Relationship Between Angiographic Vasospasm, Cerebral Blood Flow, and Cerebral Infarction After Subarachnoid Hemorrhage

Author(s):  
Rajat Dhar ◽  
Michael N. Diringer
2006 ◽  
Vol 21 (3) ◽  
pp. 1-11 ◽  
Author(s):  
Christina M. Sayama ◽  
James K. Liu ◽  
William T. Couldwell

✓Cerebral vasospasm remains a major source of morbidity and death in patients with aneurysmal subarachnoid hemorrhage (SAH). When vasospasm becomes refractory to maximal medical management consisting of induced hypertension and hypervolemia and administration of calcium channel antagonists, endovascular therapies should be considered. The primary goal of endovascular treatment is to increase cerebral blood flow to prevent cerebral infarction. Two of the more frequently studied endovascular treatments are transluminal balloon angioplasty and intraarterial papaverine infusion. These two have been used either alone or in combination for the treatment of vasospasm. Other pharmacological vasodilating agents currently being investigated are intraarterial nimodipine, nicardipine, verapamil, and milrinone. Newer intraarterial agents, such as fasudil and colforsin daropate, have also been investigated. In this article the authors review the current options in terms of endovascular therapies for treatment of cerebral vasospasm. The mechanism of action, technique of administration, clinical effect and outcomes, and complications of each modality are discussed.


2007 ◽  
Vol 107 (6) ◽  
pp. 1101-1112 ◽  
Author(s):  
Nestor R. Gonzalez ◽  
W. John Boscardin ◽  
Thomas Glenn ◽  
Fernando Vinuela ◽  
Neil A. Martin

Object The goal in this study was to create an index (vasospasm probability index [VPI]) to improve diagnostic accuracy for vasospasm after subarachnoid hemorrhage (SAH). Methods Seven hundred ninety-five patients in whom aneurysmal SAH was demonstrated by computed tomography, and in whom one or more intracranial aneurysms had been diagnosed, underwent transcranial Doppler (TCD) studies between April 1998 and January 2000. In 154 patients angiography was performed within 24 hours of the TCD examination, and in 75 133Xe cerebral blood flow (CBF) studies were obtained the same day. Seven cases were excluded because of a limited sonographic window. Forty-one women (60.3%) and 27 men (39.7%) between the ages of 35 and 84 years (58.0 ± 13.2 years [mean ± standard deviation]) were included. Clinical characteristics analyzed included age, sex, Hunt and Hess grade, Fisher grade, days after SAH, day of treatment, type of treatment (coil embolization, surgical clip occlusion, or conservative treatment), smoking history, and hypertension history. Lindegaard ratios and spasm indexes (TCD velocities/hemispheric CBF) were calculated bilaterally. Digital subtraction angiography images were measured at specific points of interest. Sensitivity, specificity, predictive values, and global accuracy of the different tests were calculated. Logistic regression was used to evaluate the possible predictive factors, and the coefficients of the logistic regression were integrated to create the VPI. Results In 18 patients (26.5%) symptomatic vasospasm was diagnosed, and 33 (48.5%) had angiographic evidence of vasospasm. For TCD velocities above 120 cm/second at the middle cerebral artery, the global accuracy was 81.1% for the diagnosis of clinical vasospasm and 77.2% for angiographic vasospasm. For a Lindegaard ratio higher than 3.0, the accuracy was 85% for clinical vasospasm and 83.2% for angiographic vasospasm. A spasm index higher than 3.5 had an accuracy of 82.0% for the diagnosis of clinical vasospasm and 81.6% for angiographic vasospasm. The selected model for estimation of clinical vasospasm included Fisher grade, Hunt and Hess grade, and spasm index. The VPI had a global accuracy of 92.9% for clinical vasospasm detection. For diagnosis of angiographic vasospasm, the model included Fisher grade, Hunt and Hess grade, and Lindegaard ratio. The VPI achieved a global accuracy of 89.9% for angiographic vasospasm detection. Conclusions The use of TCD velocities, Lindegaard ratio, and spasm index independently is of limited value for the diagnosis of clinical and angiographic vasospasm. The combination of predictive factors associated with the development of vasospasm in the new index reported here has a significantly superior accuracy compared with the independent tests and may become a valuable tool for the clinician to evaluate the individual probability of cerebral vasospasm after aneurysmal SAH.


2008 ◽  
Vol 109 (6) ◽  
pp. 1155-1164 ◽  
Author(s):  
Amanda M. Murphy ◽  
Anargyros Xenocostas ◽  
Pria Pakkiri ◽  
Ting-Yim Lee

Object The authors investigated the hemodynamic effects of recombinant human erythropoietin (rhEPO) after subarachnoid hemorrhage (SAH) in rabbits. Methods The authors used male New Zealand White rabbits in this study divided into the following groups: SAH plus saline (16 rabbits), SAH plus low-dose rhEPO (16 rabbits; 1500 IU/kg on Day 0 and 500 IU/kg on Days 2 and 4), SAH plus high-dose rhEPO (10 rabbits; 1500 IU/kg on Days 0, 2, 4, and 6), and sham (6 rabbits). Computed tomography perfusion studies and CT angiography were performed for 1 hour after SAH on Day 0, and once each on Days 2, 4, 7, 9, and 16 after SAH. Assessments of neurological function and tissue histology were also performed. Results The mortality rate was significantly lower after rhEPO treatment (12%) than after saline treatment (44%) (p < 0.05). Neurological outcomes in the low-dose and high-dose rhEPO groups were better than in the saline group after SAH (p < 0.05), and the cerebral blood flow in the high-dose rhEPO group was greater than that in the saline group (p < 0.05). The mean transit time was significantly lower on Days 2 and 4 in the low-dose and high-dose rhEPO groups than in the saline group, but increased significantly on Day 7 in both groups (p < 0.05). The hematocrit increased significantly from baseline values in the high-dose and low-dose rhEPO groups on Days 4 and 7, respectively (p < 0.05). Conclusions Treatment with rhEPO after experimental SAH is associated with improved cerebral blood flow and microcirculatory flow as reflected by lower mean transit times. Improved tissue perfusion correlated with reduced mortality and improved neurological outcomes. Further investigation of the impact of increasing hematocrit on hemodynamic changes is needed.


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