Keywords
Intraparenchymal hemorrhage - NBCA embolization - Posttraumatic middle meningeal artery
pseudoaneurysm
Introduction
Middle meningeal artery pseudoaneurysms are a rare entity. It can either be a true
aneurysm associated with high flow states or systemic hypertension or can be a delayed
complication of trauma.[1]
[2] An estimated 85% of traumatic pseudoaneurysms were documented from the temporal
region and infrequently from frontal or occipital region and approximately 70 to 90%
of traumatic MMA pseudoaneurysms arise due to the temporal bone skull fracture which
is an overlying part of the MMA.[3]
The most frequent complication of posttraumatic pseudoaneurysms is an epidural hemorrhage
which can have acute or delayed presentation. Many a times, it may manifest as subdural
or subarachnoid hemorrhage. Combined setting of large intraparenchymal with subarachnoid
hemorrhage is a rare presentation. N-butyl cyanoacrylate (NBCA) is a routinely utilized
liquid embolic agent for cerebral arteriovenous malformations and other peripheral
vascular pathologies.[4]
[5]
Our case report demonstrates endovascular embolization with NBCA is valid and safe
treatment option for middle meningeal artery pseudoaneurysm which can present as a
delayed posttraumatic complication.
Case Report
A 64-year elderly gentleman with a history of hypertension and type 2 diabetes mellitus
sustained a road traffic accident 7 months back and managed conservatively without
any residual neurological deficits. NCCT brain done at that time was suggestive of
left parietal hemorrhagic contusion.
Seven months after the accident, the patient arrived at the emergency department with
a complaint of acute onset severe headache, vomiting, altered sensorium, and right
hemiparesis since the past 8 hours. NCCT brain done at the periphery center showed
acute thalamocapsular hemorrhage with a significant mass effect and minimal subarachnoid
hemorrhage in left MCA cistern and Sylvian fissures ([Fig. 1A-B]–[C]). There was also evidence of impending uncal herniation and mild hemorrhage in the
fourth ventricle. The Baseline Glasgow coma scale on arrival was E2M4V1. In view of
the sudden deterioration in the patient's clinical status and recent CT findings,
urgent decompression and hematoma evacuation were considered. To rule out the possibility
of a ruptured aneurysm or pial arterio-venous fistula, urgent cerebral angiography
was planned prior to the surgery.
Fig. 1 Computed tomography (CT) done at periphery center prior to admission reveals (A) bone window and (B) parenchymal hemorrhage in the left thalamocapsular region and minimal subarachnoid
hemorrhage in the left sylvian cistern with mass effect.
Selective catheter angiography of the left external carotid artery showed a fusi-saccular
dissecting pseudoaneurysm involving the middle meningeal branch of the left internal
maxillary artery, measuring approximately 14.2 × 6.3 mm ([Fig. 2A and B]).
Fig. 2 Cerebral angiography of the left external carotid artery (A) showing a pseudoaneurysm (red arrow) feeding from the middle meningeal artery (MMA) (white arrow). (B) Selective contrast injection of middle meningeal artery with marathon microcatheter
revealing pseudoaneurysm. (C) Dye stasis noted in the pseudoaneurysm as well as distal MMA segment (red arrow). (D) Postembolization native DSA image (white arrow) demonstrates glue cast with contrast stasis in a pseudoaneurysm and distal MMA.
(E) (Postembolization contrast run demonstrating complete occlusion of the pseudoaneurysm
with NBCA cast (white arrow)). (F) Postprocedure DynaCT (bone window) demonstrates fracture of the left squamous temporal bone (most likely trauma sequelae).
In view of lesion complexity and preplanned neurosurgical evacuation of hematoma,
NBCA was chosen for embolization followed by surgical decompression. A 6F 70 cm Flexor
check long sheath was inserted through the right common femoral artery and navigated
into the left CCA. Subsequently, CAT 5 guiding catheter was advanced and placed in
the left internal maxillary artery. Selective catheterization of left MMA using marathon
1.5 F 165 cm microcatheter and hybrid 008 microguidewire was done. Furthermore, any
anatomical variations of MMA and dangerous anastomoses which may predispose to procedure-related
morbidity were ruled out.
A dilution of 33% concentration of the NBCA mixed with lipiodol was slowly injected
under direct vision inside the pseudoaneurysm and the feeding vessel causing parent
vessel occlusion. Final check angiogram demonstrated a complete occlusion of pseudoaneurysm
with significant stasis, without any evidence of fresh hemorrhage on the postprocedure
DynaCT scan ([Fig. 2C - E]). Retrospectively analyzing DynaCT, a left anterior squamous temporal bone fracture
was noted ([Fig. 2F]) which was not initially reported at the peripheral center. The patient was hemodynamically
stable and immediately underwent decompression and surgical evacuation. The in-hospital
course was uneventful, and postoperative CT ([Fig. 3]) revealed hyperdense material in the middle cranial fossa due to NBCA without any
fresh evidence of hemorrhage. The patient's neurological status gradually improved
over the course in the hospital and was discharged with minimal residual right hemiparesis.
Fig. 3 Postdecompressive surgery computed tomography (CT) shows hyperdense material made
by n-butyl-2-cyanoacrylate (red arrow).
Discussion
Intracranial pseudoaneurysms account for less than 1% of all intracranial aneurysms
and the leading cause is head trauma.[4]
Around 70 to 90% of cases of MMA pseudoaneurysms are due to the fracture of temporal
bone overlying the middle meningeal artery or its branches accounting for approximately
20 to 25% of mortality.[3]
Pseudoaneurysm pathogenesis in case of trauma to the middle meningeal artery involves
fractured bony rim induced injury of the adventitia and intima followed by the formation
of a contained intramural hematoma which undergoes fibrous reorganization. Clot destabilization
by the hemodynamic stress of the arterial flow renders the lesion progressively rupture
prone.[6] Among few cases, traction of the MMA has been documented in patients without any
bony deformity on the same side causing pseudoaneurysms.[7]
[8]
Rumbaugh et al[9] reported an elderly woman with a right temporal hemorrhage and sphenoid region MMA
pseudoaneurysm. Also, Montanari et al[7] reported eight cases of previous fractures of the temporal bone with small parenchymal
hemorrhage (s) out of which six patients represented delayed parenchymal bleeding
due to pseudoaneurysm rupture which occurred 7 days to 11 months after prior head
injury.
Our patient had a recent onset spontaneous multicompartment bleed, which routinely
raises clinical suspicion of a ruptured aneurysm or pial fistula. With the background
history of trauma, we also included pseudoaneurysm in our differential diagnosis.
Urgent neurosurgery was advised considering the deterioration in clinical response
and significant mass effect. With these differential diagnoses in our mind, an urgent
diagnostic cerebral angiography was planned prior to surgery. Selective contrast run
of the internal maxillary artery demonstrated middle meningeal artery pseudoaneurysm.
The most common treatment modalities preferred are neurosurgical resection, ligation
of MMA, or coagulation of the vessel. Endovascular embolization with coils or liquid
embolic agents like NBCA or onyx provides alternative and safe treatment options.
However, there is no general consensus to prefer a specific liquid embolic agent to
be used.
Jussen et al[3] reported coil embolization as a safe treatment modality for MMA pseudoaneurysms.
However, the small size, friable nature, and irregular morphology may not allow for
the accommodation of standard-sized coils. Furthermore, any manipulation with the
microcatheter or during coil placement accounts for an increased risk of intraprocedural
rupture. On the contrary, occluding the pseudoaneurysm-bearing vessels with coils
can pose a challenge. Hence, adequate embolization with parent vessel occlusion using
liquid embolic agents such as NBCA or onyx may be a safer and more effective treatment
option.
As the patient was already planned for emergency decompression, a decision to embolize
with NBCA was taken. Very few cases document the presence of large intracerebral hematoma
secondary to traumatic pseudoaneurysm in which NBCA embolization is considered to
be a preferred treatment modality in an acute setting, considering the risk of intraoperative
rerupture and hemorrhage due to the friable nature of these pseudoaneurysms. Furthermore,
NBCA was chosen in our patient considering its cost-effectiveness when compared to
onyx.
Postembolization contrast run demonstrated contrast stasis without any inflow into
the pseudoaneurysm. Kim et al[4] reported a large pseudoaneurysm with uncontrollable bleeding and contrast leakage
from a ruptured middle meningeal artery which was managed intraoperatively utilizing
NBCA.
Conclusion
Pseudoaneurysm of MMA secondary to trauma is a rare but life-threatening condition.
Patients presenting acutely with ICH or SAH with a history of trauma and delayed pseudoaneurysm
rupture should be considered a possibility and NBCA embolization as a safe, cost-effective,
and alternative treatment option.
