Clot volume and clearance rate as independent predictors of vasospasm after aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 101 (2) ◽  
pp. 255-261 ◽  
Author(s):  
Christopher Reilly ◽  
Chris Amidei ◽  
Jocelyn Tolentino ◽  
Babak S. Jahromi ◽  
R. Loch Macdonald
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clearance Rate ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Quantitative Imaging ◽  
Univariate Analysis ◽  
Ct Scans ◽  
Focal Neurological Deficit ◽  
Content Type ◽  
Fisher Grade ◽  
Fine Print

Object. This study was conducted for two purposes. The first was to determine whether a combination of measurements of subarachnoid clot volume, clearance rate, and density could improve prediction of which patients experience vasospasm. The second was to determine if each of these three measures could be used independently to predict vasospasm. Methods. Digital files of the cranial computerized tomography (CT) scans obtained in 75 consecutive patients admitted within 24 hours of subarachnoid hemorrhage (SAH) were analyzed in a blinded fashion by an observer who used quantitative imaging software to measure the volume of SAH and its density. Clot clearance rates were measured by quantifying SAH volume on subsequent CT scans. Vasospasm was defined as new onset of a focal neurological deficit or altered consciousness 5 to 12 days after SAH in the absence of other causes of deterioration, diagnosed with the aid of or exclusively by confirmatory transcranial Doppler ultrasonography and/or cerebral angiography. Univariate analysis showed that vasospasm was significantly associated with the SAH grade as classified on the Fisher scale, the initial clot volume, initial clot density, and percentage of clot cleared per day (p < 0.05). In multivariate analysis, initial clot volume and percentage of clot cleared per day were significant predictors of vasospasm (p < 0.05), whereas Fisher grade and initial clot density were not. Conclusions. Quantitative analysis of subarachnoid clot shows that vasospasm is best predicted by initial subarachnoid clot volume and the percentage of clot cleared per day.

Risk factors for ischemic lesions following aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 102 (2) ◽  
pp. 194-201 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Joona Varis ◽  
Kristiina Poussa ◽  
Matti Porras
Keyword(s):  
Risk Factors ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Univariate Analysis ◽  
Delayed Cerebral Ischemia ◽  
Artery Occlusion ◽  
Ct Scans ◽  
Content Type ◽  
Fine Print

Object. The aim of this study was to test whether enoxaparin treatment (40 mg subcutaneously once daily) reduces the risk of cerebral infarction after subarachnoid hemorrhage (SAH) and to investigate predictive risk factors for permanent ischemic lesions visible on follow-up computerized tomography (CT) scans obtained 3 months after SAH. Methods. After undergoing surgery for a ruptured aneurysm, 170 patients were randomized in a prospective, double-blind, placebo-controlled trial to test the effect of enoxaparin on the occurrence of ischemic lesions, which were demonstrated on follow-up CT scans available for 156 patients. The presence of lesions correlated highly with an impaired outcome, as assessed using both the Glasgow Outcome and modified Rankin Scales (p < 0.01). Lesions occurred in 101 (65%) of the 156 patients. In half of the patients (51 patients) no lesion was visible on the CT scan obtained on the 1st postoperative day in 51 patients. On univariate analysis, the presence of lesions at 3 months post-SAH was not associated with enoxaparin treatment but did correlate with several clinical, radiological, and prehemorrhage variables. Significant independent risk factors for lesions consisted of an impaired initial clinical condition (odds ratio [OR] 2.63, 95% confidence interval [CI] 1.03–6.73), amount of subarachnoid blood (OR 6.51, 95% CI 2.27–18.65), nocturnal occurrence of SAH (that is, between 12:01 a.m. and 8:00 a.m.; OR 4.32, 95% CI 1.28–14.52), fixed symptoms of delayed ischemia (OR 5.21, 95% CI 1.02–26.49), duration of temporary artery occlusion during surgery (OR 1.66 per minute, 95% CI 1.20–2.31), and body mass index (OR 1.13/kg/m2, 95% CI 1.01–1.28). Conclusions The presence of ischemic lesions can be predicted by the severity of bleeding, delayed cerebral ischemia, excess weight, duration of temporary artery occlusion, and occurrence of nocturnal aneurysm rupture.

Characterization of perioperative seizures and epilepsy following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 99 (6) ◽  
pp. 978-985 ◽  
Author(s):  
Chih-Lung Lin ◽  
Aaron S. Dumont ◽  
Ann-Shung Lieu ◽  
Chen-Po Yen ◽  
Shiuh-Lin Hwang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Predictive Factors ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Loss Of Consciousness ◽  
Content Type ◽  
Fisher Grade ◽  
The Mean ◽  
Fine Print

Object. The reported incidence, timing, and predictive factors of perioperative seizures and epilepsy after subarachnoid hemorrhage (SAH) have differed considerably because of a lack of uniform definitions and variable follow-up periods. In this study the authors evaluate the incidence, temporal course, and predictive factors of perioperative seizures and epilepsy during long-term follow up of patients with SAH who underwent surgical treatment. Methods. Two hundred seventeen patients who survived more than 2 years after surgery for ruptured intracranial aneurysms were enrolled and retrospectively studied. Episodes were categorized into onset seizures (≤ 12 hours of initial hemorrhage), preoperative seizures, postoperative seizures, and late epilepsy, according to their timing. The mean follow-up time was 78.7 months (range 24–157 months). Forty-six patients (21.2%) had at least one seizure post-SAH. Seventeen patients (7.8%) had onset seizures, five (2.3%) had preoperative seizures, four (1.8%) had postoperative seizures, 21 (9.7%) had at least one seizure episode after the 1st week postoperatively, and late epilepsy developed in 15 (6.9%). One (3.8%) of 26 patients with perioperative seizures (onset, preoperative, or postoperative seizure) had late epilepsy at follow up. The mean latency between the operation and the onset of late epilepsy was 8.3 months (range 0.3–19 months). Younger age (< 40 years old), loss of consciousness of more than 1 hour at ictus, and Fisher Grade 3 or greater on computerized tomography scans proved to be significantly related to onset seizures. Onset seizure was also a significant predictor of persistent neurological deficits (Glasgow Outcome Scale Scores 2–4) at follow up. Factors associated with the development of late epilepsy were loss of consciousness of more than 1 hour at ictus and persistent postoperative neurological deficit. Conclusions. Although up to one fifth of patients experienced seizure(s) after SAH, more than half had seizure(s) during the perioperative period. The frequency of late epilepsy in patients with perioperative seizures (7.8%) was not significantly higher than those without such seizures (6.8%). Perioperative seizures did not recur frequently and were not a significant predictor for late epilepsy.

Poor-grade aneurysmal subarachnoid hemorrhage: relationship of cerebral metabolism to outcome

2004 ◽  
Vol 100 (3) ◽  
pp. 400-406 ◽  
Author(s):  
Asita Sarrafzadeh ◽  
Daniel Haux ◽  
Ingeborg Küchler ◽  
Wolfgang R. Lanksch ◽  
Andreas W. Unterberg
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Metabolism ◽  
Univariate Analysis ◽  
High Morbidity ◽  
Low Grade ◽  
High Grade ◽  
Content Type ◽  
Poor Grade ◽  
Fisher Grade ◽  
Fine Print

Object. The majority of patients with poor-grade subarachnoid hemorrhage (SAH), that is, World Federation of Neurosurgical Societies (WFNS) Grades IV and V, have high morbidity and mortality rates. The objective of this study was to investigate cerebral metabolism in patients with low-compared with high-grade SAH by using bedside microdialysis and to evaluate whether microdialysis parameters are of prognostic value for outcome in SAH. Methods. A prospective investigation was conducted in 149 patients with SAH (mean age 50.9 ± 12.9 years); these patients were studied for 162 ± 84 hours (mean ± standard deviation). Lesions were classified as low-grade SAH (WFNS Grades I–III, 89 patients) and high-grade SAH (WFNS Grade IV or V, 60 patients). After approval by the local ethics committee and consent from the patient or next of kin, a microdialysis catheter was inserted into the vascular territory of the aneurysm after clip placement. The microdialysates were analyzed hourly for extracellular glucose, lactate, lactate/pyruvate (L/P) ratio, glutamate, and glycerol. The 6- and 12-month outcomes according to the Glasgow Outcome Scale and functional disability according to the modified Rankin Scale were assessed. In patients with high-grade SAH, cerebral metabolism was severely deranged compared with those who suffered low-grade SAH, with high levels (p < 0.05) of lactate, a high L/P ratio, high levels of glycerol, and, although not significant, of glutamate. Univariate analysis revealed a relationship among hyperglycemia on admission, Fisher grade, and 12-month outcome (p < 0.005). In a multivariate regression analysis performed in 131 patients, the authors identified four independent predictors of poor outcome at 12 months, in the following order of significance: WFNS grade, patient age, L/P ratio, and glutamate (p < 0.03). Conclusions. Microdialysis parameters reflected the severity of SAH. The L/P ratio was the best metabolic independent prognostic marker of 12-month outcome. A better understanding of the causes of deranged cerebral metabolism may allow the discovery of therapeutic options to improve the prognosis, especially in patients with high-grade SAH, in the future.

Volumetric quantification of Fisher Grade 3 aneurysmal subarachnoid hemorrhage: a novel approach to predict symptomatic vasospasm on admission computerized tomography scans

2002 ◽  
Vol 97 (2) ◽  
pp. 401-407 ◽  
Author(s):  
Jonathan A. Friedman ◽  
Stephan J. Goerss ◽  
Fredric B. Meyer ◽  
David G. Piepgras ◽  
Mark A. Pichelmann ◽  
...  
Keyword(s):  
Ct Scan ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Ct Scans ◽  
Content Type ◽  
Fisher Grade ◽  
Volumetric Quantification ◽  
Hemorrhage Volume ◽  
Grade 3 ◽  
Fine Print ◽  
New Onset

Object. Predicting which patients with aneurysmal subarachnoid hemorrhage (SAH) will develop delayed ischemic neurological deficit (DIND) due to vasospasm remains subjective and unreliable. The authors analyzed the utility of a novel software-based technique to quantify hemorrhage volume in patients with Fisher Grade 3 aneurysmal SAH. Methods. Patients with aneurysmal SAH in whom a computerized tomography (CT) scan was performed within 72 hours of ictus and demonstrated Fisher Grade 3 SAH were analyzed. Severe DIND was defined as new onset complete focal deficit or coma. Moderate DIND was defined as new onset partial focal deficit or impaired consciousness without coma. Fifteen consecutive patients with severe DIND, 13 consecutive patients with moderate DIND, and 12 consecutive patients without DIND were analyzed. Software-based volumetric quantification was performed on digitized admission CT scans by a single examiner blinded to clinical information. There was no significant difference in age, sex, admission Hunt and Hess grade, or time to admission CT scan among the three groups (none, moderate, or severe DIND). Patients with severe DIND had a significantly higher cisternal volume of hemorrhage (median 30.5 cm3) than patients with moderate DIND (median 12.4 cm3) and patients without DIND (median 10.3 cm3; p < 0.001). Intraparenchymal hemorrhage and intraventricular hemorrhage were not associated with DIND. All 13 patients with cisternal volumes greater than 20 cm3 developed DIND, compared with 15 of 27 patients with volumes less than 20 cm3 (p = 0.004). Conclusions. The authors developed a simple and potentially widely applicable method to quantify SAH on CT scans. A greater volume of cisternal hemorrhage on an admission CT scan in patients with Fisher Grade 3 aneurysmal SAH is highly associated with DIND. A threshold of cisternal hemorrhage volume (> 20 cm3) may exist above which patients are very likely to develop DIND. Prospective application of software-based volumetric quantification of cisternal SAH may predict which patients will develop DIND.

Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study

2002 ◽  
Vol 97 (4) ◽  
pp. 771-778 ◽  
Author(s):  
Jan Hillman ◽  
Steen Fridriksson ◽  
Ola Nilsson ◽  
Zhengquan Yu ◽  
Hans Säveland ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Tranexamic Acid ◽  
Hospital Admission ◽  
Acid Treatment ◽  
Aneurysm Rupture ◽  
Clinical Findings ◽  
Ct Scans ◽  
Content Type ◽  
Fisher Grade ◽  
Fine Print

Object. By pursuing a policy of very early aneurysm treatment in neurosurgical centers, in-hospital rebleeds can be virtually eliminated. Nonetheless, as many as 15% of patients with aneurysm rupture suffer ultraearly rebleeding with high mortality rates, and these individuals are beyond the reach of even the most ambitious protocol for diagnosis and referral. Only drugs given immediately after the diagnosis of subarachnoid hemorrhage (SAH) has been established at the local hospital level can, in theory, contribute to the minimization of such ultraearly rebleeding. The object of this randomized, prospective, multicenter study was to assess the efficacy of short-term antifibrinolytic treatment with tranexamic acid in preventing rebleeding. Methods. Only patients suffering SAH verified on computerized tomography (CT) scans within 48 hours prior to the first hospital admission were included. A 1-g dose of tranexamic acid was given intravenously as soon as diagnosis of SAH had been verified in the local hospitals (before the patients were transported), followed by doses of 1 g every 6 hours until the aneurysm was occluded; this treatment did not exceed 72 hours. In this study, 254 patients received tranexamic acid and 251 patients were randomized as controls. Age, sex, Hunt and Hess and Fisher grade distributions, as well as aneurysm locations, were congruent between the groups. Outcome was assessed at 6 months post-SAH by using the Glasgow Outcome Scale (GOS). Vasospasm and delayed ischemic neurological deficits were classified according to clinical findings as well as by transcranial Doppler (TCD) studies. All events classified as rebleeding were verified on CT scans or during surgery. Conclusions. More than 90% of patients reached the neurosurgical center within 12 hours of their first hospital admission after SAH; 70% of all aneurysms were clipped or coils were inserted within 24 hours of the first hospital admission. Given the protocol, only one rebleed occurred later than 24 hours after the first hospital admission. Despite this strong emphasis on early intervention, however, a cluster of 27 very early rebleeds still occurred in the control group within hours of randomization into the study, and 13 of these patients died. In the tranexamic acid group, six patients rebled and two died. A reduction in the rebleeding rate from 10.8 to 2.4% and an 80% reduction in the mortality rate from early rebleeding with tranexamic acid treatment can therefore be inferred. Favorable outcome according to the GOS increased from 70.5 to 74.8%. According to TCD measurements and clinical findings, there were no indications of increased risk of either ischemic clinical manifestations or vasospasm that could be linked to tranexamic acid treatment. Neurosurgical guidelines for aneurysm rupture should extend also into the preneurosurgical phase to guarantee protection from ultraearly rebleeds. Currently available antifibrinolytic drugs can provide such protection, and at low cost. The number of potentially saved lives exceeds those lost to vasospasm.

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.

Serial changes of hemostasis in aneurysmal subarachnoid hemorrhage with special reference to delayed ischemic neurological deficits

1997 ◽  
Vol 86 (4) ◽  
pp. 594-602 ◽  
Author(s):  
Yukihiko Fujii ◽  
Shigekazu Takeuchi ◽  
Osamu Sasaki ◽  
Takashi Minakawa ◽  
Tetsuo Koike ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Multivariate Analyses ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Ct Scans ◽  
Blood Samples ◽  
Content Type ◽  
Significant Difference ◽  
D Dimer ◽  
Fine Print

✓ This study was undertaken to elucidate comprehensively the serial changes occurring in hemostatic systems after aneurysmal subarachnoid hemorrhage (SAH) and thereby to ascertain whether the examination of the integrity of these systems is helpful in predicting delayed ischemic neurological deficits (DINDs). The authors examined 117 patients admitted to the hospital within 24 hours after onset of SAH. Blood samples were collected from each patient on Days 0 (at admission), 3, 6, 14, and 30. A number of hemostatic parameters were examined in these samples, and the relationships between their changes and DINDs were assessed. Eighteen (15.4%) of the patients exhibited DINDs, and their frequency increased as the severity of subarachnoid clotting increased. Also, the frequency of DINDs was significantly higher in the patients with hydrocephalus on initial computerized tomography (CT) scans than in those without hydrocephalus. Regarding the hemostatic parameters at admission, there was no significant difference between the patients with and without DINDs. On Day 3, however, the fibrinogen and D-dimer levels were higher in the patients with than in those without DINDs. The fibrinogen and thrombin—antithrombin complex levels on Day 6 and the D-dimer level on Day 14 in the patients with DINDs were higher than the corresponding levels in those without DINDs. Multivariate analyses revealed that the following variables (in order of importance) were independent predictors of DINDs: the levels of D-dimer on Day 3, fibrinogen on Day 6, and the presence of hydrocephalus on admission. These data indicate that the levels of hemostatic parameters in concert with the CT findings may enable us to predict the appearance of DINDs.

The prophylactic use of transluminal balloon angioplasty in patients with Fisher Grade 3 subarachnoid hemorrhage: a pilot study

1999 ◽  
Vol 91 (1) ◽  
pp. 51-58 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Marike Zwienenberg ◽  
Nancy A. Rudisill ◽  
Stephen T. Hecht
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Pilot Study ◽  
Balloon Angioplasty ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Pilot Trial ◽  
Neurological Deficits ◽  
Content Type ◽  
Fisher Grade ◽  
Grade 3 ◽  
Fine Print

Object. Recent advances in neuroradiology have made it possible to dilate vasospastic human cerebral arteries after aneurysmal subarachnoid hemorrhage (SAH), but the time window is short and the success rate for reversal of delayed ischemic neurological deficits (DINDs) varies between 31% and 77%. In a dog model of vasospasm, transluminal balloon angioplasty (TBA) performed on Day 0 totally prevented the development of angiographically demonstrated narrowing on Day 7. Because the effect of preventive TBA in this animal model was better than any pharmacological treatment described previously for experimental vasospasm, the authors conducted a pilot trial in humans to assess the safety and efficacy of TBA performed within 3 days of SAH.Methods. The study group consisted of 13 patients with Fisher Grade 3 SAH who had a very high probability of developing vasospasm. In all patients, regardless of the site of the ruptured aneurysm, target vessels for prophylactic TBA were as follows: the internal carotid artery, A1 segment, M1 segment, and P1 segment bilaterally; the basilar artery; and one vertebral artery. Prophylactic TBA was considered satisfactory when it could be performed in at least two of the three parts of the intracranial circulation (right and/or left carotid system and/or vertebrobasilar system), and included the aneurysm-bearing part of the circulation. Of the 13 patients, none developed a DIND or more than mild vasospasm according to transcranial Doppler ultrasonography criteria. At 3 months posttreatment eight patients had made a good recovery, two were moderately disabled, and three had died; one patient died because of a vessel rupture during TBA and two elderly individuals died of medical complications associated with poor clinical condition on admission.Conclusions. Compared with large series of patients with aneurysmal SAH reported in the literature, the results of this pilot study indicate an extremely low incidence of vasospasm and DIND after treatment with prophylactic TBA. A larger randomized study is required to determine whether prophylactic TBA is efficacious enough to justify the risks, and which vessels need to be dilated prophylactically.

Cerebral hemodynamic impairment after aneurysmal subarachnoid hemorrhage as evaluated using transcranial Doppler ultrasonography: relationship to delayed cerebral ischemia and clinical outcome

2001 ◽  
Vol 95 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Tõnu Rätsep ◽  
Toomas Asser
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Outcome ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Content Type ◽  
Unfavorable Clinical Outcome ◽  
Hemodynamic Impairment ◽  
Fine Print

Object. In this study the authors evaluated the relative role of cerebral hemodynamic impairment (HDI) in the pathogenesis of delayed cerebral ischemia and poor clinical outcome after aneurysmal subarachnoid hemorrhage (SAH). Methods. Cerebral hemodynamics were assessed daily with transcranial Doppler (TCD) ultrasonography in 55 consecutive patients with verified SAH. Hemodynamic impairment was defined as blood flow velocity (BFV) values consistent with vasospasm in conjunction with impaired autoregulatory vasodilation as evaluated using the transient hyperemic response tests in the middle cerebral arteries. A total of 1344 TCD examinations were performed, in which the evaluation of HDI was feasible during 80.9% and HDI was registered during 12% of the examinations. It was found that HDI occurred in 60% of patients and was frequently recorded in conjunction with severe vasospasm (p < 0.05) and a rapid increase of BFV values (p < 0.05). Detection of HDI was closely associated with the development of delayed ischemic brain damage after SAH (p < 0.05). Furthermore, because delayed ischemia was never observed in cases in which vasospasm had not led to the development of HDI, its occurrence increased significantly the likelihood of subsequent cerebral ischemia among the patients with vasospasm (p < 0.05). Detection of HDI was independently related to unfavorable clinical outcome according to Glasgow Outcome Scale at 6 months after SAH (p < 0.05). Conclusions. The results showed that HDI is common after SAH and can be evaluated with TCD ultrasonography in routine clinical practice. Detection of HDI could be useful for identifying patients at high or low risk for delayed ischemic complications and unfavorable clinical outcome after SAH.

No effect of enoxaparin on outcome of aneurysmal subarachnoid hemorrhage: a randomized, double-blind, placebo-controlled clinical trial

2003 ◽  
Vol 99 (6) ◽  
pp. 953-959 ◽  
Author(s):  
Jari Siironen ◽  
Seppo Juvela ◽  
Joona Varis ◽  
Matti Porras ◽  
Kristiina Poussa ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Molecular Weight ◽  
Subarachnoid Hemorrhage ◽  
Low Molecular Weight Heparin ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Intracranial Bleeding ◽  
Low Molecular Weight ◽  
Double Blind ◽  
Content Type ◽  
Fine Print

Object. From the moment an intracranial aneurysm ruptures, cerebral blood flow is impaired, and this impairment mainly determines the outcome in patients who survive after the initial bleeding. The exact mechanism of impairment is unknown, but activation of coagulation and fibrinolysis correlate with clinical condition and outcome after aneurysmal subarachnoid hemorrhage (SAH). The purpose of this study was to determine whether enoxaparin, a low-molecular-weight heparin, which is a well-known anticoagulating agent, has any effect on the outcome of aneurysmal SAH postoperatively. Methods. In this randomized, double-blind, single-center clinical trial, 170 patients (85 per group) with aneurysmal SAH were randomly assigned to receive either enoxaparin (40 mg subcutaneously once daily) or a placebo, starting within 24 hours after occlusion of the aneurysm and continuing for 10 days. Analysis was done on an intention-to-treat basis. Outcome was assessed at 3 months on both the Glasgow Outcome and modified Rankin Scales. Patients were eligible for the study if surgery was performed within 48 hours post-SAH, and no intracerebral hemorrhage was larger than 20 mm in diameter on the first postoperative computerized tomography scan. At 3 months, there were no significant differences in outcome by treatment group. Of the 170 patients, 11 (6%) died, and only 95 (56%) had a good outcome. Principal causes of unfavorable outcome were poor initial condition, delayed cerebral ischemia, and surgical complications. There were four patients with additional intracranial bleeding in the group receiving enoxaparin. The bleeding was not necessarily associated with the treatment itself, nor did it require treatment, and there were no such patients in the placebo group. Conclusions. Enoxaparin seemed to have no effect on the outcome of aneurysmal SAH in patients who had already received routine nimodipine and who had received triple-H therapy when needed. Routine use of low-molecular-weight heparin should be avoided during the early postoperative period in patients with SAH, because this agent seems to increase intracranial bleeding complications slightly, with no beneficial effect on neurological outcome.

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