter is introduced into the
proximal end of the guide catheter, along with the microcatheter (through
the side port). When the coil is nearing the aneurysm, the balloon is filled
with 100% contrast. Subsequent coils can then be delivered, mindful of
distal ischemia time while the balloon is inflated. Somatosensory evoked
potentials and motor evoked potentials can be useful monitoring techniques, particularly in anesthetized patients, and if changes occur, the
balloon can be temporarily deflated to restore distal blood flow. Once the
coil mass is delivered, the balloon is deflated. If the coil mass does not
herniate out of the aneurysm, then the microcatheter is removed. If the
coil mass appears unstable, then deployment of a stent may be required.

Double-Microcatheter Technique
Stent- or balloon-assisted coiling for wide-necked recurrences have
specific risks for thromboembolic complications. Stent-assisted coiling

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Ebook Decision making in neurovascular disease: Part 2

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