Prognosis with 500 ruptured and operated intracranial arterial aneurysms

Based on a series of 500 operated intracranial aneurysms in 486 patients, we have analyzed the results of current neurosurgical treatment. The overall results (75% cures, 13% poor results, 12% deaths) depend on several factors, which have all to be analyzed: the age and general condition of the patient; the topography and mode of rupture of the aneurysm; and the timing of the surgical intervention.     

Endovascular management of ruptured cerebral mycotic aneurysms

The purpose of this investigation was to evaluate the current endovascular management of cerebral mycotic aneurysms. We report the retrospective evaluation of data of patients with cerebral mycotic aneurysms treated with endovascular approach. Thirteen consecutive patients with cerebral mycotic aneurysms were treated between April 2001 and March 2007. There were seven men and six women with ages ranging from 20 to 52 years (mean age 33 years.). All 13 patients had rheumatic heart disease (RHD) with endocarditis. The aneurysms were located within the distal cerebral circulation (n = 12) or in the circle of Willis (n = 1). All were ruptured aneurysms. Distal aneurysms were treated by parent vessel occlusion. Proximal saccular aneurysms were selectively treated. Endovascular treatment was technically successful in all patients. No patient had a rebleed after embolization during the clinical follow-up. Two patients deteriorated and died after endovascular treatment. Repeat CT scan showed increased mass effect because of earlier intracerebral bleed. The late clinical outcome in the other 11 patients was normal neurological status (n = 8) or permanent disability that was related to the initial stroke (n = 3). Endovascular approach is a reliable and safe technique for management of cerebral mycotic aneurysms.     

Paraparesis associated with ruptured anterior cerebral artery territory aneurysms

BACKGROUND: Paraparesis is a rare but characteristic manifestation of ruptured anterior communicating artery or anterior cerebral artery (ACA) aneurysms, but the pathogenesis remains unclear. This study investigated the neuroimaging and clinical features of patients with such paraparesis to evaluate possible causes. METHODS: Nine of 178 patients with ruptured anterior communicating artery or ACA aneurysms presented with paraparesis among 462 patients with subarachnoid hemorrhage (SAH) admitted between May 1996 and November 2001. Diffusion-weighted magnetic resonance (MR) imaging was performed within 48 hours of the onset of SAH in 4 of these 9 patients. The clinical course and neuroimaging studies of these 4 patients were retrospectively reviewed. RESULTS: Diffusion-weighted MR imaging revealed -intensity areas in the medial aspects of the bilateral frontal lobes, which were supplied by the ACAs and distal to the aneurysms, in all 4 patients. These high-intensity lesions had normal to subnormal values of apparent diffusion coefficient (ADC). Most of the high-intensity lesions recovered and did not result in the final lesions regardless of the ADC values, but some lesions with subnormal ADC values resulted in cerebral infarction. Paraparesis was transient and almost completely resolved in 3 patients. CONCLUSIONS: Diffusion-weighted MR imaging detected primary brain damage in the ACA territories caused by acute SAH, which was compatible with the clinical paraparesis. Primary brain damage caused by SAH may include 3 types of lesions: reversible with normal ADC value, reversible with subnormal ADC value, and irreversible with subnormal ADC value.     

Fenestrated basilar artery with ruptured cerebral aneurysms: case report

Two cases of aneurysms with basilar artery fenestration are presented. A 45 year-old lady had a saccular aneurysm associated with a fenestrated basilar artery. The fenestration was located in the proximal third of the basilar artery. The aneurysm arose from the proximal end of the fenestration, projecting antero-inferiorly. Via a left retromastoid craniectomy, the aneurysm was successfully obliterated through the space between the eighth cranial nerve and the lower cranial nerve complexes. Postoperative deficit in the lower cranial nerves was minimal and transient. The other patient, a 63 year-old lady, had multiple aneurysms arising from the anterior circulation associated with a basilar artery fenestration. These aneurysms were clipped uneventfully. Surgical approach to an aneurysm arising from the basilar artery fenestration is discussed with other related literature. Full study of posterior circulation with multiple projection is mandatory to detect basilar artery fenestration, and the possible presence of saccular aneurysm at the site of the anomaly.     

Rebleeding after endovascular embolization of ruptured cerebral aneurysms

This study retrospectively reviewed 227 patients with ruptured solitary cerebral aneurysm who underwent endovascular embolization with detachable coils between March 1997 and March 2006 to establish the incidence of rebleeding after endovascular treatment for ruptured cerebral aneurysm and identify the risk factors. The site and size of the aneurysm, the interval between treatment and rebleeding, and the outcome were investigated in six of the 227 patients (2.6%) who rebled after treatment. Four patients had large or giant aneurysms located on the internal carotid artery at the origin of the posterior communicating artery. The interval between treatment and rebleeding was less than 1 year in four patients (mean 394.2 days). Two patients died, and the survivors had modified Rankin Scale scores of 0, 2, 3, and 4. Re-embolization was performed in four patients and no further bleeding occurred during the mean follow-up period of 1.9 years after re-treatment. Patients with giant aneurysms of the internal carotid artery are at increased risk for rebleeding. Re-treatment should be considered if there is conventional and/or magnetic resonance angiographic evidence of dome filling. Patients with ruptured cerebral aneurysms must be followed up with diagnostic imaging closely during the first 12 months post-embolization because rebleeding frequently occurs within 1 year after initial treatment. Re-embolization is safe and effective in patients with recurrent hemorrhage from aneurysms previously embolized with detachable coils.     

Epilepsy after operative treatment of ruptured cerebral aneurysms

Summary A retrospective analysis of 183 consecutive patients operated on for ruptured cerebral aneurysms and surviving at least one year revealed appearance of postoperative epilepsy in 14 cases (8 per cent) on an average of 10 months (range 0–23 months) after the operation. Factors associated with the development of secondary epilepsy were localization of the aneurysm on the middle cerebral artery, temporary clipping intraoperatively, wrapping technique to treat the aneurysm, and vasospasm seen on the postoperative control angiogram. Intraoperative and/or postoperative ischaemia seems to be the crucial phenomenon favouring the development of epilepsy. Identification of the risk factors may help to focus the anti-epileptic prophylaxis in cases prone to develop seizures.     

Analysis of 53 ruptured middle cerebral artery aneurysms

In spite of a recent remarkable progress in operative results of ruptured middle cerebral artery aneurysms, a mortality rate of 2-8% appears to be unavoidable. In the present study, 53 ruptured MCA aneurysms were retrospectively analyzed to determine causative factors of unfortunate outcome (fair, poor and dead). Surgical results of 53 ruptured MCA aneurysms are shown in Table 1, where the outcome was unfortunate in 7 cases (17%). Intracerebral hematoma was responsible for 4 cases, two of which were fatal and postoperative vasospasm for 3 cases. There were 13 cases with intracerebral hematomas (25%) ranging from 21 mm to 68 mm in diameter. Although hematomas less than 40 mm in diameter localized in temporal or frontal subcortical areas and yielded no neurological deficits, those more than 60mm extended to the caudate nucleus or thalamus through the internal capsule and led to deep coma (Table 2, Fig. 1). Intracerebral hematoma with the diameter between 50 to 60 mm seems to be critical in regard to postoperative outcome. Repeated rupture caused intracerebral hematoma (50%) more frequently than single rupture (21%) and aneurysm with intracerebral hematoma was liable to bleed (27%), resulting in acute deterioration of neurological conditions by marked enlargement of the hematoma (Fig. 2). Accordingly it is essential for the cases with intracerebral hematoma to prevent rerupture. Subarachnoid hemorrhage and symptomatic vasospasm were observed less frequently in hematoma group than in non-hematoma group. However, prophylactic treatment of vasospasm is important even in the cases with intracerebral hematoma since more than half of them suffer from relatively thicker subarachnoid clot.     

Gastrointestinal bleeding in cases of ruptured cerebral aneurysms

Among 1,000 cases of patients undergoing direct surgery on cerebral aneurysms, two, showed clear signs of preoperative, and 19 cases showed postoperative gastrointestinal bleeding. We have made a clinical analysis of various aspects of the 19 cases in which the bleeding developed postoperatively. 1. Gastrointestinal bleeding was most frequent postoperatively in cases of AComA aneurysms (4.3%) and ICA aneurysms (2.0%), and less common in MCA and ACA aneurysm cases. 2. Gastrointestinal bleeding was most frequently seen in those cases operated on between the third and seventh days after the last subarachnoid haemorrhage (8.9%) and was more common in cases with a relatively poor preoperative grade. 3. The development of such bleeding in cases with a good preoperative grade was due to problems with the surgical operation in most cases, although the influence of vasospasm must not be ignored. The development of bleeding in cases with a poor preoperative grade is thought to be due primarily to vasospasm and transitory brain damage to the hypothalamus and the orbital portion of the anterior lobe due to a haematoma caused by aneurysm rupture. 4. First, the location of gastrointestinal bleeding should be determined endoscopically and, if haemostasis is not achieved by coagulation, then the desirability of surgery should be considered early. Abdominal surgery may be performed.     

Regional cerebral blood flow in patients with ruptured intracranial aneurysms.

Eighty-five studies of regional cerebral blood flow (rCBF) were performed on 49 patients with ruptured intracranial aneurysms. The changes in rCBF were analyzed under various pathophysiological conditions, The degree of flow abnormalities correlated well with the clinical severity of neurological deficits. All of the patients with diffuse vasospasm of severe grade, to less than half of their control value, showed focal areas of decreased flow below 30 ml/100 gm/min, in addition to a reduction in mean CBF. The relief or disappearance of vasospasm in angiograms was followed by the increase of rCBF in the ischemic focus and mean CBF. Marked reduction in rCBF was found in patients with intracerebral hematoma and ventricular dilatation. Impaired CO2 response and autoregulation were found in patients with severe neurological deficits, a severe degree of vasospasm and marked depression of CBF. In this series direct operation was delayed in patients with impaired vascular reactivity as well as marked decrease of mean CBF below 30 ml/100 gm/min; good clinical results were obtained in thses patients.     

Mesenteric ischaemia after endovascular coiling of ruptured cerebral aneurysms

Summary Three patients were referred to a national neurosurgical centre following CT evidence of subarachnoid haemorrhage. The three patients, who were referred from different institutions within a seven week period, were Fisher grade 3 and WFNS Grade I at all times. Angiography showed a PCOM aneurysm in one case, a ruptured Basilar tip aneurysm and an unruptured ACOM aneurysm in another case, and an ACOM aneurysm in the third case. It was decided that the aneurysms were suitable for endovascular coiling. These patients had unremarkable intraoperative catheterizations and coiling but subsequently deteriorated post-operatively due to mesenteric ischaemia. Two patients required colectomy for mesenteric ischaemia, and the third arrested secondary to sepsis from bowel perforation. We discuss the various causes that may explain this association, and we alert the neurosurgical community for this complication which has not been reported before. Correspondence: Mahmoud Hamdy Kamel, Neurosurgery Department, 4F ward, Royal Victoria Hospital, Belfast, UK.     

Hydrocephalus and vasospasm after subarachnoid hemorrhage from ruptured intracranial aneurysms

The incidence of hydrocephalus and vasospasm and the relationship between them were analyzed retrospectively in 87 patients with subarachnoid hemorrhage from ruptured intracranial aneurysms. Sixty-seven per cent of the patients showed ventricular enlargement on a computed tomographic scan done within 30 days of the hemorrhage; in patients whose first scan was done within 3 days of the hemorrhage, 63% seemed to have ventricular enlargement by a neuroradiologist's interpretation. Shunts were required in 14% of the patients because of delayed neurological deterioration or enlarging ventricles; 3% required ventriculostomy shortly after admission. Seventy-four per cent of the patients had angiographic spasm on an angiogram done within the first 30 days after hemorrhage. Sixty-two per cent of the patients had both hydrocephalus and vasospasm: 22% had neither. Five per cent had hydrocephalus, but no spasm; 11% had spasm, but no hydrocephalus. Hydrocephalus and vasospasm were significantly associated (P less than 0.01, chi2). These data document a high incidence of mild ventricular enlargement and angiographic vasospasm after subarachnoid hemorrhage. They also emphasize that these two sequelae of subarachnoid hemorrhage are closely linked, probably by the presence of blood in the basal cisterns obstructing cerebrospinal fluid flow and surrounding arteries there.     

Effects of intravascular volume expansion on cerebral blood flow in patients with ruptured cerebral aneurysms

To clarify the effect of intravascular volume expansion on cerebral blood flow (CBF) in patients after subarachnoid hemorrhage (SAH), we performed 55 pairs of regional CBF measurements using the xenon-133 inhalation method before and after volume expansion in 35 patients with ruptured cerebral aneurysms. CBF was calculated as the hemispheric mean value of the initial slope index. To accomplish volume expansion, we transfused 500 ml of 5% human serum albumin in half an hour. After volume expansion with albumin, the hemoglobin value decreased significantly (P less than 0.005). Volume expansion did not change the mean arterial blood pressure. During the first 2 weeks after SAH, CBF decreased significantly after volume expansion (P less than 0.005). During the 3rd week after SAH and subsequently to the 4th week after SAH, volume expansion produced no change in CBF. In patients with symptomatic vasospasm, CBF decreased significantly after volume expansion (P less than 0.005). In patients without symptomatic vasospasm, volume expansion produced no change in CBF. The results of this study suggest that increasing the intravascular volume above normal by volume expansion does not increase CBF or reverse symptomatic vasospasm.     

Ventriculostomy-related intracranial hemorrhage following surgical and endovascular treatment of ruptured aneurysms

Endovascular therapy of ruptured aneurysms is regularly accompanied by periprocedural heparinization and requires the use of periprocedural antiplatelets in more complex cases. This raises concerns regarding increased bleeding risks in the case of frequently required ventriculostomy. The aim of this study was to analyze risk factors for ventriculostomy-related intracranial hemorrhages (VS-ICH) in endovascular or surgical treatment of ruptured aneurysms with a focus on antithrombotic therapy. In this retrospective analysis, we included patients admitted to our institution over a 12-year period who had received at least one ventriculostomy due to subarachnoid hemorrhage-related hydrocephalus. Patients were dichotomized into an endovascular and surgical group and rates of VS-ICH were compared. Risk factors for VS-ICH were assessed in uni- and multivariate analyses. A total of 606 ventriculostomies were performed in 328 patients. Within the endovascular group, antiplatelet therapy was used in 44.8% of cases. The overall rate of ventriculostomy-related intracranial hemorrhage was 13.1%. Endovascular treatment was associated with a higher rate of VS-ICH compared to surgical treatment (p?=?0.011), but not in cases without antiplatelet therapy (p?=?0.166). Application of any antiplatelet therapy (odds ratio, 2.647 [95% confidence interval, 1.141–6.143]) and number of ventriculostomies (odds ratio, 2.513 [95% confidence interval, 1.859–3.395]) were independent predictors of ventriculostomy-related hemorrhages. Our findings indicate an increased risk of VS-ICH in the endovascular group if administration of antiplatelets was required. While this aspect has to be included into treatment decision-making, it must be weighed against the benefits of endovascular techniques.