Concurrent aneurysm rupture and thrombosis of high grade internal carotid artery stenosis: Report of two cases

ELSEVIER

CONCURRENT ANEURYSM RUPTURE AND THROMBOSIS OF HIGH GRADE INTERNAL CAROTID ARTERY STENOSIS: REPORT OF Two CASES Randall W. Porter, M.D.,* Michael T. Lawton, M.D.,* Mark G. Hamilton, M.D.C.M., F.R.C.S.(C),“( and Robert F. Spetzler, M.D., F.A.C.S.* *Barrow Neurological Institute, Division of Neurological Surgery, St. Joseph3 Hospital and Medical Center, Phoenix, Arizona; and TAlberta Children’s Hospital, Division of Neurosurgery, Calgary, Alberta, Canada

Porter RW, Lawton MT, Hamilton MG, Spetzler RF. Concurrent aneurysm rupture and thrombosis of high grade internal carotid artery stenosis: report of two cases. Surg Neural 1997;47:532-40. BACKGROUND

The simultaneous presentation of aneurysmal subarachnoid hemorrhage and thrombosis of a high-grade internal carotid artery stenosis is rare, and their management raises several treatment dilemmas. METHODS

Two such patients with ruptured aneurysms are presented: one with high-grade internal carotid artery stenosis that progressed to occlusion and one with acute internal carotid artery occlusion. RESULTS

Both patients were treated with craniotomy ping

of the

ruptured

aneurysm

followed

for clipby carotid

thromboendarterectomy. CONCLUSlONS

We advocate urgent surgical treatment of both lesions, dealing with the most symptomatic lesion first. These two cases demonstrate the importance of reestablishing blood flow in patients with an acutely thrombosed carotid artery. 0 1997 by Elsevier Science Inc. KEY

WORDS

Aneurysm, hemodynamic stress,internal carotid artery stenosis,subarachnoid hemorrhage, thromboendarterectomy, thrombosis.

A

neurysmal subarachnoid hemorrhage (SAH) is a common neurosurgical entity and the management of these patients is well-established [8,15, 32,401. Symptomatic high-grade internal carotid artery (KA) stenosis is also a common neurosurgical Address reprint requests to: Robert F. Spetzler, M.D., % Neuroscience Publications, Barrow Neurological Institute, 350 West Thomas Road; Phoenix, AZ 850134496. Received April 28, 1995; accepted June 8, 1996. 0090-3019/97/$17.00 PI1 s0090-3019(96)00392-8

entity and the guidelines for management have been suggested by the North American Symptomatic Carotid Endarterectomy Trial (NASCET) 1281. However, simultaneous occurrence of these two symptomatic clinical entities is uncommon and raises treatment dilemmas. Several authors have described patients in whom either the carotid stenosis or aneurysm was symptomatic and the other lesion was asymptomatic, but there are few reports of patients in whom both lesions are symptomatic [3,30]. We present two patients with a ruptured cerebral aneurysm and thrombosis of a stenotic internal carotid artery. These patients represent the first report of aneurysm clipping and thromboendarterectomy for concurrent symptomatic lesions. Treatment strategies and the role of reopening an acutely thrombosed internal carotid artery are discussed.

CASE REPORTS CASE

1

This 65year-old female suddenly developed a severe headache, nausea, and vomiting. During the next 24 hours she deteriorated from an alert to a comatose state. She was intubated at the referring hospital and transferred to this institution. The patient had a history of hypertension, peripheral vascular disease, and smoking. Her Glasgow Coma Scale (GCS) score [21] was 8 (eyes = 2, motor = 5, verbal = 1; intubated). Cranial nerve function was intact and she localized painful stimuli with both upper extremities. The patient’s Hunt-Hess grade was 4 [ 191. 655 Avenue

0 1997 by Elsevier Science Inc. of the Americas, New York, NY 10010

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Case 1. (A) Preoperative 0scan computed tomography demonstrates thick subarachnoid blood in the basal cisterns; @) anteroposterior, and (C) lateral vertebrobasilar angiograms show the basilar artery bifurcation aneurysm. Note filling of the left middle cerebra1 and anterior cerebra1 arteries via the posterior communicating artery.

A computed tomography (CT) scan demonstrated thick subarachnoid blood in the basal cisterns with intraventricular blood (Fisher Grade 4) [9], and moderate hydrocephalus (Figure 1A). Cerebral angiography revealed an 8 mm aneurysm at the basilar artery bifurcation (Figure 1 B,C). In addition, she had 90% stenosis of the left ICA at the cervical bifurcation with a filling defect extending up the internal carotid artery, consistent with intraluminal thrombus (Figure lD,E). The posterior circulation provided collateral blood flow to the left anterior circulation via the posterior communicating artery. A right pterional craniotomy was performed and a basilar bifurcation saccular aneurysm was clipped through a standard transsylvian approach [44]. Intraoperatively, the patient received intravenous barbiturates to achieve EEG-burst suppression [37, 381. Blood clot was clearly identified on the aneurysm wall at the site of rupture. During the operation, the compressed spectral analysis signal over the left cerebral hemisphere, which initially had

been symmetric with the right side, diminished and disappeared. A left carotid endarterectomy was performed immediately after the craniotomy was completed. The ICA distal to the bifurcation had no pulsations, suggesting that occlusion had occurred. No vessel clips were initially placed on the ICA. An arteriotomy was performed and plaque with acute thrombus was found (Figure 2). The thrombus was expelled through the arteriotomy by retrograde blood flow through ICA. The endarterectomy was completed and blood flow was reestablished. Postoperative angiograms demonstrated no residual aneurysm and a patent left ICA supplying blood flow to the left anterior circulation (Figure 3A,B,C). The patient had an uneventful postoperative course and was discharged to a rehabilitation program. At her l-year follow-up examination, her Glasgow outcome score was good, [20] and a carotid Doppler ultrasonography study revealed a patent left ICA with no stenosis. The patient re sumed a normal, independent life with no neurologic deficits.

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Continued. Left (D) lateral and (E) anteroposterior internal carotid artery (KA) angiograms demonstrating stenosis and an intraluminal filling defect, consistent with thrombus.

CASE 2 This 59-year-old male collapsed at work and was intubated, resuscitated, and transferred to our institution. His medical history was unremarkable. On neurologic examination, his GCS was 9 (eyes = 2, motor = 6, verbal = 1, intubated) and cranial nerve function was intact. He obeyed commands with the right upper extremity and withdrew the left upper extremity to painful stimuli. His Hunt-Hess grade was 4. CT demonstrated a Fisher Grade 3 SAH. An angiogram from the referring hospital demonstrated an anterior communicating artery (ACoA) aneurysm and a right ICA occlusion with cross-filling from the left ICA (Figure 4A). There was no collateral flow from the posterior circulation via posterior communicating artery. Given this angiographic information and the patient’s left hemiparesis, his cerebrovascular reserve was considered inadequate and flow to the right middle cerebral artery (MCA) territory would need augmentation to treat ongoing ischemia. A right frontal ventriculostomy was inserted, and

the patient underwent a right pterional craniotomy with direct clipping of the saccular aneurysm. Intraoperative inspection confirmed rupture of the ACoA aneurysm. In addition, a right superficial temporal artery-to-MCA bypass was completed. The postoperative angiogram demonstrated good aneurysm clipping (Figure 4B) and, unexpectedly, also showed delayed retrograde filling of the right ICA down to the petrous segment (Figure 4C), a finding not evident on the angiogram from the other institution and suggestive of acute rather than chronic ICA occlusion. The patient was immediately returned to the operating room where a right thromboendarterectomy was completed, the acute nature of the thrombus was confirmed, and blood flow was reestablished (Figure 4D). The patient’s postoperative course was uncomplicated. He required a ventriculoperitoneal shunt for a cerebrospinal fluid absorptive defect and was discharged to a rehabilitation program. At 6-month follow-up examination, the patient had minima1 leftsided weakness and had returned to light physical work.

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operation was reported by Bidzinski [3], who performed craniotomy for aneurysm clipping followed by extracranial-intracranial bypass in a patient with SAH who developed hemiparesis and decreased level of consciousness one day after his hemorrhage. Our case 1 is the first reported surgical treatment of both lesions in a single operation using thromboendarterectomy.

specimen: left G?IOperative plaque with thrombus.

internal

carotid artery

DISCUSSION Simultaneous occurrence of symptomatic aneurysm and symptomatic carotid stenosis is rare. Five percent of patients with symptomatic carotid stenosis or occlusion will have incidental aneurysms [ 1,24,25,34,35], and approximately 0.5% of patients with symptomatic aneurysms will have incidental carotid stenosis or occlusion [3,7,22,29,39]. The number of reported patients with symptoms referable to both an aneurysm and carotid stenosis or occlusion is limited to five [3,30]. Two of these patients were treated nonoperatively: one died from the initial subarachnoid hemorrhage and the other recovered. One patient presented with SAH, underwent endarterectomy, and died from a recurrent hemorrhage. The first successful surgical treatment of both lesions was reported by Portnoy and Avellanosa [30], who performed endarterectomy and craniotomy for aneurysm clipping in two operations. The first surgical treatment of both lesions in a single

MANAGEMENTOFCONCURRENT ANEURYSM RUPTURE AND CAROTID STENOSIS OR OCCLUSION A critical question that arises with concurrent lesions concerns the order of treatment: which of the two pathologies should be treated first? For patients who present with two disease entities, one symptomatic and the other asymptomatic, the symptomatic lesion should be treated first on an urgent or emergency basis, followed by later treatment of the asymptomatic lesion. When a patient presents with symptomatic carotid stenosis or occlusion, it is safe to perform an endarterectomy without acutely increasing the risk of rupture of an incidental aneurysm [ 7,24,29,39]. Similarly, when a patient presents with aneurysmal SAH and asymp tomatic carotid stenosis, craniotomy for aneurysm clipping can be performed first without compromising cerebral blood flow intraoperatively [3,39,41]. However, when a patient’s symptomatic aneurysm is left untreated and an endarterectomy is performed for asymptomatic carotid stenosis, the risk of hemorrhage is increased [7,10,39]. Because the patients reported here presented with two acute disease entities, the order in which to treat these problems posed a dilemma. The philosophy of first treating the initial symptomatic lesion was applied: each patient’s neurologic state was due to SAH so the aneurysm was clipped first. In case 1, the carotid lesion became “symptomatic” when the patient was in the operating room, as manifested by the loss of cortical activity on routine monitoring. The thromboendarterectomy was therefore performed during the same operative setting. In case 2, the carotid occlusion was symptomatic as manifested by the contralateral hemiparesis, but the acuteness of the occlusion was not apparent until after postoperative angiography was performed. A single surgical stage with aneurysm clipping and thromboendarterectomy (rather than an STA-MCA bypass) would have been performed had this information been available preoperatively. Treatment recommendations are summarized in Table 1.

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Postoperative (A) anteroEl posterior and @) lateral vertebrobasilar angiograms

showing no residual aneurysm; (C) left internal carotid artery angiogram demonstrates normal anatomy and restored flow.

THROMBOENDARTERECTOMY The role of thromboendarterectomy to restore blood flow in a symptomatic occluded internal carotid artery remains controversial. The natural history of spontaneous ICA occlusion involves an ipsilateral stroke rate of about 5% [4,6,7,11]. Our experience in selected symptomatic patients without profound ischemic neurologic deficits or intracerebral hemorrhage suggests that an occluded ICA can be reopened successfully in a significant num-

ber of patients, with low surgical morbidity and mortality [25]. Key technical points include: (1) avoiding manipulation of the ICA to minimize the risk of dislodging the thrombus; (2) performing the arteriotomy without occluding the ICA, allowing backflow to spontaneously express the clot; (3) attempting to deliver the clot with a Fogarty catheter if the clot does not express itself; and (4) performing a stumpectomy if a thrombectomy is unsuccessful. In both of our cases, the patient’s thrombus was

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Treatment Recommendations ASVMPT~MATIC

Asymptomatic carotid Symptomatic carotid

NASCET = North American treat one aneurysm first.

INTRACRANIAL

ANEURYSM

(1) Elective aneurysm clipping (2) Stenosis >60%: elective carotid endarterectomy (1) Complete occlusion: thromboendarterectomy High-grade (70%-99%) stenosis: carotid endarterectomy Moderate-grade (30%-69%) stenosis: NASCETenrollment (2) Elective aneurysm clipping Symptomatic

Carotid

Endarterectomy

Trial. *Exception:

easily expressed, backflow

was brisk, and restoration of normal flow in the ICA was achieved after a standard endarterectomy [25]. Thrombolytic therapy was not considered in either case because of the risk of thrombolysis at the site of aneurysm rupture and subsequent rehemorrhage.

EFFECTS OF ALTERED HEMODYNAMICS ON ANEURYSM RUPTURE The coexistence of high-grade carotid stenosis and a cerebral aneurysm raises the suspicion that altered hemodynamics may have precipitated the rupture of the aneurysm. Changes in collateral blood flow after carotid ligation have been linked to aneurysm formation and rupture [2,5,12-14,16,23, 26,27,31,33,36,42,43]. Carotid ligation in experimental animals has been shown to contribute to the formation of aneurysms in the circle of Willis [ 17, 181. The appearance of aneurysms on feeding arteries to arteriovenous malformations and their propensity to rupture support the belief that high flow is important in the pathogenesis of aneurysms. In the two cases presented, ICA stenosis/occlusion may have increased collateral blood flow through the communicating arteries and led to aneurysm formation and rupture. Therefore, although carotid stenosis may not have been the initial symptomatic lesion, it may have caused the aneurysm to rupture. REFERENCES 1. Baker HL. Medical and surgical care of stroke. Circulation 1965;32:559-62. 2. Batjer H, Mickey B, SamsonD. Enlargement and rup ture of distal basilar artery aneurysm after iatrogenic carotid occlusion. Neurosurgery 1987;20:624-8. 3. Bidzinski J, Bonicki W, Kolity GV, Zareba A. Ruptured intracranial aneurysm with spontaneous occlusion of internal carotid artery. Experience with 5 cases.Acta Neurochir (Wien) 1989;100:43-45.

SYMPTOMATIC

INTR.~xAN~

ANEURYSM

(1) Aneurysm clipping (2) Stenosis >60%: elective carotid endarterectomy (1) Aneurysm clipping and carotid endarterectomy Treat initial symptomatic lesion first*

if an aneurysm

is located downstream

from the carotid

stenosis,

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COMMENTARY

Porter et al have provided a nice report of two cases of simultaneous aneurysm rupture and symptomatic internal carotid artery thrombosis presenting as concurrent disease processes. The simultaneous presence of two separate and distinct problems makes for an interesting discussion of the appropriate treatment of each symptomatic lesion. There is not much dispute that with subarachnoid hemorrhage (SAH), the surgical treatment of a ruptured cerebral aneurysm needs to take precedence over virtually every other disease process, due to the risk of catastrophic aneurysm rebleeding. The only significant question is the timing and technical considerations for treatment of symptomatic carotid thrombosis concurrent with acute SAH. In case 1, the authors diagnosed a severe stenosis of the left internal carotid artery at the cervical bifurcation and the presence of an intraluminal filling defect extending up the cervical internal carotid artery on the preoperative arteriogram. With this information we would have recommended a simultaneous aneurysm clipping and subsequent carotid thromboendarterectomy regardless of changes on compressed spectral EEC analysis intraoperatively. We would initially repair the ruptured aneurysm