|Year : 2015 | Volume
| Issue : 3 | Page : 172-175
Postaneurysmal subarachnoid hemorrhage vasospasm: a review of the incidence of radiographic and clinical vasospasm
Ahmed M Ali Mahmoud BSc, MSc, MD
Department of Neurosurgery, Kasr Al-Ainy Medical School, Cairo University, Giza, Egypt
|Date of Submission||23-Jan-2015|
|Date of Acceptance||01-Mar-2015|
|Date of Web Publication||13-Aug-2015|
Ahmed M Ali Mahmoud
Department of Neurosurgery, Kasr Al-Ainy Medical School, Cairo University, Giza
Source of Support: None, Conflict of Interest: None
Vasospasm following ruptured intracranial aneurysms has always been a challenging condition to treat.
The aim of this study was to correlate between clinical and radiographic vasospasms after aneurysmal subarachnoid hemorrhage (SAH) and to point out the other important causes of neurological deterioration.
This is a retrospective study conducted on 25 consecutive patients between June 2013 and February 2014 who presented with SAH. Altogether there were 18 male and seven female patients with ages ranging from 42 to 65 years. All patients underwent initial four-vessel or computed tomography (CT) angiography. All patients were treated by direct surgical clipping and all of them were operated upon 48-72 h from admission. All patients were assessed clinically and radiologically by CT scan and conventional angiography or CT angiography at day 10 of postbleeding.
Out of 25 cases with aneurysmal SAH, 20 developed radiographic vasospasm, with only 11 cases developing clinical vasospasm.
The incidence of radiographic (angiographic) vasospasm was 80%, with only 55% of cases developing clinical vasospasm. Proper evaluation with laboratory tests and neuroimaging should be carried out in all cases to detect the actual cause of neurological deterioration and to start the proper treatment.
Keywords: aneurysmal subarachnoid hemorrhage, clinical vasospasm, radiographic vasospasm
|How to cite this article:|
Ali Mahmoud AM. Postaneurysmal subarachnoid hemorrhage vasospasm: a review of the incidence of radiographic and clinical vasospasm. Egypt J Neurol Psychiatry Neurosurg 2015;52:172-5
|How to cite this URL:|
Ali Mahmoud AM. Postaneurysmal subarachnoid hemorrhage vasospasm: a review of the incidence of radiographic and clinical vasospasm. Egypt J Neurol Psychiatry Neurosurg [serial online] 2015 [cited 2022 Jul 1];52:172-5. Available from: http://www.ejnpn.eg.net/text.asp?2015/52/3/172/162024
| Introduction|| |
Intracranial arterial vasospasm usually occurs following rupture of intracranial aneurysms and subarachnoid hemorrhage (SAH). The vasospasm can be either clinical, also known as delayed ischemic neurologic deficit, or it can be radiographic vasospasm, known as angiographic vasospasm . The radiographic (angiographic) vasospasm can be as high as 90% .
In aneurysmal SAH, at least one cerebral artery will show moderate vasospasm in two-thirds of cases. Half of these patients will become symptomatic as a result of ischemia, and a cerebral infarct will develop in about half of these patients . Cerebral infarction is significantly associated with increasing patient age, worse neurological grade on admission, history of hypertension or diabetes mellitus, large aneurysms, induced hypertension, fever, and a diagnosis of symptomatic vasospasm .
A large volume of persistent subarachnoid clot is the most important risk factor predictive of vasospasm after SAH . The original Fisher grading scale in which clot volume and distribution on admission computed tomography (CT) are related to risk for vasospasm has been modified [Table 1], and in a single-center study the scale was found to have greater predictive value for delayed ischemia and prognosis . Other risk factors for the development of vasospasm have been identified, including poor neurological grade or loss of consciousness on admission, cigarette smoking, and pre-existing hypertension .
Symptoms of ischemia resulting from cerebral vasospasm most commonly appear 1 week after aneurysm rupture but often occur later; accordingly, it is important to remain vigilant for this complication for at least 2 weeks after SAH. Regular and careful bedside examination remains the simplest and most effective means of detecting early ischemia in awake, examinable patients; one should concentrate on subtle findings such as diminished attention, changes in verbal output, or a slight but new pronator drift of the upper extremity. Symptomatic vasospasm usually has a gradual onset, sometimes heralded by increased headache and either agitation or somnolence - a change in patient behavior. It then follows a progressive course if untreated. A smaller group of patients will experience precipitous deterioration .
There are several causes of delayed deterioration after SAH: increased edema surrounding hematomas, contusions, or infarcts; rebleeding of aneurysms or aneurysmal remnant; hydrocephalus; infection including ventriculitis; hyponatremia; hypoxemia; and cerebral vasospasm causing cerebral ischemia . To diagnose clinical vasospasm, the other causes of neurological deterioration must be ruled out by proper laboratory and radiological investigations.
This study aims to review and clinically correlate the degree and relationship between clinical and radiological vasospasm and its impact on the patients' outcome.
| Patients and methods|| |
This is a retrospective study of 25 patients with postaneurysmal SAH admitted to Kasr Al-Ainy Hospitals, Cairo University, between June 2013 and February 2014. Patients with postaneurysmal SAH despite the location of the aneurysm were studied both radiographically and clinically. Only cases with spontaneous bleeding were included in this study. Hunt and Hess grading was used to grade the patients' neurological status after clinical spasm [Table 2] and the Fisher grading system to grade the degree of expected vasospasm. The Glasgow Coma Scale (GCS) was used to determine the level of consciousness. Initial four-vessel or CT angiography was performed immediately as soon as the SAH was detected in the CT scan. All patients were treated by direct surgical clipping. All patients were operated upon within 48-72 h from admission. The study was approved by ethical committee of Kasr Al-Ainy Hospitals, Cairo University.
There were 18 male and seven female patients with ages ranging from 42 to 65 years. All patients were assessed clinically and radiologically by CT scan and four-vessel angiography or CT angiography at day 10 of postbleeding.
All 25 patients were operated upon in Cairo University Hospitals by the author. All of them were assessed using the GCS and Hunts and Hess grading system [Table 2]. Different approaches were used according to the site of the aneurysm. All cases received routine preoperative nimodipine once diagnosed with SAH and were continued on nimodipine for 3 weeks or until discharge from the hospital with no neurological deficits. Intraoperative irrigation with papaverine and saline was used in all cases. Triple-H therapy was started once clipping of the aneurysm was done. Patients without complications were discharged 2 weeks after surgery.
| Results|| |
Out of 25 patients, 20 (80%) developed radiographic vasospasm and five (20%) developed neither clinical nor radiographic vasospasm [Table 3]. Out of these 20 cases only 11 (55%) developed clinical vasospasm: in the form of conscious level deterioration in six (30%) cases and neurological deficits in five (25%) [Figure 1]. In the six cases, whose conscious level deteriorated, the GCS dropped from 15 to 13 or 14. Among those with focal neurological deficits, three developed lower-limb weakness and dysphasia. Two patients developed right-side weakness of grade III [Table 4]. All patients recovered well in the postoperative period.
|Figure 1: (a) Computed tomography of a 45-year-old male patient showing extensive subarachnoid hemorrhage (SAH). The patient developed new weakness on day 8 after SAH. (b, c) Lateral and superior views of computed tomographic angiography show right-sided posterior communicating irregular aneurysm. (d) Postclipping angiogram performed at day 10 of bleeding shows severe spasm of the carotid and middle cerebral arteries.|
Click here to view
|Table 3: Number of patients with vasospasm in relation to total number of cases|
Click here to view
|Table 4: Neurological deficits of 11 patients with radiographic and clinical vasospasm|
Click here to view
In the nine patients who developed radiographic but not clinical vasospasm, two died at day 7 and day 8 postoperatively. They were patients with poor Hunt and Hess grade on admission (grade IV) and developed severe chest infection postoperatively. Three patients had no neurological deficits or conscious level deterioration from the start. Two cases had dysphasia, which improved totally in the postoperative period. Two had lower-limb weakness of grades II or III, which improved and became ambulant with support [Table 5]. Five patients did not develop radiological spasm and all had a smooth postoperative period and were discharged well [Table 3].
| Discussion|| |
The vasospasm that occurs following aneurysmal SAH is considered one of the most important factors determining morbidity and mortality in such patients. Even after successful uneventful surgical clipping, vasospasm still composes a challenge in the perioperative management. Two types of vasospasm are identified, radiographic and clinical. In this study, clinical and radiological vasospasm has been reviewed and correlated with each other.
The results published in the literature show a strong relationship between the radiographic vasospasm and the development of later cerebral infarction . The percentage of cereb ral infarction in patients with angiographic vasospasm ranges from 34 to 70% in different studies .
In this study follow-up CT angiography or four-vessel angiography was performed after 10 days of bleeding. The radiographic (angiographic) vasospasm can be as high as 90% . As reported in the literature, the radiological vasospasm is identified early in 97% of patients between days 5 and 7 from aneurysmal rupture and late in 3% between days 12 and 15 . This study reported that 80% of cases had developed radiological spasm when angiography was performed on day 10 of bleeding. There is a significant association between the development of neurological deterioration and possibly late cerebral infarctions and the degree of vasospasm. In studies by Crowley et al.  and Weidaeur and colleagues, most vasospasm-related ischemia was in patients with severe vasospasm. In this study there were 11 patients out of the 20 with radiographic vasospasm who developed clinical vasospasm as well. Nine patients developed only radiological spasm. Two of these patients died because of poor general condition and poor Hunt and Hess grade and chest infection. Three cases were clinically free. The last four patients out of the nine with only radiographic vasospasm developed neurologic deterioration. This deterioration was attributed to postoperative edema and lobe contusions, as evident by CT scan, rather than clinical vasospasm. Of these four patients two (22.2%) were back to being normal on late follow-up and two were ambulant with support (22.2%). The result in this study coincides with the results of Awad et al.  In their study, 35.6% of patients developed clinical vasospasm. Eighty percent of patients in this study developed radiological vasospasm, similar to the study by Newell et al.  in which 92% of patients developed radiological spasm.
The data from the literature recommend controlled CT scanning after 6 weeks following SAH to diagnose definitive cerebral infarction .
| Conclusion|| |
The incidence of radiographic vasospasm is high after SAH, especially in cases with dense SAH. Not all cases with radiographic vasospasm pass into clinical vasospasm. In addition, some cases with evident neurological deterioration can be due to several other factors than the clinical vasospasm. Proper evaluation with laboratory tests and neuroimaging should be performed in all cases to detect the actual cause of neurological deterioration and to start proper treatment.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Harrod CG, Bendok BR, Batjer HH. Prediction of cerebral vasospasm in patients presenting with aneurysmal subarachnoid hemorrhage: a review. Neurosurgery 2005; 56
Dorsch NW, King MT. A review of cerebral vasospasm in aneurysmal subarachnoid haemorrhage. Part I: incidence and effects. J Clin Neurosci 1994; 1
Fergusen S, Macdonald RL. Predictors of cerebral infarction in patients with aneurysmal subarachnoid hemorrhage. Neurosurgery 2007; 60
Proust F, Hannequin D, Langlois O, Freger P, Creissard P. Causes of morbidity and mortality after ruptured aneurysm surgery in a series of 230 patients. The importance of control angiography. Stroke 1995; 26
Reilly C, Amidei C, Tolentino J, Jahromi BS, Macdonald RL. Clot volume and clearance rate as independent predictors of vasospasm after aneurysmal subarachnoid hemorrhage. J Neurosurg 2004; 101
Kramer AH, Hehir M, Nathan B, Gress D, Dumont AS, Kassell NF, Bleck TP. A comparison of 3 radiographic scales for the prediction of delayed ischemia and prognosis following subarachnoid hemorrhage. J Neurosurg 2008; 109
Fisher CM, Roberson GH, Ojemann RG. Cerebral vasospasm with ruptured saccular aneurysm - the clinical manifestations. Neurosurgery 1977; 1
Brown RJ, Kumar A, Dhar R, Sampson TR, Diringer MN. The relationship between delayed infarcts and angiographic vasospasm after aneurysmal subarachnoid hemorrhage. Neurosurgery 2013; 72
:702-707 discussion 707-708.
Etminan N, Vergouwen MD, Macdonald RL. Angiographic vasospasm versus cerebral infarction as outcome measures after aneurysmal subarachnoid hemorrhage. Acta Neurochir Suppl 2013; 115
Weidauer S, Lanfermann H, Raabe A, Zanella F, Seifert V, Beck J. Impairment of cerebral perfusion and infarct patterns attributable to vasospasm after aneurysmal subarachnoid hemorrhage: a prospective MRI and DSA study. Stroke 2007; 38
Crowley RW, Medel R, Dumont AS, Ilodigwe D, Kassell NF, Mayer SA, et al.
Angiographic vasospasm is strongly correlated with cerebral infarction after subarachnoid hemorrhage. Stroke 2011; 42
Awad IA, Carter LP, Spetzler RF, Medina M, Williams FC Jr. Clinical vasospasm after subarachnoid hemorrhage: response to hypervolemic hemodilution and arterial hypertension. Stroke 1987; 18
Newell DW, Grady MS, Eskridge JM, Winn HR. Distribution of angiographic vasospasm after subarachnoid hemorrhage: implications for diagnosis by transcranial Doppler ultrasonography. Neurosurgery 1990; 27
Siironen J, Porras M, Varis J, Poussa K, Hernesniemi J, Juvela S. Early ischemic lesion on computed tomography: predictor of poor outcome among survivors of aneurysmal subarachnoid hemorrhage. J Neurosurg 2007; 107
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]