Cerebellar Hemorrhage after Coil Embolization for a Ruptured Vertebral Dissecting Aneurysm Motohiro Nomura, M.D.,* Shinya Kida, M.D.,* Daisuke Kita, M.D.,* Takuro Kaneko, M.D.,* Ryo Higashi, M.D.,* Jun Yoshikawa, M.D.,† Osamu Matsui, M.D.,† and Junkoh Yamashita, M.D.* *Departments of Neurosurgery and †Radiology, Kanazawa University School of Medicine, Kanazawa, Japan Nomura M, Kida S, Kita D, Kaneko T, Higashi R, Yoshikawa J, Matsui O, Yamashita J. Cerebellar hemorrhage after coil embolization for a ruptured vertebral dissecting aneurysm. Surg Neurol 2000;53:239 – 42. BACKGROUND We present a case of ruptured vertebral dissecting aneurysm that exhibited cerebellar hemorrhage after successful embolization of the vertebral artery including the dissected site. CASE PRESENTATION A 59-year-old man suffered a sudden onset of severe occipital headache when he looked up. Computed tomography demonstrated subarachnoid hemorrhage. Angiography revealed a right vertebral dissecting aneurysm distal to the posterior inferior cerebellar artery. Endovascular embolization of the aneurysm was performed with preservation of the posterior inferior cerebellar artery. The next day, the patient suffered a cerebellar hemorrhage in the vermis. The intracranial pressure was controlled by external ventricular drainage. The patient was discharged with mild cerebellar ataxia and bilateral abducens nerve palsy. CONCLUSION In a case of vertebral dissecting aneurysm distal to the posterior inferior cerebellar artery, blood circulation in the vertebral arterial system may change after embolization of the aneurysm. In our case, the preserved posterior inferior cerebellar artery might have been hemodynamically stressed postoperatively, resulting in cerebellar hemorrhage. Therefore, strict control of blood pressure is essential in the acute stage after occlusion of the aneurysm. © 2000 by Elsevier Science Inc. KEY WORDS Dissecting aneurysm, subarachnoid hemorrhage, vertebral artery, posterior inferior cerebellar artery, cerebellar hemorrhage, endovascular embolization. Address reprint requests to: Dr. Motohiro Nomura, Department of Neurosurgery, Kanazawa University School of Medicine, 13-1 Takara-machi, Kanazawa 920-8641, Japan Received September 13, 1999; accepted November 2, 1999. © 2000 by Elsevier Science Inc. 655 Avenue of the Americas, New York, NY 10010 issecting aneurysms involving the vertebral artery (VA) frequently cause subarachnoid hemorrhage (SAH) [4]. To prevent subsequent rupture, many kinds of surgical treatment have been reported [3]. These include proximal clipping, trapping, wrapping, and so on [3,4]. In the field of endovascular treatment, occlusion of the parent artery with a detachable balloon has been performed [6]. However, this technique is not always able to prevent rerupture of the dissecting aneurysm [8]. Recent advancements in endovascular techniques make it possible to occlude the dissected site less invasively. Yamaura et al [8] reported five cases of ruptured vertebral dissecting aneurysms that were treated successfully by endovascular embolization using platinum coils [8]. On the other hand, complications related to the endovascular procedure are not fully undersood. Recently, we encountered a case of ruptured vertebral dissecting aneurysm complicated by cerebellar hemorrhage after successful coil embolization. In this article, we present our experience, and discuss the mechanism of the cerebellar hemorrhage and the perioperative management of ruptured vertebral dissecting aneurysms. D Case Report A 59-year-old man suffered a sudden onset of severe occipital headache when he looked up. The headache did not improve and he consulted another neurosurgical hospital on the next day. Computed tomography (CT) revealed a slight high-density area in the basal cistern, indicating possible SAH. He was transferred to our hospital by ambulance. Just before his arrival at our hospital, he complained of severe headache and nausea, and lost 0090-3019/00/$–see front matter PII S0090-3019(99)00191-3 240 Surg Neurol 2000;53:239 –42 1 CT on admission showing SAH, mainly in the posterior fossa, and ventricular dilatation. consciousness. CT showed SAH, especially in the posterior fossa, and ventricular dilatation (Figure 1). Blood was also seen in the lateral ventricles. He regained consciousness within 30 minutes. Angiography revealed a dissecting aneurysm of the right VA distal to the posterior inferior cerebellar artery (PICA) (Figure 2A). This vertebral dissecting aneurysm was considered to be the origin of the SAH. The diameter of the affected VA was almost equal to that of the contralateral VA. After angiography, endovascular embolization of the dissecting aneurysm was performed under local Nomura et al anesthesia. As his right brachiocephalic and subclavian arteries were tortuous because of arteriosclerotic changes, the right VA could not be approached via the femoral artery. Therefore, a 6F guiding catheter was inserted into the right VA via the right brachial artery. To navigate the microcatheter to the true lumen of the dissected site, a J-shaped micro guidewire was advanced to the distal VA through the dissected portion. A Turbotracker (Target Therapeutics, Fremont, CA) microcatheter was then navigated into the dissecting aneurysm. First, a Guglielmi detachable coil (GDC) 6 mm in diameter and 20 cm in length was placed in the aneurysm. Six more GDCs were subsequently added. A 5F catheter was positioned in the left VA origin via the right femoral artery to confirm the patency of the basilar artery and right VA distal to the dissected site during the procedure. The postoperative angiogram revealed complete occlusion of the right VA distal to the PICA including the dissected site (Figure 2B). The opacification of the right VA and PICA and washout of the contrast medium from these arteries were delayed. These findings indicated delayed circulation in the right vertebral system, creating a risk of thrombosis. To prevent thrombosis, intravenous administration of argatroban with volume expansion by low molecular dextran was begun. Postoperatively, the patient (A) The right vertebral angiogram (VAG) on admission revealing a dissecting aneurysm arising from the right VA distal to the origin of the PICA. (B) Angiogram obtained 14.76 seconds after starting injection of contrast medium. Postoperative right VAG showing complete obliteration of the aneurysm including the dissected site and preservation of the right PICA. Delayed opacification of the right VA and PICA, and delayed washout of the contrast medium from these arteries were observed. 2 Cerebellar Hemorrhage in VA Dissection 3 Surg Neurol 241 2000;53:239 –42 CT obtained after respiratory arrest showing fresh blood in the cerebellar vermis. Angiogram obtained 4.70 seconds after starting injection of contrast medium. Right VAG performed after cerebellar hemorrhage demonstrating no change from that taken just after the embolization, except that the delayed blood circulation is improved. 4 was initially well and had no neurological deficits. A spinal drain was inserted to drain the bloody cerebrospinal fluid and to control hydrocephalus. Because his systolic blood pressure was high (ranging from 150 to 180 mmHg), continuous intravenous administration of nicardipine hydrochloride was started. Twenty-three hours after the embolization, the patient’s respiration suddenly arrested and his systolic blood pressure dropped to 50 mmHg. Fresh blood was seen in the spinal drainage. We suspected recanalization and rerupture of the dissecting aneurysm. CT revealed that a cerebellar hemorrhage in the vermis had ruptured into the fourth ventricle (Figure 3). Emergency angiography demonstrated that the dissecting aneurysm had not recanalized, and that the PICA was patent (Figure 4). The delayed blood circulation in the right VA and PICA was improved compared with that immediately after the embolization. Anticoagulation therapy using argatroban was stopped. An external ventricular drain was inserted in the right lateral ventricle to control the intracranial pressure. The patient showed consciousness disturbance and complete bilateral abducens nerve palsy, which improved gradually. The follow-up angiogram performed 30 days after the embolization showed complete occlusion of the aneurysm and patency of the right PICA. The blood circulation time in the right VA and PICA was normal. Forty-five days after the cerebellar hemorrhage, a right ventriculoperitoneal shunt was placed. The patient’s condition improved gradually. Six months after admission, he was discharged with cer- ebellar ataxia and mild left abducens nerve palsy. He could walk with the aid of a cane 9 months after onset. Discussion Although vertebral dissecting aneurysm is recognized as a cause of SAH, the best therapeutic strategy remains controversial [3]. The goal of treatment for a ruptured dissecting aneurysm is isolation of the dissected site from the circulation to prevent rerupture [2]. Recently, endovascular occlusion of the VA, including the dissected site, with platinum coils has been reported [1]. Yamaura et al [8] mentioned that endovascular occlusion of the dissected site with GDCs is a safe, minimally invasive and reliable treatment for some vertebral dissecting aneurysms. Their basic method for endovascular embolization of a dissecting aneurysm is to place the permanent occlusion devices at the dissected site in the true lumen and then collapse the false lumen to induce thrombosis. In our case, endovascular embolization was performed successfully with short-segment occlusion of the dissected site. Recanalization of the VA was not observed during the follow-up period. Although this endovascular technique may be considered to be an effective treatment, the intra- and postoperative complications are not fully understood. In our case, cerebellar hemorrhage occurred postoperatively. 242 Surg Neurol 2000;53:239 –42 The worst possible complication that could occur during the endovascular procedure would be aneurysm rupture [8]. Other possible complications include damage to the branching arteries and intra- or postoperative thrombosis. According to a Japanese nationwide study [7], 127 of 206 ruptured vertebral dissecting aneurysms, were treated by open or endovascular surgery. In this population, complications occurred in 32 cases (25%). These included 16 cases of Wallenberg syndrome, 12 cases of cranial nerve palsy, 3 cases of rerupture, and 3 other complications. There have been no reports describing complications related to the procedure for occlusion of the dissected site. In our case, cerebellar hemorrhage occurred 23 hours after embolization. To our knowledge, this is the first report presenting a case of vertebral dissecting aneurysm with cerebellar hemorrhage after embolization of the VA including the dissected site. In our case, cerebellar hemorrhage was observed in the vermis. This observation indicated that the hemorrhage might have been due to destruction of the vermian branch of the right PICA. Angiography performed immediately after embolization revealed delayed blood circulation in the right VA and PICA. These angiographical findings were also observed after embolization of the unruptured aneurysm [5]. After occlusion of the distal VA, all blood normally draining to the right distal VA may flow into the PICA. Therefore, the right PICA might be hemodynamically stressed and disrupted under hypertension. In a case of vertebral dissecting aneurysm distal to the PICA, the blood flow into the PICA may increase after embolization of the lesion. In our case, angiography performed after cerebellar hemorrhage showed improvement of the delayed blood circulation in the VA and distal PICA. This observation indicated that the blood circulation might normalize to some degree within 24 hours after embolization of the VA. Therefore, treatment to reduce hemodynamic stress on the peripheral artery is required in the acute stage after embolization. In our case, although nicardipine hydrochloride was administered intravenously to regulate the patient’s blood pressure, his postoperative blood pressure was relatively high. Induced hypertension Nomura et al is effective in preventing thrombosis and vasospasm; however, careful control of blood pressure is recommended in the acute stage of vertebral dissecting aneurysm after embolization. Conclusion We present a case of ruptured vertebral dissecting aneurysm that developed cerebellar hemorrhage after endovascular obliteration of the affected VA including the dissected site. It was suspected that the hemodynamically stressed PICA was disrupted and bled. Although our experience is limited to only one case, we recommend strict control of the blood pressure in the acute stage after obliteration of vertebral dissecting aneurysms. REFERENCES 1. Halbach VV, Higashida RT, Dowd CF, Fraser KW, Smith TP, Teitelbaum GP, Wilson CB, Hieshima GB. 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