Keywords
carotid artery stenosis - intracranial aneurysm - staged treatment - carotid endarterectomy
- microsurgical clipping
Introduction
The coexistence of an ipsilateral unruptured intracranial aneurysm (UIA) in the setting
of significant cervical internal carotid artery (ICA) stenosis occurs in approximately
3.2% of cases.[1]
[2] These concomitant pathologies require unique treatment considerations, including
the appropriate selection of endovascular, open surgical, or hybrid technique as well
as timing the procedure to mitigate both ischemic and hemorrhagic risks and managing
the use of antiplatelet agents. Treating the ICA stenosis before securing the coexisting
aneurysm may alter intracranial hemodynamics and thereby increase aneurysm rupture
risk.[3]
[4] Conversely, UIA treatment before ICA stenosis management may increase the risk of
perioperative stroke from hypoperfusion and/or traversing catheters/wires through
a stenotic ICA.[5] Moreover, the potential need for dual antiplatelet therapy (DAPT) after endovascular
aneurysm treatments that require stenting or flow diversions must be considered with
any subsequent open surgical intervention.
There is no consensus treatment and limited evidence regarding the safest, most effective
treatment strategy for this patient population. We present a patient with ipsilateral
ICA stenosis and an A1–2 intracranial aneurysm who underwent a successful, staged,
open carotid endarterectomy (CEA) and microsurgical aneurysm clipping to demonstrate
the rationale for this approach.
Case Report
History
A 69-year-old woman with a history of myocardial infarction, hypertension, hyperlipidemia,
hypothyroidism, and Bell's palsy with a residual right-sided facial droop developed
diplopia, headaches, and mild difficulty walking after a ground-level fall. A head
computed tomography (CT) scan demonstrated no acute findings. Magnetic resonance imaging
(MRI) and CT angiography (CTA) demonstrated multifocal atherosclerotic disease and
an intracranial aneurysm, prompting a neurosurgical consultation. In the neurosurgery
clinic, the patient reported improved diplopia, mild dizziness, and headaches. Her
neurologic examination was unremarkable, aside from a chronic right-sided facial droop.
She was taking low-dose aspirin, clopidogrel, and a statin for her atherosclerotic
disease.
Preoperative Neuroimaging
Brain MRI revealed scattered microvascular ischemic changes but no acute strokes.
CTA and diagnostic cerebral angiogram demonstrated bilateral proximal ICA stenosis
(right 90%, left 65%), multifocal left vertebral artery stenosis (proximal 77%, V4
50%), and mild scattered intracranial atherosclerotic disease. A wide-necked, 4.8-mm
aneurysm with multiple secondary excrescences was seen arising from the right A1–2
region with a small, poorly visualized anterior communicating artery (Acomm) ([Fig. 1]).
Fig. 1 Preoperative imaging. A 69-year-old woman was found to have a high-grade right ICA
stenosis and an ipsilateral unruptured intracranial aneurysm on workup for headache,
dizziness, and diplopia. Coronal (A) and axial (B) CTA demonstrated a calcified atherosclerotic plaque resulting in 90% stenosis of
the right ICA (white arrows). Coronal CTA (C) and right ICA injection oblique view on digital cerebral angiography (D) showing a wide-necked (2.9-mm neck, 4.8-mm dome) anterior–inferior projecting aneurysm
with multiple secondary excrescences arising from the right A1–2 region (black arrows).
CTA, computed tomography angiography; ICA, internal carotid artery.
Preoperative Assessment and Patient Counseling
Treatment for both pathologies was recommended after multidisciplinary review, with
proposed treatment of the ICA first and subsequent aneurysm treatment as soon as safely
possible thereafter. Open, endovascular, and hybrid options were discussed with the
patient, who selected a staged, open surgical strategy. Her antiplatelet regimen was
switched to full-dose aspirin monotherapy in preparation for surgery.
Treatment and Outcome
A right CEA was performed first, followed by a second-stage right frontotemporal craniotomy
for microsurgical aneurysm clipping 5 days later. Both procedures were performed without
complications. The patient was admitted to the neurocritical care unit after each
procedure (with strict blood pressure control of 110–140 mm Hg between stages). A
carotid duplex ultrasound after CEA demonstrated ICA patency. This was confirmed on
CTA after the craniotomy, which also demonstrated no residual aneurysm or strokes.
The patient was discharged 1 week after the craniotomy at her neurologic baseline
and remained neurologically stable with unchanged imaging over 3-month follow-up ([Fig. 2]).
Fig. 2 Follow-up imaging. The patient was treated successfully with a staged right carotid
endarterectomy followed by microsurgical aneurysm clipping 5 days later. Follow-up
CTA imaging demonstrated wide patency of the right ICA (white arrows on coronal [A] and axial [B] CTA) and no residual aneurysm (black arrow on coronal CTA [C]). CTA, computed tomography angiography; ICA, internal carotid artery.
Discussion
In cases of concomitant ICA stenosis and a UIA, the risk of embolic stroke and ischemia
from carotid artery stenosis must be balanced with the risk of aneurysmal subarachnoid
hemorrhage (aSAH). UIAs have an annual rupture risk of 1 to 3%, and the mortality
rate is up to 50% in the setting of aSAH.[6]
[7] Rupture risk is associated with aneurysm size (>7 mm), smoking, female sex, hypertension,
and a family/personal history of aSAH.[8]
[9] Aneurysms within the posterior circulation, those in the Acomm region, and those
with irregular angioarchitecture also carry more risk.[9]
[10] In the presented case, the aneurysm diameter (4.8 mm), irregular shape, associated
daughter sac, and Acomm region location prompted treatment.
Carotid artery stenosis is a similarly nonbenign condition and an independent risk
factor for ischemic stroke.[11] A CEA or carotid artery stent (CAS) is generally recommended for asymptomatic patients
with stenosis ≥ 60% or symptomatic patients with stenosis ≥50%.[12]
[13] Our patient presented with >90% asymptomatic stenosis and met criteria for treatment.
Treatment options for concomitant lesions typically address the carotid disease first
to avoid ischemic complications and include CEA with open microsurgical aneurysm clipping
(commonly staged), CAS plus staged or simultaneous endovascular aneurysm treatment
(coiling, stent-coiling, flow diversion, or intrasaccular device), CEA plus staged
or simultaneous endovascular aneurysm treatment, CAS followed by delayed clipping
of the aneurysm (after a period of DAPT), and isolated CEA or CAS followed by close
monitoring of the aneurysm. Each strategy has advantages and disadvantages stemming
from the distinct clinical scenario.
With staged approaches, the timing between stages requires consideration, because
there is a greater theoretical risk of rupture of downstream aneurysms after carotid
revascularization from increased hemodynamic pressure and disruptions in autoregulation.[3]
[4]
[14] The associated risks and optimal treatment timing in this setting nonetheless remain
unclear.[15]
[16]
[17] In a subgroup analysis of 32 patients from the North American Symptomatic Carotid
Endarterectomy Trial who underwent carotid revascularization with a concurrent UIA,
only one patient experienced aSAH within 30 days of revascularization.[1] Similarly, in a retrospective study of 198 patients who underwent carotid revascularization
with a concomitant UIA, one patient experienced aSAH within 30 days of CEA, and two
patients experienced aSAH more than 30 days after CEA, with an overall 0.87% risk
of rupture per patient year.[15] Given these data, Tallarita et al[15] argued that the risk of aneurysmal rupture is not imminent after CEA, and treatment
of an aneurysm may be delayed if indicated. However, neither of these studies was
limited to patients with ipsilateral aneurysms/carotid stenosis, where the risk of
rupture is theoretically the highest. In a systematic review, Khan et al[18] reported that 5/140 (4%) patients who underwent carotid revascularization experienced
rupture of a coexisting UIA, with ipsilateral stenosis and UIA carrying the highest
risk. In our case, CEA and microsurgical aneurysm clipping were performed within a
5-day span (with blood pressure strictly controlled between surgeries) to mitigate
rupture risk, while also allowing for recovery from the initial surgery and anesthesia.
A shorter interval timeframe (i.e., between 2 and 4 days) could, nonetheless, have
been selected with likely similar results.
Hybrid open and endovascular options also exist, most commonly with CEA followed by
a staged endovascular aneurysm treatment.[15] A nonstaged hybrid approach has also been reported, with simultaneous CEA and ipsilateral
intracranial aneurysm coiling in a patient with 90% stenosis of a tortuous left ICA
and an Acomm aneurysm.[2] However, this approach is technically challenging, requires use of a hybrid operating
room, and involves crossing a freshly repaired ICA with a sheath.
Endovascular treatment of both lesions is yet another possible management strategy,
particularly in patients on DAPT for other reasons. If pursued, CAS is typically performed
before the aneurysm treatment because traversing a significant stenosis with endovascular
devices before carotid revascularization may increase the risk of thromboembolic complications.[19] Although this approach can be performed simultaneously or in a staged fashion, staged
treatment (of at least 3 weeks) is preferred to allow for neointimal growth within
the stent, with careful interval blood pressure management.[14] In cases of noncritical ICA stenosis and a stable plaque, first-line endovascular
aneurysm treatment with a subsequent CAS up to 1 month later has also been reported.[20]
Single-stage endovascular treatment of both lesions may also be performed. Kaçar et
al[21] reported a series of seven patients treated with simultaneous CAS and endovascular
aneurysm securement; they reported no hemorrhagic events or technical failures except
one contralateral transient ischemic attack, and all aneurysms were adequately occluded
on follow-up imaging. Similarly good results were reported with this technique by
Ni et al[22] in a series of 10 patients. Park et al[19] also demonstrated this method's effectiveness in a series of 17 patients, although
complications occurred in 11.7% of patients, namely acute in-stent thrombosis and
premature aneurysmal rupture.
Although not as common, UIA treatment before carotid revascularization can also mitigate
the risk of aneurysm rupture. In this strategy, the patient has a theoretical risk
of perioperative cerebral ischemia from reduced cerebral perfusion secondary to the
carotid stenosis, particularly if bilateral carotid stenosis is present.[5] A retrospective series of 60 patients nonetheless suggests this can be a safe strategy.[23] CAS followed by a delayed microsurgical clipping of the aneurysm is less common
but viable option. However, the need for DAPT after CAS (typically for at least 6
months, which can limit treatment options in case of aneurysm rupture) and its associated
hemorrhage risk must be considered.[24]
[25]
Isolated carotid disease treatment with close aneurysm monitoring can also be pursued.
Although the risk of aneurysm rupture with this strategy is relatively low (ranging
from 0 to 5.3%),[2] this approach is likely best suited for relatively small aneurysms without high-risk
features and should include close blood pressure monitoring.
Conclusion
Multiple management strategies for concomitant ICA stenosis and UIAs exist. Selection
of treatment approaches and timing should be tailored to the patient to minimize ischemic
and hemorrhagic risks. Although permutations of the endovascular options are increasingly
preferred, in our case, a staged open strategy was selected to optimally minimize
ischemic and hemorrhagic risks.
