Factors associated with the development of vasospasm after planned surgical treatment of aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 99 (4) ◽  
pp. 644-652 ◽  
Author(s):  
R. Loch Macdonald ◽  
Axel Rosengart ◽  
Dezheng Huo ◽  
Theodore Karrison
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ct Scan ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Factors Associated ◽  
Symptomatic Vasospasm ◽  
Aneurysm Size ◽  
Induced Hypertension ◽  
History Of ◽  
Fine Print

Object. The goal of this study was to determine factors associated with the development of symptomatic vasospasm among patients with aneurysmal subarachnoid hemorrhage (SAH) who participated in the randomized, double-blind, placebo-controlled trials of tirilazad between 1991 and 1997. Methods. Data obtained from 3567 patients entered into trials of tirilazad were analyzed using uni- and multivariate logistic regression to determine factors that predict the development of symptomatic vasospasm. Symptomatic vasospasm was defined by clinical criteria accompanied by laboratory- and radiologically determined exclusion of other causes of neurological deterioration. Transcranial Doppler ultrasonographic and/or angiographic confirmation was not required. In these patients, the aneurysms were scheduled to be treated surgically, and no patient undergoing endovascular treatment was included. A multivariate analysis showed that factors significantly associated with vasospasm were age 40 to 59 years, history of hypertension, worse neurological grade, thicker blood clot on the cranial computerized tomography (CT) scan obtained on hospital admission, larger aneurysm size, presence of intraventricular hemorrhage (IVH), prophylactic use of induced hypertension, and not participating in the first European tirilazad study. Conclusions. Symptomatic vasospasm was associated with the amount of SAH on the CT scan, the presence of IVH, and the patient's neurological grade. The association with patient age may reflect alterations in vessel reactivity associated with age. A history of hypertension may render the brain more susceptible to symptoms from vasospasm. The explanation for the relationships with aneurysm size, use of prophylactic induced hypertension, and the particular study is unclear.

Smaller cerebral aneurysms producing more extensive subarachnoid hemorrhage following rupture: a radiological investigation and discussion of theoretical determinants

2003 ◽  
Vol 99 (2) ◽  
pp. 248-253 ◽  
Author(s):  
Stephen M. Russell ◽  
Ke Lin ◽  
Sigrid A. Hahn ◽  
Jafar J. Jafar
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ct Scan ◽  
Cerebral Aneurysms ◽  
Radiological Investigation ◽  
Content Type ◽  
Aneurysm Size ◽  
History Of ◽  
The Mean ◽  
The Relationship ◽  
Fine Print

Object. The goal of this study was to determine the relationship between aneurysm size and the volume of subarachnoid hemorrhage (SAH). Methods. One hundred consecutive patients who presented with acute SAH, which was diagnosed on the basis of a computerized tomography (CT) scan within 24 hours postictus and, subsequently, confirmed to be aneurysmal in origin by catheter angiography, were included in this study. The data were collected prospectively in 32 patients and retrospectively in 68. The volume of SAH on the admission CT scan was scored in a semiquantitative manner from 0 to 30, according to a previously published method. The mean aneurysm size was 8.3 mm (range 1–25 mm). The mean SAH volume score was 15 (range 0–30). Regression analysis revealed that a smaller aneurysm size correlated with a more extensive SAH (r2 = 0.23, p < 0.0001). Other variables including patient sex and age, intraparenchymal or intraventricular hemorrhage, multiple aneurysms, history of hypertension, and aneurysm location were not statistically associated with a larger volume of SAH. Conclusions. Smaller cerebral aneurysm size is associated with a larger volume of SAH. The pathophysiological basis for this correlation remains speculative.

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

Hyperglycemia, excess weight, and history of hypertension as risk factors for poor outcome and cerebral infarction after aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 102 (6) ◽  
pp. 998-1003 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Johanna Kuhmonen
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Patient Outcomes ◽  
Plasma Glucose ◽  
Clinical Condition ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Poor Outcome ◽  
History Of ◽  
Fine Print

Object. Stress-induced hyperglycemia has been shown to be associated with poor outcome after aneurysmal subarachnoid hemorrhage (SAH). The authors prospectively tested whether hyperglycemia, independent of other factors, affects patient outcomes and the occurrence of cerebral infarction after SAH. Methods. Previous diseases, health habits, medications, clinical condition, and neuroimaging variables were recorded for 175 patients with SAH who were admitted to the hospital within 48 hours after bleeding. The plasma level of glucose was measured at admission and the fasting value of glucose was measured in the morning after aneurysm occlusion. Factors found to be independently predictive of patient outcomes at 3 months after SAH onset and the appearance of cerebral infarction were tested by performing multiple logistic regression. Plasma glucose values at admission were found to be associated with patient age, body mass index (BMI), history of hypertension, clinical condition, amount of subarachnoid or intraventricular blood, shunt-dependent hydrocephalus, outcome variables, and the appearance of cerebral infarction. When considered independently of age, clinical condition, or amount of subarachnoid, intraventricular, or intracerebral blood, the plasma glucose values at admission predicted poor outcome (per millimole/liter the odds ratio [OR] was 1.24 with a 95% confidence interval [CI] of 1.02–1.51). After an adjustment was made for the amount of subarachnoid blood, the clinical condition, and the duration of temporary artery occlusion during surgery, the BMI was found to be a significant predictor (per kilogram/square meter the OR was 1.15 with a 95% CI of 1.02–1.29) for the finding of cerebral infarction on the follow-up computerized tomography scan. Hypertension (OR 3.11, 95% CI 1.11–8.73)—but not plasma glucose (OR 1.06, 95% CI 0.87–1.29)—also predicted the occurrence of infarction when tested instead of the BMI. Conclusions. Independent of the severity of bleeding, hyperglycemia at admission seems to impair outcome, and excess weight and hypertension appear to elevate the risk of cerebral infarction after SAH.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Paradoxical aggravation of vasospasm with papaverine infusion following aneurysmal subarachnoid hemorrhage

1996 ◽  
Vol 84 (4) ◽  
pp. 690-695 ◽  
Author(s):  
Brent L. Clyde ◽  
Andrew D. Firlik ◽  
Anthony M. Kaufmann ◽  
MichaelP. Spearman ◽  
Howard Yonas
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Artery ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Left Middle Cerebral Artery ◽  
Xenon Ct ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fine Print

✓ Reports of intraarterial papaverine infusion as treatment for cerebral vasospasm are few and documented complications are uncommon. The authors report the case of a patient with paradoxical aggravation of cerebral arterial narrowing during selective intraarterial papaverine infusion intended to treat vasospasm following aneurysmal subarachnoid hemorrhage (SAH). A 48-year-old man presented to the authors' service with symptomatic vasospasm 10 days after experiencing an SAH. The ruptured anterior communicating artery aneurysm was surgically obliterated the following day, and thereafter maximum hypervolemic and hypertensive therapies were used. However, the patient remained lethargic, and a stable xenon—computerized tomography (CT) cerebral blood flow (CBF) study revealed CBF to be 15 cc/100 g/minute in the left anterior cerebral artery (ACA) and 25 cc/100 g/minute in the right ACA territories. Cerebral arteriography demonstrated diffuse severe left ACA and mild left middle cerebral artery (MCA) vasospasm. In response intraarterial papaverine was infused into the internal carotid artery just proximal to the ophthalmic artery. During the infusion the patient became aphasic and exhibited right hemiplegia. Arteriography performed immediately after the intraarterial papaverine infusion revealed diffuse exacerbation of vasospasm in the distal ACA and MCA territories. A repeat xenon—CT CBF study showed that CBF in the left ACA and the MCA had drastically decreased (2 cc/100 g/minute and 10 cc/100 g/minute, respectively). Despite aggressive management, infarction ultimately developed. This is the first clinical case to illustrate a paradoxical effect of intraarterial papaverine treatment for vasospasm following aneurysmal SAH. The possible mechanisms of this paradoxical response and potential therapeutic reactions are reviewed.

Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 101 (3) ◽  
pp. 408-416 ◽  
Author(s):  
Gregory G. Heuer ◽  
Michelle J. Smith ◽  
J. Paul Elliott ◽  
H. Richard Winn ◽  
Peter D. Leroux
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Grade ◽  
Icp Monitoring ◽  
Content Type ◽  
Poor Grade ◽  
Symptomatic Vasospasm ◽  
Increased Icp ◽  
Fine Print

Object. Increased intracranial pressure (ICP) is well known to affect adversely patients with head injury. In contrast, the variables associated with ICP following aneurysmal subarachnoid hemorrhage (SAH) and their impact on outcome have been less intensely studied. Methods. In this retrospective study the authors reviewed a prospective observational database cataloging the treatment details in 433 patients with SAH who had undergone surgical occlusion of an aneurysm as well as ICP monitoring. All 433 patients underwent postoperative ICP monitoring, whereas only 146 (33.7%) underwent both pre- and postoperative ICP monitoring. The mean maximal ICP was 24.9 ± 17.3 mm Hg (mean ± standard deviation). During their hospital stay, 234 patients (54%) had elevated ICP (> 20 mm Hg), including 136 of those (48.7%) with a good clinical grade (Hunt and Hess Grades I–III) and 98 (63.6%) of the 154 patients with a poor grade (Hunt and Hess Grades IV and V) on admission. An increased mean maximal ICP was associated with several admission variables: worse Hunt and Hess clinical grade (p < 0.0001), a lower Glasgow Coma Scale (GSC) motor score (p < 0.0001); worse SAH grade based on results of computerized tomography studies (p < 0.0001); intracerebral hemorrhage (p = 0.024); severity of intraventricular hemorrhage (p < 0.0001); and rebleeding (p = 0.0048). Both intraoperative cerebral swelling (p = 0.0017) and postoperative GCS score (p < 0.0001) were significantly associated with a raised ICP. Variables such as patient age, aneurysm size, symptomatic vasospasm, intraoperative aneurysm rupture, and secondary cerebral insults such as hypoxia were not associated with raised ICP. Increased ICP adversely affected outcome: 71.9% of patients with normal ICP demonstrated favorable 6-month outcomes postoperatively, whereas 63.5% of patients with ICP between 20 and 50 mm Hg and 33.3% with ICP greater than 50 mm Hg demonstrated favorable outcomes. Among 21 patients whose raised ICP did not respond to mannitol therapy, all experienced a poor outcome and 95.2% died. Among 145 patients whose elevated ICP responded to mannitol, 66.9% had a favorable outcome and only 20.7% were dead 6 months after surgery (p < 0.0001). According to results of multivariate analysis, however, ICP was not an independent outcome predictor (odds ratio 1.26, 95% confidence interval 0.28–5.68). Conclusions. Increased ICP is common after SAH, even in patients with a good clinical grade. Elevated ICP post-SAH is associated with a worse patient outcome, particularly if ICP does not respond to treatment. This association, however, may depend more on the overall severity of the SAH than on ICP alone.

A randomized controlled trial of high-dose intravenous nicardipine in aneurysmal subarachnoid hemorrhage

1993 ◽  
Vol 78 (4) ◽  
pp. 537-547 ◽  
Author(s):  
E. Clarke Haley ◽  
Neal F. Kassell ◽  
James C. Torner ◽  
_ _
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Controlled Trial ◽  
Treated Group ◽  
High Dose ◽  
Similar Frequency ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

✓ Because of their action as cerebral vasodilators, dihydropyridine calcium antagonists have received intense scrutiny for their potential benefit in ameliorating the devastating consequences of delayed cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). From October, 1987, to September, 1989, 41 North American neurosurgical centers in the Cooperative Aneurysm Study accrued 906 patients with recent (Days 0 to 7) aneurysmal SAH into a prospective randomized double-blind placebo-controlled trial of high-dose intravenous nicardipine to test whether treatment with this agent improved overall outcome. Eligible patients received 0.15 mg/kg/hr of either nicardipine or placebo by continuous infusion for up to 14 days following hemorrhage. The 449 patients randomly assigned to the nicardipine-treated group and the 457 patients assigned to the placebo-treated group were balanced with regard to prognostic factors for ischemic deficits from vasospasm and for overall outcome. Other medical and surgical interventions were used with similar frequency in both groups, except that antihypertensive agents were used less frequently in the nicardipine-treated patients (26% of the nicardipine-treated group vs. 43% of the placebo-treated group, p < 0.001), and more patients in the placebo-treated group had intentional hypervolemia, induced hypertension, and/or hemodilution administered therapeutically for symptomatic vasospasm (38% of the placebo-treated group vs. 25% of the nicardipine-treated group, p < 0.001). The incidence of symptomatic vasospasm during the treatment period was higher in the placebo-treated group (46%) than in the nicardipine-treated group (32%) (p < 0.001). Despite the reduction in symptomatic vasospasm in the nicardipine-treated group, overall outcome at 3 months was similar between the two groups. Fifty-five percent of nicardipine-treated patients were rated as having a good recovery according to the Glasgow Outcome Scale at follow-up review and 17% were dead, compared to 56% and 18%, respectively, in the placebo-treated group (not statistically significant). These data suggest that high-dose intravenous nicardipine treatment is associated with a reduced incidence of symptomatic vasospasm in patients with recent aneurysmal SAH, but not with an improvement in overall outcome at 3 months when compared to standard management in North America. It is postulated that, while nicardipine prevents vasospasm, hypertensive/hypervolemic therapy may be effective in reversing ischemic deficits from vasospasm once they occur.

Symptomatic vasospasm and outcomes following aneurysmal subarachnoid hemorrhage: a comparison between surgical repair and endovascular coil occlusion

2003 ◽  
Vol 98 (2) ◽  
pp. 319-325 ◽  
Author(s):  
Alejandro A. Rabinstein ◽  
Mark A. Pichelmann ◽  
Jonathan A. Friedman ◽  
David G. Piepgras ◽  
Douglas A. Nichols ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Acute Hydrocephalus ◽  
Treatment Groups ◽  
Symptomatic Vasospasm ◽  
Coil Occlusion ◽  
Clip Application ◽  
Fine Print

Object. The authors studied patients with aneurysmal subarachnoid hemorrhage (SAH) to determine whether the incidence of symptomatic vasospasm or overall clinical outcomes differed between patients treated with craniotomy and clip application and those treated by endovascular coil occlusion. Methods. The authors reviewed 415 consecutive patients with aneurysmal SAH who had been treated with either craniotomy and clip application or endovascular coil occlusion at a single institution between 1990 and 2000. Three hundred thirty-nine patients underwent surgical clip application procedures, whereas 76 patients underwent endovascular coil occlusion. Symptomatic vasospasm occurred in 39% of patients treated with clip application, 30% of patients treated with endovascular coil occlusion, and 37% of patients overall. Compared with patients treated with clip application, patients treated with endovascular coil occlusion were more likely to suffer acute hydrocephalus (50 compared with 34%, p = 0.008) and were more likely to harbor aneurysms in the posterior circulation (53 compared with 20%, p < 0.001). Logistic regression models controlling for patient age, admission World Federation of Neurosurgical Societies (WFNS) grade, acute hydrocephalus, aneurysm location, and day of treatment revealed that, among patients with an admission WFNS grade of I to III, endovascular coil occlusion carried a lower risk of symptomatic vasospasm (odds ratio [OR] 0.34, 95% confidence interval [CI] 0.14—0.8) and death or permanent neurological deficit due to vasospasm (OR 0.28, 95% CI 0.08–1) compared with craniotomy and clip application. Similar models revealed no difference in the likelihood of a Glasgow Outcome Scale score of 3 or less at the longest follow-up review (median 6 months) between treatment groups (OR 0.58, 95% CI 0.28–1.21). Conclusions. Patients with better clinical grades (WFNS Grades I–III) at hospital admission were less likely to suffer symptomatic vasospasm when treated by endovascular coil occlusion, compared with craniotomy and clip application. Nevertheless, there was no significant difference in overall outcome at the longest follow-up examination between the two treatment groups.

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (6) ◽  
pp. 1222-1226 ◽  
Author(s):  
Matthew J. McGirt ◽  
John C. Mavropoulos ◽  
Laura Y. McGirt ◽  
Michael J. Alexander ◽  
Allan H. Friedman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Leukocyte Count ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Increased Risk ◽  
Grade 3 ◽  
Fine Print

Object. The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm. Methods. A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 ± 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5–15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02–1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01–0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04–0.45). A serum leukocyte count greater than 15 × 109/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74–6.38). Conclusions. During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 × 109/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

Magnesium sulfate therapy after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 96 (3) ◽  
pp. 510-514 ◽  
Author(s):  
Richard S. Veyna ◽  
Donald Seyfried ◽  
Don G. Burke ◽  
Chris Zimmerman ◽  
Mark Mlynarek ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Magnesium Sulfate ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
High Dose ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Male Patients ◽  
The Mean ◽  
Fine Print

Object. Vasospasm remains a significant source of neurological morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH), despite advances in current medical, surgical, and endovascular therapies. Magnesium sulfate therapy has been demonstrated to be both safe and effective in preventing neurological complications in obstetrical patients with eclampsia. Evidence obtained using experimental models of brain injury, cerebral ischemia, and SAH indicate that Mg may also have a role as a neuroprotective agent. The authors hypothesize that MgSO4 therapy is safe, feasible, and has a beneficial effect on vasospasm and, ultimately, on neurological outcome following aneurysmal SAH. Methods. A prospective randomized single-blind clinical trial of high-dose MgSO4 therapy following aneurysmal SAH (Hunt and Hess Grades II–IV) was performed in 40 patients, who were enrolled within 72 hours following SAH and given intravenous MgSO4 or control solution for 10 days. Serum Mg++ levels were maintained in the 4 to 5.5 mg/dl range throughout the treatment period. Clinical management principles were the same between groups (including early use of surgery or endovascular treatment, followed by aggressive vasospasm prophylaxis and treatment). Daily transcranial Doppler (TCD) ultrasonographic recordings were obtained, and clinical outcomes were measured using the Glasgow Outcome Scale (GOS). The patients' GOS scores and the TCD recordings were analyzed using the independent t-test. Forty patients were enrolled in the study: 20 (15 female and five male patients) received treatment and 20 (11 female and nine male patients) comprised a control group. The mean ages of the patients in these groups were 46 and 51, respectively, and the mean clinical Hunt and Hess grades were 2.6 ± 0.68 in the MgSO4 treatment group and 2.3 ± 0.73 in the control group (mean ± standard deviation [SD], p = 0.87). Fisher grades were similar in both groups. Mean middle cerebral artery velocities were 93 ± 27 cm/second in MgSO4-treated patients and 102 ± 34 cm/second in the control group (mean ± SD, p = 0.41). Symptomatic vasospasm, confirmed by angiography, occurred in six of 20 patients receiving MgSO4 and in five of 16 patients receiving placebo. Mean GOS scores were 3.8 ± 1.6 and 3.6 ± 1.5 (mean ± SD, p = 0.74) in the treatment and control groups, respectively. Significant adverse effects from treatment with MgSO4 did not occur. Conclusions. Administration of high-dose MgSO4 following aneurysmal SAH is safe, and steady Mg++ levels in the range of 4 to 5.5 mg/dl are easily maintained. This treatment does not interfere with neurological assessment, administration of anesthesia during surgery, or other aspects of clinical care. We observed a trend in which a higher percentage of patients obtained GOS scores of 4 or 5 in the group treated with MgSO4, but the trend did not reach a statistically significant level. A larger study is needed to evaluate this trend further.

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