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Endovascular therapy using flow diversion for giant internal
carotid artery pseudoaneurysm arising in the setting of an
invasive pituitary macroadenoma
Amin F. Saad, MD, Almas Syed, MD, Keyan B. Marashi, MD, Brian D. O’Rourke, MD, Joseph H. Hise, MD,
Michael J. Opatowsky, MD, MBA, and Kennith F. Layton, MD, MS
This report illustrates the unusual occurrence of a pseudoaneurysm
arising in the setting of a skull base mass and describes the first
reported use of endovascular flow diversion therapy in such a setting.
A 63-year-old man with occasional headaches during the preceding month presented with the acute onset of severe left retroorbital
headache and oculomotor nerve palsy. Computed tomography (CT)
and CT angiogram revealed a destructive skull base mass with an
associated giant probable pseudoaneurysm of the cavernous segment
of the left internal carotid artery. The patient underwent endoscopic
transsphenoidal biopsy with a subsequent diagnosis of prolactinoma.
Endovascular therapy utilizing two Pipeline™ flow diversion embolization devices was performed with subsequent resolution of the patient’s
headache and improvement in his cranial nerve deficits/cavernous
sinus syndrome.
A
neurysms coincident with invasive skull base masses are
unusual. An association between pituitary neoplasms
and intracranial aneurysms has been documented.
The acute development of a cavernous sinus syndrome
with associated cranial nerve deficits in conjunction with an
aneurysm entirely encased within a neoplastic lesion supports
the diagnosis of an acutely enlarging pseudoaneurysm, and we
describe the first reported use of endovascular flow diversion
therapy in such a setting. This case illustrates a diagnostic pitfall
with the potential for grave implications in patient outcome if
an associated vascular lesion is not appreciated at the time an
intracranial mass is diagnosed.
CASE PRESENTATION
A 63-year-old man with minor headaches in the preceding month presented to the emergency department following
the acute onset of severe left retroorbital headache, ptosis,
mydriasis, ophthalmoplegia, and diplopia. Noncontrast head
computed tomography (CT) (Figure 1a) revealed a large
destructive central skull base mass. Subsequently pre- and
postgadolinium brain magnetic resonance imaging (MRI)
(Figure 1b, 1c) delineated the margins and character of the
skull base mass, which was centered in the clivus and extended
to encase the left greater than right cavernous segments of the
internal carotid arteries (ICAs) with partial destruction of the
Proc (Bayl Univ Med Cent) 2017;30(1):47–49
petrous carotid canals. A hypointense T2 signal was identified with heterogeneous enhancement following gadolinium
administration. A suspicious large flow void within the region
of the cavernous segment of the left ICA was confirmed to
reflect a probable pseudoaneurysm on postgadolinium imaging and subsequent CT and catheter angiography (Figure 2),
which revealed additional dysplastic irregular lobular projections arising from the pseudoaneurysm sac. The patient underwent an endoscopic transsphenoidal biopsy of the lesion.
Histopathologic findings showed a pituitary adenoma, and
subsequent laboratory testing showed serum prolactin levels
to be 14191.5 ng/mL (normal range 2.1–17.7), compatible
with the diagnosis of a prolactinoma.
The patient was loaded with aspirin and clopidogrel for 1
day and subsequently underwent endovascular therapy utilizing
two overlapping PipelineTM flow diversion embolization devices
(Medtronic, Minneapolis, MN) measuring 4.25 × 30 mm and
4.5 × 16 mm (Figure 3), extending to the supraclinoid ICA. This
resulted in an immediate and marked decrease in contrast flow
within the pseudoaneurysm sac and contrast stasis. Cabergoline
medical therapy was initiated to treat his prolactinoma.
The patient’s headache resolved, and he was discharged in
good condition 5 days following endovascular therapy. The
patient continued to experience ptosis, mydriasis, and mild
diplopia at the time of discharge, although he did experience
an improvement in his ophthalmoplegia. On follow-up catheter
angiography, the pseudoaneurysm was markedly decreased in
size with only trace filling of a subcentimeter residual pseudoaneurysm sac. The patient’s cranial nerve palsies also greatly
improved during the 6 months following discharge, and he has
continued to do well.
DISCUSSION
The incidence of intracranial aneurysms arising in association with pituitary adenomas is greater than the incidence
From the Departments of Diagnostic and Neurointerventional Radiology, Baylor
University Medical Center at Dallas. Dr. Saad is now with Stanford University, and
Dr. Marashi is now with University of Utah, Salt Lake City.
Corresponding author: Amin F. Saad, MD , Department of Radiology,
Neuroradiology Division, Stanford University, 300 Pasteur Drive, MC 5105,
Stanford, CA 94305 (e-mail: [email protected]).
47
a
b
c
Figure 1. (a) Axial noncontrast head CT in bone windows demonstrates extensive lytic destruction of the central skull base (arrow). (b) Axial T2-weighted image
reveals hypointense signal within the mass (arrow) in addition to a large flow void in the region of the cavernous left internal carotid artery (arrowhead). (c) Axial
T1-weighted postgadolinium image shows heterogeneous contrast enhancement of the mass with robust enhancement (arrowhead) of the flow void noted on the
T2-weighted image.
a
b
c
d
Figure 2. (a) Axial source image, (b) sagittal, and (c) coronal reformatted images from a CT angiogram show a giant
pseudoaneurysm of the cavernous segment of the left internal carotid artery (arrows) with a dysplastic cephalad projecting lobule (arrowheads). These findings are confirmed on a (d) lateral projection digital subtraction angiography image
following a left internal carotid artery injection.
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Baylor University Medical Center Proceedings
of aneurysms arising in the general population (0.5%–7.4%)
(1), as well as the incidence of
aneurysms coexistent with intracranial masses of nonpituitary
origin. The pathogenesis of this
increased incidence is uncertain.
Proposed etiologies include increased blood flow through
vessels supplying the tumor, hormonal effects, and direct neoplastic infiltration (1). The concept
of increased tumoral blood flow
via internal carotid branch vessels
is supported by the fact that the
greatest proportion of adenomaassociated aneurysms arise from
the ICA (50%) (1). A hormonal
influence on the incidence of aneurysm formation is supported
by the fact that the greatest incidence of adenoma-associated
aneurysms occurs in the context
of acromegaly (50%) (1), with
associated increased insulin-like
growth factor–1 potentially playing a role in the formation of intracranial aneurysms, as well as
the more diffuse vasculopathic
changes that can be seen in these
patients, to include widespread
cerebrovascular dolichoectasia
(2). The contribution of tumor
infiltration is supported by the
statistically significant increase in
aneurysm incidence in the setting of cavernous sinus invasion
Volume 30, Number 1
a
b
Figure 3. Frontal (a) oblique and (b) lateral projection digital subtraction angiography images show placement of two
overlapping Pipeline embolization devices (arrows) traversing the wide pseudoaneurysm neck with associated sluggish
flow of contrast within the pseudoaneurysm sac.
(3), as well as a case reported by Mangiardi et al that described
a macroadenoma invading the walls of a giant cavernous carotid aneurysm on a postmortem examination (4). In our case,
the fact that the entire pseudoaneurysm was encased within
the mass that had invaded the cavernous sinus may provide
additional support for the theory of direct neoplastic infiltration, particularly the clinical evidence of acute pseudoaneurysm
enlargement supporting an underlying loss of integrity of the
vessel wall.
January 2017
1.
2.
3.
4.
The utility of flow diversion
devices has been realized in treating giant aneurysms not amenable
to traditional coiling, as well as in
therapy of pseudoaneurysms arising
secondary to trauma or iatrogenic
causes. Vascular remodeling following flow diversion embolization is an
established phenomenon that also
occurs in pseudoaneurysms with an
associated decrease in sac size and
is particularly desirable in cases of
symptomatic mass effect. Improvement in associated cranial nerve palsies is variable, although the degree
of improvement likely relates to the
duration and degree of compression.
Choi HS, Kim MS, Jung YJ, Kim OL. Incidental superior hypophygeal
artery aneurysm embedded within pituitary adenoma. J Korean Neurosurg
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Weir B. Pituitary tumors and aneurysms: case report and review of the
literature. Neurosurgery 1992;30(4):585–591.
Oh MC, Kim EH, Kim SH. Coexistence of intracranial aneurysm in
800 patients with surgically confirmed pituitary adenoma. Neurosurg
2012;116(5):942–947.
Mangiardi JR, Aleksic SN, Lifshitz M, Pinto R, Budzilovic GN, Pearson J.
Coincidental pituitary adenoma and cerebral aneurysm with pathological
findings. Surg Neurol 1983;19(1):38–41.
Endovascular therapy using flow diversion
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