scholarly journals Management of cerebral vasospasm in subarachnoid hemorrhage

2019 ◽  
pp. S58-S66
Author(s):  
Dewi Prahaztuti ◽  
Hanik Badriyah Hidayati ◽  
Achmad Firdaus Sani
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Adhesion Molecule ◽  
Neurological Deficit ◽  
Medical Management ◽  
Treatment Modalities ◽  
Intercellular Adhesion Molecule ◽  
Delayed Ischemic Neurological Deficit

Subarachnoid hemorrhage (SAH) has been shown to result in cerebral vasospasm at day 4 to day 14, which is the main cause of mortality and morbidity after SAH. Outcome after SAH depends on many factors, including the severity of the event, medical management, and prevention of several serious complications. The principal goal in management of vasospasm after SAH is to prevent delayed ischemic neurological deficit (DIND) by decreasing intracranial pressure (ICP), optimizing cerebral oxygen demand rate and improving cerebral blood flow (CBF). Therapeutic management has been applied to prevent or treat vasospasm, including hemodynamic therapy, and endovascular therapy. Endovascular therapies, including mechanical angioplasty and chemical angioplasty with administration of intra-arterial (IA) vasodilator, have been widely used and given a good outcome. The purpose of this article is to describe the management of vasospasm including medical management and endovascular treatment. This review will describe the treatment modalities and management strategies to treat vasospasm.Abbreviations: SAH – subarachnoid hemorrhage; aSAH – aneurysmal subarachnoid hemorrhage; TCD – transcranial Doppler; ROS – reactive oxygen species; ICAM – intercellular adhesion molecule; VCAM – vascular cell adhesion molecule; IL – interleukin; CTA – computed tomography angiography; MRA – magnetic resonance angiography; CBF – cerebral blood flow; DIND – delayed ischemic neurological deficit; RCT - randomized controlled trialsCitation: Prahaztuti D, Hidayati HB, Sani AF. Management of cerebral vasospasm in subarachnoid hemorrhage. Anaesth Pain & Intensive Care 2018;22(3 Suppl 1):S58-S66.Received: 19 Oct 2018 Reviewed: 4, 11 Nov 2018 Accepted: 12 Nov 2018

Intra-Aortic Balloon Counterpulsation Augments Cerebral Blood Flow in a Canine Model of Subarachnoid Hemorrhage-Induced Cerebral Vasospasm

Neurosurgery ◽  
1995 ◽  
Vol 36 (4) ◽  
pp. 879-886 ◽  
Author(s):  
Eric S. Nussbaum ◽  
Roberto C. Heros ◽  
Eric E. Solien ◽  
Michael T. Madison ◽  
Leslie A. Sebring ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Canine Model ◽  
Intra Aortic Balloon Counterpulsation ◽  
Balloon Counterpulsation

scholarly journals Concentrations of estradiol, progesterone and testosterone in sefrum and cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage correlate weakly with transcranial Doppler flow velocities

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jan Martin ◽  
Eva Plank ◽  
Bernhard Ulm ◽  
Jens Gempt ◽  
Maria Wostrack ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Blood Flow Velocities ◽  
Flow Velocities

Abstract Background The implication of the steroids estradiol, progesterone and testosterone in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) has not been comprehensively assessed. In rodents, studies suggested beneficial effects of steroids on cerebral vasospasm after experimental SAH. Studies in humans are warranted, however, a general dilemma of human studies on neuroactive substances is that the brain is not directly accessible and that concentrations in the periphery may not adequately parallel concentrations in the central compartments. In the present study, concentrations of estradiol, progesterone and testosterone in serum and cerebrospinal fluid (CSF) of patients with aSAH were determined. Blood flow velocities in cerebral arteries were measured by transcranial Doppler sonography (TCD). The aim of this study was to evaluate the correlations between the cerebral blood flow velocities and levels of estradiol, progesterone and testosterone in CSF and serum. Results Samples of serum and CSF of 42 patients with aSAH were collected concomitantly daily or every other day via the arterial line and the external ventricular drainage for two weeks after the hemorrhage. Blood flow velocities in the cerebral arteries were determined by TCD. Total estradiol, progesterone and testosterone concentrations were measured by electro-chemiluminescence immunoassay. The strength of correlation was assessed by Spearman’s rank correlation coefficient. The correlation analysis revealed very weak correlations between cerebral blood flow velocities and concentrations of estradiol, progesterone and testosterone levels in both compartments with correlation coefficients below 0.2. Conclusions In humans with aSAH, merely very weak correlations between flow velocities in cerebral arteries and concentrations of estradiol, progesterone and testosterone in serum and CSF were demonstrated. These results suggest a limited influence of the respective steroids on cerebral vascular tone although vasodilatory effects were described in rodent studies. Thus, the implication of steroids in processes of neurological deterioration warrants further clarification.

scholarly journals Update on endovascular therapies for cerebral vasospasm induced by aneurysmal subarachnoid hemorrhage

2006 ◽  
Vol 21 (3) ◽  
pp. 1-11 ◽  
Author(s):  
Christina M. Sayama ◽  
James K. Liu ◽  
William T. Couldwell
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Infarction ◽  
Cerebral Vasospasm ◽  
Mechanism Of Action ◽  
Clinical Effect ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Calcium Channel Antagonists ◽  
Induced Hypertension

✓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.

Rise in serum soluble intercellular adhesion molecule—1 levels with vasospasm following aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (3) ◽  
pp. 537-541 ◽  
Author(s):  
J Mocco ◽  
William J. Mack ◽  
Grace H. Kim ◽  
Alan P. Lozier ◽  
Ilya Laufer ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Adhesion Molecule ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Intercellular Adhesion Molecule ◽  
Adhesion Molecule Expression ◽  
Intercellular Adhesion Molecule 1 ◽  
Content Type ◽  
Soluble Intercellular Adhesion Molecule ◽  
Fine Print

Object. Proinflammatory adhesion molecule expression has been demonstrated to be elevated in patients with aneurysmal subarachnoid hemorrhage (SAH). Recent studies have shown that elevations in soluble intercellular adhesion molecule—1 (ICAM-1) may be predictive of poor outcome in patients with good grade (Hunt and Hess Grades 1–2) aneurysmal SAH at delayed time points that correspond with the risk period for cerebral vasospasm. In addition, ICAM-1 is upregulated in experimental models of vasospasm. Unfortunately, the relationship of adhesion molecule expression to human vasospasm remains unclear. The authors hypothesized that the delayed elevation of soluble ICAM-1 in patients with aneurysmal SAH is associated with the development of cerebral vasospasm. Methods. Eighty-nine patients with aneurysmal SAH were prospectively enrolled in a study and stratified according to the presence or absence of vasospasm, as evidenced by daily monitoring of transcranial Doppler (TCD) velocities (presence, > 200 cm/second; absence, ≤ 120 cm/second). Levels of soluble ICAM-1 were determined using enzyme-linked immunosorbent assay every other day for 12 days post-SAH. An analysis of covariance model was used to evaluate trends in soluble ICAM-1 levels from 2 days prior to 6 days after the occurrence of documented vasospasm. Two groups of patients, matched for admission admission Hunt and Hess grade, were compared: nine patients with TCD velocities greater than 200 cm/second and nine patients with TCD velocities less than 120 cm/second. From among the patients with TCD velocities greater than 200 cm/second six patients with angiographically documented vasospasm were selected. Patients with TCD velocities less than 120 cm/second and matched admission Hunt and Hess grades but without angiographically documented vasospasm were selected. Patients with TCD-demonstrated vasospasm showed a significant mean rate of rise (p < 0.01) in soluble ICAM-1 levels during the perivasospasm period, but admission Hunt and Hess grade—matched control patients did not (p = not significant [NS]). There was a significant difference between these groups' rates of soluble ICAM increase (p < 0.01). Patients with both TCD- and angiographically demonstrated vasospasm likewise showed a highly significant mean rate of increase in soluble ICAM-1 levels during the perivasospasm period (p < 0.01), whereas admission Hunt and Hess grade—matched controls did not (p = NS). The difference beween these groups' rates of increase was highly significant (p < 0.001). Conclusions. These data suggest a role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae. As this relationship is further elucidated, adhesion molecules such as ICAM-1 may provide novel therapeutic targets in the prevention of vasospasm or its ischemic consequences.

Vasospasm and Regional Cerebral Blood Flow (rCBF) in Patients with Ruptured Intracranial Aneurysm: Serial rCBF Studies with the Xenon-133 Inhalation Method

Neurosurgery ◽  
1983 ◽  
Vol 13 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Iwao Yamakami ◽  
Katsumi Isobe ◽  
Akira Yamaura ◽  
Takao Nakamura ◽  
Hiroyasu Makino
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurological Deficit ◽  
Mean Value ◽  
Initial Slope ◽  
Delayed Ischemic Neurological Deficit ◽  
Ruptured Intracranial Aneurysm ◽  
The Mean ◽  
Xenon 133 ◽  
Head Probe

Abstract To clarify the relationship of vasospasm to the reduction of cerebral blood flow (CBF) and the delayed ischemic neurological deficit, serial rCBF studies with the use of the xenon-133 inhalation method were conducted in 35 postoperative patients with ruptured intracranial aneurysms. The CBF was calculated as an initial slope index (ISI) derived from the desaturation curve of each head probe, and the hemispheric mean value of the ISI (mean ISI) was calculated in both hemispheres. The mean ISI in the hemisphere ipsilateral to the operation was low compared to that of the contralateral hemisphere. In relation to the presence of vasospasm, angiographic findings were classified into the following five types: diffuse, peripheral, proximal-severe, proximal-mild, and no spasm. Patients with vasospasm of the diffuse, peripheral, and proximal-severe types showed a markedly decreased mean ISI, and vasospasm of the diffuse type caused the greatest degree of reduction. The mean ISI of the patients who developed delayed ischemic neurological deficit (DIND) due to vasospasm was significantly decreased (37.4± 4.6) compared to that of the patients who did not develop DIND (52.2± 5.6). None of 3 cases of no spasm and only 1 of 14 cases of proximal-mild spasm developed DIND. On the other hand, all of 4 cases of diffuse, 2 of 3 cases of peripheral, and 2 of 6 cases of proximal-severe spasm developed DIND. Thus, if these three types of vasospasm are joined together as severe vasospasm, 8 of 13 cases with severe vasospasm developed DIND. These results suggest that severe vasospasm causes a reduction of CBF and that the reduced CBF brings about DIND.

Experimental cerebral vasospasm

1974 ◽  
Vol 41 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Hajime Nagai ◽  
Yoshiaki Suzuki ◽  
Mitsuo Sugiura ◽  
Satoshi Noda ◽  
Hideo Mabe
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Posterior Communicating Artery ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Experimental Subarachnoid Hemorrhage ◽  
Fine Print

✓The authors describe a model for making an experimental subarachnoid hemorrhage that closely simulates human aneurysmal rupture. A needle previously inserted into the posterior communicating artery is subsequently withdrawn by traction on a thread. Using this model they demonstrate biphasic spasm by measurement of cerebral blood flow and angiography after rupture of the artery; the early spasm lasted 60 minutes and the late spasm began 3 or 4 hours after subarachnoid hemorrhage and continued for several days. The authors discuss the pathogenesis of early and late spasm.

Sign in / Sign up

Export Citation Format

Share Document