Intraprocedure aneurysm rupture in embolization: Clinical outcome with imaging correlation : Journal of the Chinese Medical Association

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Original Article

Intraprocedure aneurysm rupture in embolization: Clinical outcome with imaging correlation

Luo, Chao-Baoa,b,c,*; Teng, Michael Mu-Huoa,b; Chang, Feng-Chia,b; Lin, Chung-Junga,b; Guo, Wan-Yuoa,b; Chang, Cheng-Yena,b

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Journal of the Chinese Medical Association: June 2012 - Volume 75 - Issue 6 - p 281-285
doi: 10.1016/j.jcma.2012.04.008

    Abstract

    1. Introduction

    Endovascular detachable coil embolization of intracranial aneurysms has increasingly become an alternative treatment modality to neurosurgical aneurysm clipping, with a better clinical outcome than endovascular and neurosurgical therapies.1 Despite increasing clinical experienceSymbol and technologic improvements, endovascular treatment still has inherent risks of morbidity and mortality.2 The most feared complication of endovascular embolization is intraprocedural aneurysm rupture (IPAR) during embolization. The technical considerations, management, and clinical outcomes of IPARs have been sporadically reported.3–7 However, imaging findings of IPAR has not been well evaluated.

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    The purpose of our study was to report the immediate and/or long-term imaging findings of cerebral angiography and brain computed tomography (CT) of IPARs as well as their correlation with clinical outcomes.

    2. Methods

    From September 2001 to August 2010, 376 consecutive patients harboring 412 intracranial saccular aneurysms were treated with endovascular coiling at our institute. In accordance with a standardized protocol, inform consent was obtained from each patient before the intervention. All patient underwent endovascular procedures under general anesthesia, and their femoral arteries were catheterized. A bolus of intravenous heparin was routinely administered into the aneurysm sac after the first coil was successfully detached, and we maintained an activated clotting time from 1.5–2 times baseline throughout the entire procedure. For all patients, systolic blood pressure (SBP) was maintained between 110 and 140mm Hg during the procedure. From this database, we found 10 patients (2.7% per patient, 2.4% per aneurysm embolization) who had experienced IPAR during the endovascular procedure (Table 1). There were two men and eight women, ranging in age from 40–71 years (mean: 52 years). Nine patients had initial aneurysmal subarachnoid hemorrhage (SAH) that occurred within 96 hours of the procedure with various grading (Table 1). Immediately after IPAR, hypertension was noted in nine patients; maximal SBP varied from 150–280mm Hg. After recognition of IPAR, anticoagulation therapy was immediately reversed with intravenously administered protamine sulfate and blood pressure was controlled and decreased with an intravenously administered antihypertensive drug. Coiling was rapidly completed in nine cases, while in one patient the procedure was discontinued because of a difficulty in identifying the aneurysm due to the flow arrest of the internal carotid artery (ICA). At the end of procedure, all patients had postembolization cerebral angiography and brain CT to evaluate the IPAR, including hemodynamic change of the cerebral circulation and intracranial hemorrhage. Seven patients who survived from IPAR had clinical and brain CT follow-up varying from 7 days to 96 months (mean: 38 months) to detect the progression of the IPAR. Each patient's final clinical outcome was defined by using the modified Rankin scale (mRS).

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    Table 1:
    Demography, imaging, and clinical outcomes in 10 patients with IPAR.

    3. Results

    All ruptured aneurysms were small, with the largest dimension being less than 10mm. The mean aneurysm size was 4.6mm (range: 3–9.5mm) with a mean neck of 3mm (Table 1). The locations of the aneurysms were in the anterior (n=5) and posterior (n=4) communicating arteries or the anterior cerebral artery (n=1). The mechanisms of IPARs were detachable coilSymbol protrusion beyond the aneurysm sac in seven cases (Fig. 1) or microcatheter perforation in two cases (Fig. 2), while one patient was assumed to have a spontaneous rupture. The hemodynamic change of the cerebral angiography at the end of procedure showed a flow arrest of ICA in one patient and persistent delays in the contrast transit time of the ICA in three patients (Fig. 1), while six patients showed no changes (Fig. 2). One patient (Patient 5) with an unruptured aneurysm received emergent ventriculostomy to relieve intracranial pressure; one patient (Patient 10) underwent surgical removal of a frontal lobe hematoma and clipping of the reruptured aneurysm because of the vicinity of the hematoma and aneurysm (Fig. 2). Postembolization brain CT demonstrated contrast media retention in the subarachnoid space and/or ventricular systems in all 10 patients, SAH expansion in six cases, new intracerebral hematoma (ICH) in three, and intraventricular hemorrhage in two. Seven patients surviving from the IPAR had follow-up brain CT longer than 3 months. Mild ventricular dilatation was found in three, while focal cerebral tissue loss was demonstrated as a result of immediate or delayed ischemic change (n=3) or ICH (n=3). On more than 90 days of clinical follow-up, six patients presented with good recoveries (mRS: ≤ 2). One patient exhibited a moderate disability (mRS: 4), and three patients died within 10 days of IPAR (mRS: 6). Six of the seven patients with IPAR had angiographic imaging follow-up that varied from 6 months to 3 years. No significant morphologic change of treated aneurysms was found in five patients; one aneurysm had mild coil compaction.

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    Fig. 1:
    (A) A woman 47 year of age presented with unruptured aneurysm in the left ICA-posterior communicating artery; (B) postembolization carotid angiography revealed a coil perforation of the aneurysm leading to contrast media leakage (arrowhead) and an IICP as well as slow flow of the carotid territory; note the early opacification of the ophthalmic vein due to IICP (arrow); (C) immediate postembolization brain CT depicted contrast retention in the subarachnoid space; (D) follow-up CT on Day 2 following aneurysm rupture demonstrated complete resolution of contrast media; (E, F) brain CT on Day 4 showed low-density ischemia in the left frontotemporal lobe and progression to chronic infarction with cerebral tissue loss and mild ventricular dilatation on Day 186. The patient exhibited moderate disability on discharge (mRS: 4). CT = computed tomography; IICP = increase in intracranial pressure; mRS = modified Rankin scale.
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    Fig. 2:
    (A) A woman 43 years of age presented with acute rupture of an anterior communicating aneurysm; (B, C) a microcatheter was seen to have perforated the aneurysm (arrow), with contrast leakage (arrowhead); (D) postembolization carotid angiogram demonstrated unchanged carotid hemodynamics; (E) immediate postembolization brain CT scan depicted high-density contrast media and hematoma in the right frontal lobe with a mild midline shift; (F) the patient underwent craniotomy with surgical clipping and removal of hematoma; postoperative brain CT showed small residual contrast and/or hematoma in the right frontal lobe; (G) follow-up CT on Day 145 showed focal brain tissue loss in the right frontal lobe. The patient was discharged with minimal neurologic deficit (mRS: 1). CT = computed tomography; mRS = modified Rankin scale.

    4. Discussion

    The incidence of IPAR during embolization is about 2%–3% (varied from 0%–10%).3–7 Murayama and colleagues8 reported 19 IPAR (2.3%) in 818 aneurysms embolized. Henkes and others9 reported 47 IPARs (4.7%) in 1818 aneurysms from a multicenter trial. We have experienced this complication 10 times among 412 aneurysmal coiling procedures (2.4%); the incidence of our series is similar to previous reported data. However, of these 10 IPARs, seven occurred in the first 206 aneurysms (3.4%), while the other three were observed among other 206 aneurysms (1.5%). Although few studies emphasized that IPARs occurred sporadically,3,10 in some series, investigators found IPAR occurred early in their experienceSymbol, as also occurred in our series.11,12 In our series, all IPARs were observed in the anterior circulation, which just reflected the relative by small number of aneurysms in posterior circulation referred for embolization as compared with those in anterior circulation (66 vs. 346 aneurysms).

    Many causative mechanisms may be correlated with IPAR, including microcatheter, guidewire, coil perforation, or high-pressure contrast media injection.3–7 Among these are built-up pressure of microcatheter/microguidewire during manipulation to sudden forward jump of the device and aneurysm perforation. This occurred in our series of two aneurysms located in an anterior communicating or cerebral artery. The most common inciting factor of IPAR is coil perforation.3–7 Attempts to totally obliterate the aneurysm may lead to overpacking with rupture/rerupture. In other cases, the deployment of coils may increase intraluminal pressure or irritate a vulnerable site of the aneurysm, causing IPAR. Other coil-related risks are oversizing the coils or the selection of stiffer coils with increasing intraluminal pressure against the aneurysm wall. Seven of the 10 IPARs in our series occurred during coil placement. In our experience, we have found that avoiding high intraluminal pressure inside the microcatheter during coiling is the most obvious preventative for IPAR. In this series, all IPARs occurred in small aneurysms less than 10mm. It is known that smaller aneurysms have little space to allow the “paintbrush movement” of the tip of microcatheter during coiling. Furthermore, in the initial microcatheter navigation to the sac of a smaller aneurysm, the margin of error for microcatheter tip positioning relative to the aneurysm wall is smaller than in those with larger aneurysm; overmanipulating the microcatheter and guidewire may lead to IPAR.

    In this series, nine IPARs were found in previously ruptured aneurysms. These findings were compatible with those of previous reports. In a meta-analysis, Cloft and coworkers6 determined that the risk of IPAR during coil embolization in patients with previously unruptured aneurysms was significantly lower than in those patients with previously ruptured aneurysms (0.7% vs. 4.1%). Sluzewski and others5 did a literature review and found 39 IPARs in 2030 aneurysms embolized; all but one aneurysm was prior SAH to perforate. IPARs in previously ruptured aneurysms occurred due to dislodgement of a clot that occluded the site of the original rupture or because of second tearing of an already torn and fragile aneurysm wall. Furthermore, ruptured aneurysms may also have an extremely fragile wall compared with those of unruptured lesions.

    The direct imaging signs of IPARs are microguidewire, microcatheter, or coil perforating the aneurysm locating beyond the confine of the aneurysm sac and/or leaking of contrast media into the subarachnoid space and/or ventricular systems. However, an IPAR may not always be seen on the angiography of those patients with small tear of aneurysm or small leak associated with better outcomeSymbol. The only warning sign is the gradual elevation of a patient's blood pressure. With more extensive extravasation, persistence of contrast delays of contrast transit time in the parent artery and/or frank opacification of the subarachnoid space/ventricles may occur. In a more severe case with an significant increase in intracranial pressure (IICP), it can result in stagnation or flow arrest of the ICA with flow redirection to external carotid artery and unusual early opacification of ophthalmic vein, such as what occurred in Patient 4 (Fig. 1D). Global fatal ischemia may occur in more extreme case. By contrast to open surgical clipping, endovascular management is performed in a closed system. In case of an IPAR association with IICP, it is initially a protective mechanism and contributes to the halting of SAH. However, its persistence is usually associated with decreasing cerebral perfusion pressure and brain ischemia complication.13–15

    CT is a good imaging tool to evaluate the progression of IPAR in terms of cerebral injury. Immediate brain CT usually demonstrates contrast media retention in the subarachnoid space, ventricular system, and/or cerebral parenchyma, and some IPARs may associate with ventricular dilatation. These are important guidelines for subsequent neurosurgical intervention. In some patients harboring an aneurysm in anterior or middle cerebral arterial territory, IPAR may demonstrate ICH, such as occurred in Patients 3, 6 and 10; the cerebral hematoma can be removed through surgical craniotomy. Ischemic brain injury resulting from blood flow compromise of the carotid artery due to IICP and/or vasospasm may occur later. Craniotomy with decompression is mandatory in some patients with ischemic mass effect and midline shift. In patients surviving IPAR, the follow-up CT showed more or less cerebral tissue loss. These imaging findings are well correlated with final clinical patient outcomes.

    Some investigators have asserted that poor outcomes are related to the worst pre-existing neurologic conditions, aneurysm in posterior circulation, elderly patients, and the timing of normalization of IICP.16,17 Other observations also suggest patients with prolonged systemic hypertension and persistent extravasation of contrast media or early phase of endovascular procedure might associate with poor outcomes.3–7 Apart from these, the type of hemorrhage and/or angiographic hemodynamics may be an important indicator to determine the outcomeSymbol of IPAR. In this series, Patients 1, 7, 8, and 10 experienced good outcomeSymbol (mRS < 2) largely because of the only presence with ICH and/or cerebral hemodynamic on angiography was unchanged. In comparison, four patients exhibited poor outcomes (mRS ≥ 4); these were likely attributable to prolong periods of brain ischemia as a resulting of IICP with flow arrest (n=1) and/or the blood flow compromise of the carotid territory (n=3).

    In conclusion, IPAR is an uncommon complication in endovascular embolization. Previously ruptured aneurysms seem to be more susceptible to perforation than unruptured ones, and it usually occurs during the advancement of a coil into the aneurysm sac. Angiographic hemodynamics is an important indicator to determine the outcome of the IPAR. Brain CT demonstrates the progression of the IPAR associated with cerebral injury and tissue loss resulting from ischemic or hemorrhagic events.

    Acknowledgments

    This work was supported in part by a grant from the Taipei Veterans General Hospital (V98C1-153, V99C1-012) and the National Science Council (97-2314-B-075-062-my2, 99-2314-B-075-045-my2).

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    Keywords:

    cerebral aneurysm; complication; endovascular embolization

    © 2012 by Lippincott Williams & Wilkins, Inc.