Thick Clot Research Articles

Predictors of Symptomatic Vasospasm After Subarachnoid Hemorrhage: A Single Center Study of 457 Consecutive Cases.

We set forth to identify predictors of symptomatic vasospasm in patients with subarachnoid hemorrhage (SAH). We used multivariate logistic regression analysis of the prospective, hospital based, single center register of the Department of Neurosurgery, University of Debrecen, Hungary. Evaluated patients' characteristics were: sex, age, Hunt-Hess grade on admission, location of aneurysm, thickness of blood clot on initial CT scan (Fisher grade), hypertension. Between 1987 and 2004, 567 SAH cases were registered, 457 were included in this study. Symptomatic vasospasm developed in 22.5% of the cases. In univariate analysis, Hunt-Hess grades 2 and 3 and female sex were predictive for symptomatic vasospasm. In multivariate analysis, female sex remained a significant predictor: OR: 1.8 (1.005-3.2). Women are at more danger of developing symptomatic vasospasm after subarachnoid hemorrhage.

Systematic review of clinical prediction tools and prognostic factors in aneurysmal subarachnoid hemorrhage.

Background:Clinical prediction tools assist in clinical outcome prediction. They quantify the relative contributions of certain variables and condense information that identifies important indicators or predictors to a targeted condition. This systematic review synthesizes and critically appraises the methodologic quality of studies that derive both clinical predictors and clinical predictor tools used to determine outcome prognosis in patients suffering from aneurysmal subarachnoid hemorrhage (SAH).Methods:This systematic review included prospective and retrospective cohort studies, and randomized controlled trials (RCTs) investigating prognostic factors and clinical prediction tools associated with determining the neurologic outcome in adult patients with aneurysmal SAH.Results:Twenty-two studies were included in this systemic review. Independent, confounding, and outcome variables were studied. Methodologic quality of individual studies was also analyzed. Included were 3 studies analyzing databases from RCTs, 8 prospective cohort studies, and 11 retrospective cohort studies. The most frequently retained significant clinical prognostic factors for long-term neurologic outcome prediction include age, neurological grade, blood clot thickness, and aneurysm size.Conclusions:Systematic reviews for clinical prognostic factors and clinical prediction tools in aneurysmal SAH face a number of methodological challenges. These include within and between study patient heterogeneity, regional variations in treatment protocols, patient referral biases, and differences in treatment, and prognosis viewpoints across different cultures.

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

Treatment of Acute Subdural Hematoma

Clinical presentation, neurologic condition, and imaging findings are the key components in establishing a treatment plan for acute SDH. Location and size of the SDH and presence of midline shift can rapidly be determined by computed tomography of the head. Immediate laboratory work up must include PT, PTT, INR, and platelet count. Presence of a coagulopathy or bleeding diathesis requires immediate reversal and treatment with the appropriate agent(s), in order to lessen the risk of hematoma expansion. Reversal protocols used are similar to those for intracerebral hemorrhage, with institutional variations. Immediate neurosurgical evaluation is sought in order to determine whether the SDH warrants surgical evacuation. Urgent or emergent surgical evacuation of a SDH is largely influenced by neurologic examination, imaging characteristics, and presence of mass effect or elevated intracranial pressure. Generally, evacuation of an acute SDH is recommended if the clot thickness exceeds 10mm or the midline shift is greater than 5mm, regardless of the neurologic condition. In patients with patients with an acute SDH with clot thickness <10mm and midline shift <5mm, specific considerations of neurologic findings and clinical circumstances will be of importance. In addition, consideration will be given as to whether an individual patient is likely to benefit from surgery. For an acute SDH, evacuation by craniotomy or craniectomy is preferred over burr holes based on available data. Postoperative care includes monitoring of resolution of pneumocephalus, mobilization and drain removal, and monitoring for signs of SDH reaccumulation. Medical considerations include seizure prophylaxis and management as well as management and resumption of antithrombotic and anticoagulant medication.

Predictors of rapid spontaneous resolution of acute subdural hematoma

ObjectiveAcute subdural hematoma (ASDH) usually requires emergency surgical decompression, but rare cases exhibit rapid spontaneous resolution. The aim of this retrospective study was to identify factors predictive of spontaneous ASDH resolution. MethodsA total of 366 consecutive patients with ASDH treated between January 2006 and September 2012 were identified in our hospital database. Patients with ASDH clot thickness >10mm in the frontoparietotemporal region and showing a midline shift >10mm on the initial computed tomography (CT) scan were divided into two groups according to subsequent spontaneous resolution. Univariate and multivariate logistic regression analyses were used to identify factors predictive of rapid spontaneous ASDH resolution. ResultsFifty-six ASDH patients met study criteria and 18 demonstrated rapid spontaneous resolution (32%). Majority of these patients were not operated because of poor prognosis/condition and in accordance to family wishes. Univariate analysis revealed significant differences in use of antiplatelet agents before head injury and in the incidence of a low-density band between the hematoma and inner wall of the skull bone on the initial CT. Use of antiplatelet agents before head injury (OR 19.6, 95% CI 1.5–260.1, p=0.02) and the low-density band on CT images (OR 40.3, 95% CI 3.1–520.2, p=0.005) were identified as independent predictive factors by multivariate analysis. ConclusionsOur analysis suggested that use of antiplatelet agents before head injury and a low-density band between the hematoma and inner skull bone on CT images (indicative of cerebrospinal fluid infusion into the subdural space) increase the probability of rapid spontaneous resolution.

The relationship between ruptured aneurysm location, subarachnoid hemorrhage clot thickness, and incidence of radiographic or symptomatic vasospasm in patients enrolled in a prospective randomized controlled trial

Cerebral vasospasm following subarachnoid hemorrhage (SAH) causes significant morbidity in a delayed fashion. The authors recently published a new scale that grades the maximum thickness of SAH on axial CT and is predictive of vasospasm incidence. In this study, the authors further investigate whether different aneurysm locations result in different SAH clot burdens and whether any concurrent differences in ruptured aneurysm location and maximum SAH clot burden affect vasospasm incidence. Two hundred fifty patients who were part of a prospective randomized controlled trial were reviewed. Most outcome and demographic variables were included as part of the prospective randomized controlled trial. Additional variables were also collected at a later time, including vasospasm data and maximum clot thickness. Aneurysms were categorized into 1 of 6 groups: intradural internal carotid artery aneurysms, vertebral artery (VA) aneurysms (including the posterior inferior cerebellar artery), basilar trunk or basilar apex aneurysms, middle cerebral artery aneurysms, pericallosal aneurysms, and anterior communicating artery aneurysms. Twenty-nine patients with nonaneurysmal SAH were excluded. Patients with pericallosal aneurysms had the least average maximum clot burden (5.3 mm), compared with 6.4 mm for the group overall, but had the highest rate of symptomatic vasospasm (56% vs 22% overall, OR 4.9, RR 2.7, p = 0.026). Symptomatic vasospasm occurrence was tallied in patients with clinical deterioration attributable to delayed cerebral ischemia. There were no significant differences in maximum clot thickness between aneurysm sites. Middle cerebral artery aneurysms resulted in the thickest mean maximum clot (7.1 mm) but rates of symptomatic and radiographic vasospasm in this group were statistically no different compared with the overall group. Vertebral artery aneurysms had the worst 1-year modified Rankin scale (mRS) scores (3.0 vs 1.9 overall, respectively; p = 0.0249). A 1-year mRS score of 0-2 (good outcome) was found in 72% of patients overall, but in only 50% of those with pericallosal and VA aneurysms, and in 56% of those with basilar artery aneurysms (p = 0.0044). Patients with stroke from vasospasm had higher mean clot thickness (9.71 vs 6.15 mm, p = 0.004). The location of a ruptured aneurysm minimally affects the maximum thickness of the SAH clot but is predictive of symptomatic vasospasm or clinical deterioration from delayed cerebral ischemia in pericallosal aneurysms. The worst 1-year mRS outcomes in this cohort of patients were noted in those with posterior circulation aneurysms or pericallosal artery aneurysms. Patients experiencing stroke had higher mean clot burden.

Dissecting Aneurysm of Vertebral Artery Manifestating as Contralateral Abducens Nerve Palsy

Isolated abducens nerve paresis related to ruptured vertebral artery (VA) aneurysm is rare. It usually occurs bilaterally or ipsilaterally to the pathologic lesions. We report the case of a contralateral sixth nerve palsy following ruptured dissecting VA aneurysm. A 38-year-old man was admitted for the evaluation of a 6-day history of headache. Abnormalities were not seen on initial computed tomography (CT). On admission, the patient was alert and no signs reflecting neurologic deficits were noted. Time of flight magnetic resonance angiography revealed a fusiform dilatation of the right VA involving origin of the posterior inferior cerebellar artery. The patient suddenly suffered from severe headache with diplopia the day before the scheduled cerebral angiography. Neurologic examination disclosed nuchal rigidity and isolated left abducens nerve palsy. Emergent CT scan showed high density in the basal and prepontine cistern compatible with ruptured aneurismal hemorrhage. Right vertebral angiography illustrated a right VA dissecting aneurysm with prominent displaced vertebrobasilar artery to inferiorly on left side. Double-stent placement was conducted for the treatment of ruptured dissecting VA aneurysm. No diffusion restriction signals were observed in follow-up magnetic resonance imaging of the brain stem. Eleven weeks later, full recovery of left sixth nerve palsy was documented photographically. In conclusion, isolated contralateral abducens nerve palsy associated with ruptured VA aneurysm may develop due to direct nerve compression by displaced verterobasilar artery triggered by primary thick clot in the prepontine cistern.

Abstract 43: Effect of Clazosentan on Clinical Outcome After Aneurysmal Subarachnoid Hemorrhage and Endovascular Coiling: Results of the CONSCIOUS-3 Study

Introduction: In CONSCIOUS-1, clazosentan, an endothelin receptor antagonist, significantly and dose-dependently reduced angiographic vasospasm (VSP) after aneurysmal subarachnoid hemorrhage (aSAH). CONSCIOUS-3 aimed to assess whether clazosentan improves VSP-related morbidity/all cause mortality after aSAH. Methods: This was a randomized, double-blind, placebo-controlled trial. Patients included in the study were 18-75 years old with SAH due to ruptured saccular aneurysm secured by endovascular coiling, any thick clot and WFNS grades I-IV prior to coiling procedure. Patients were randomized 1:1:1 to intravenous clazosentan (5 or 15 mg/h) or placebo for ≤2 weeks. The primary composite endpoint (all-cause mortality; VSP-related new cerebral infarcts; delayed ischemic neurological deficit [DIND] due to VSP; rescue therapy in the presence of confirmed angiographic VSP) was evaluated 6 weeks post-aSAH and assessed centrally by a blinded critical events committee, with significance determined using logistic regression adjusted for WFNS. The main secondary endpoint was the extended Glasgow Outcome Scale (GOSE; dichotomized) at week 12. Results: CONSCIOUS-3 was halted prematurely following nonsignificant results from the parallel CONSCIOUS-2 clipping study. There were 571 treated patients (placebo n=189, clazosentan 5 mg/h n=194, clazosentan 15 mg/h n=188). The primary endpoint occurred in 27% of the placebo group compared with 24% and 15% in the 5 and 15 mg/h clazosentan groups, respectively; significant improvement was seen with 15 mg/h clazosentan (odds ratio [OR] 0.474, 95% CI 28-82%; p=0.007) but not 5 mg/h (OR 0.786, 95% CI 48-129%; p=0.340). DIND decreased with increasing clazosentan dose (placebo 21%; clazosentan 5 mg/h 18%; clazosentan 15 mg/h 10%). VSP-related new cerebral infarct occurred in 13%, 16% and 7% in the placebo, clazosentan 5 and 15 mg/h groups, respectively. A 3-fold greater use of rescue therapy was seen in patients receiving placebo (21%) compared with 15 mg/h clazosentan (7%). Poor functional outcome (GOSE score ≤4) occurred in 24% of patients in the placebo group compared with 25% (OR 0.918, 95% CI 55-154%; p=0.748) and 28% (OR 1.337, 95% CI 80-223%; p=0.266) in the clazosentan 5 and 15 mg/h groups, respectively. At week 12, mortality rates were 6%, 4% and 6% with placebo, clazosentan 5 and 15 mg/h, respectively. Treatment-emergent adverse events of specific interest were lung complications (21%, 36%, 37%), anemia (10%, 13%, 13%) and hypotension (7%, 11%, 16%) in the placebo, clazosentan 5 and 15 mg/h groups, respectively. Conclusions: Clazosentan (15 mg/h) significantly reduced mortality/VSP-related morbidity; however, no significant effect on GOSE occurred, possibly due to greater use of rescue therapy with placebo. Pulmonary complications, anemia and hypotension were more common in patients receiving clazosentan.

Development of Nicardipine Prolonged-Release Implants After Clipping for Preventing Cerebral Vasospasm: From Laboratory to Clinical Trial

We have developed a drug delivery system using a vasodilating drug that can be implanted intracranially at the time of surgery for aneurysm clipping, without systemic side effects or side effects associated with long-term intrathecal drug administration. We started our project on 1994 for making a slowly releasing drug delivery system in vitro because cerebral vasospasm occurs 4–14 days following subarachnoid hemorrhage (SAH). A rod-shaped pellet containing 1 mg of nicardipine for animal study was prepared by heat compression. We presented the efficacy and safety of this drug delivery system using both canine double-hemorrhage and clot placement models. Since October 1999, nicardipine prolonged-release implants (NPRIs) containing 4 mg of nicardipine have been used to prevent vasospasm in patients with SAH. NPRIs were placed in the cistern of the cerebral arteries, where thick clots existed; therefore, vasospasm related to delayed ischemic neurological deficits (DINDs) was highly probable. Vasospasm was completely prevented in the arteries by placing NPRIs adjacent to the arteries during surgery. No complications were experienced. We have performed three studies (a single-center study with consecutive patients; a single-center, randomized, double-blind trial; and a multicenter cooperative study) and have proved that implantation of NPRIs reduces the incidence of cerebral vasospasm and DINDs and improves clinical outcome after SAH.

Effect of country or continent of treatment on outcome after aneurysmal subarachnoid hemorrhage

Prognostic factors for outcome after aneurysmal subarachnoid hemorrhage (SAH) include the clinical and pathological characteristics of the patient and hemorrhage as well as some aspects of treatment. Because treatment can vary between countries and continents, the authors used a large database of patients with SAH to determine the effect of the geographic location of treatment on outcome. Data obtained in 3567 patients who were entered into randomized trials of tirilazad between 1991 and 1997 were analyzed. Patients underwent treatment in 162 neurosurgical centers in 21 countries in North America, Europe, Africa, and Australia. The dependent variable was clinical outcome assessed 3 months after SAH with the Glasgow Outcome Scale, which was analyzed as a 5-point variable and dichotomized into favorable (good recovery or moderate disability) and unfavorable (severe disability, vegetative state, or death) outcomes. The effect of country or continent of treatment on outcome was assessed using univariate and multivariate logistic regression and proportional odds modeling before and after adjusting for numerous other factors significantly associated with outcome. The authors constructed several multivariate analysis models and demonstrated that for almost every model, country was not a significant predictor of outcome (p>0.05). There was variation in outcome between countries, but this was mostly due to differences in other admission characteristics that influence outcome such as age, clinical grade, and subarachnoid clot thickness. Because the number of patients entered from some countries was small, countries were grouped, and the data were analyzed by continent. This grouping gave more stable estimates and created an appropriate model for both logistic and proportional odds models and again showed that continent had no significant effect on outcome. Despite the variations in treatment that undoubtedly exist between countries and continents, the location of treatment had minimal effect on outcome. Outcome was influenced mostly by clinical characteristics on admission such as neurological grade, patient age, and amount of SAH.

Hemorrhagic cerebral infarction in carbon monoxide poisoning: a case report

IntroductionAlmost every known central neurological syndrome has been reported as a complication of carbon monoxide poisoning. Hemorrhagic infarct has rarely been considered as an early manifestation of carbon monoxide poisoning. A case of cerebral hemorrhagic infarction is presented. Typical findings, neuropathology and the role of vascular injury are described.Case presentationThe symptoms and clinical course of acute poisoning with carbon monoxide in a 7-year-old boy are described. To evaluate the possible causes, a brain computed tomography (CT) was performed that showed thick clot in the left medial temporal and parasellar area, left sylvian fissure(acute intravascular thrombus) accompanied by left diffuse frontotemporal hypodensity and midline shift. Four-vessel digital subtraction angiography two weeks after intoxication was not indicative of any vascular lesion.ConclusionHemorrhagic infarction is a rare presentation of carbon monoxide poisoning. When found in a child, in addition to conservative treatment to reduce the neurocognitive squeal, other probable causes should be ruled out.

Prognostic Factors and Targets for Intervention After Subarachnoid Hemorrhage

See related article, pages 2315–2321. Aneurysmal subarachnoid hemorrhage is associated with a high risk of morbidity and mortality. Treatment requires early aneurysm repair to prevent catastrophic rebleeding and intensive medical care to manage associated problems including hydrocephalus, cerebral vasospasm, electrolyte disorders, infection, and seizures. Prognosis after SAH is determined in part by factors that are present from the outset and not modifiable, but recent evidence suggests potential opportunities to improve outcomes. Rosengart et al1 analyzed a large series of patients with ruptured aneurysms and determined that the most important factors leading to unfavorable outcome were cerebral infarction, worse clinical grade on admission, advanced age, fever, and symptomatic vasospasm. Other significant variables were greater clot thickness on admission CT …

Smoking, Haemostatic Factors, and Cardiovascular Risk

There is a strong relationship between cigarette smoking and haemostatic parameters to increase the risk of cardiovascular events. Smoking influences negatively coagulation-fibrinolysis cascade at any level, although it acts primarily on those pathways that are most important for an effective clot formation: endothelium, platelets, and fibrinogen. Endothelial dysfunction is a main consequence of smoke compounds with significant changes in initiating physiologic coagulation process; platelet adhesiveness and aggregation increases as a result of smoking; finally, fibrinogen/fibrin framework strengthens clot thickness. Therefore, the whole coagulation cascade activates the thrombi formation pathway under smoking action. The risk of thrombotic cardiovascular events increases its frequency with more severe atherosclerotic alterations if compared to similar events in nonsmokers. Changes in haemostatic factors produced by smoking appear to be related to female sex, especially for those women who use oral contraceptives. Thrombosis of coronary and cerebral arteries are found with a major incidence in young women who are users. In conclusion, cigarette smoking modifies haemostatic parameters via thrombosis with consequently more rate of cardiovascular events.

Nicardipine Prolonged-Release Implants for Preventing Cerebral Vasospasm After Subarachnoid Hemorrhage: Effect and Outcome in the First 100 Patients

Vasospasm following subarachnoid hemorrhage (SAH) remains difficult to prevent despite extensive investigative efforts. Nicardipine prolonged-release implants (NPRIs) have been used to prevent vasospasm in patients with SAH since October 1999. The present study analyzed the efficacy and safety of NPRIs in 100 patients with SAH and thick subarachnoid clot (mainly Fisher group 3) treated with NPRIs (diameter 2 mm, length 10 mm, containing 4 mg of nicardipine) during surgery after clipping of the aneurysm. The number and location of pellets depended on the amount and site of the subarachnoid clot on preoperative computed tomography and on the type of craniotomy. Two to 12 pellets were implanted in the cisterns of the internal carotid artery, middle cerebral artery, and/or anterior cerebral artery, where thick clots were present and vasospasm related to delayed ischemic neurological deficit (DIND) was highly likely. Only seven patients developed DIND and five patients suffered cerebral infarction. Angiography performed on days 7-12 revealed no vasospasm in any of the arteries close to the site of NPRI placement. NPRI placement can completely prevent vasospasm in arteries within the cisterns containing thick clots, but is less effective in remote locations.

Application of Nicardipine Prolonged-release Implants: Analysis of 97 Consecutive Patients with Acute Subarachnoid Hemorrhage

Since October 1999, nicardipine prolonged-release implants (NPRIs) have been used to prevent vasospasm in patients with subarachnoid hemorrhage. This study was conducted to examine the incidence of cerebral vasospasm and outcome after the application of NPRIs. Ninety-seven consecutive patients among 125 patients with subarachnoid hemorrhage who were surgically treated within 72 hours were analyzed. NPRIs were applied principally to patients with thick clots (Fisher Group 3) through a frontotemporal or frontal craniotomy. Sixty-nine patients, including five in Fisher Group 2, were treated with NPRIs, and 28 were not. NPRIs were placed in the cisterns of thick clots where vasospasm was highly probable. Four (6%) of the 69 patients treated with NPRIs and 3 (11%) of the 28 patients not treated with NPRIs developed delayed ischemic neurological deficits (DINDs). Of these patients, clinical deterioration with infarction occurred in two patients (3%). Current smoking (P = 0.0088) and intraventricular hemorrhage on admission computed tomographic (CT) scans (P = 0.0077) were correlated with DIND. CT groupings on admission and postoperatively were not correlated, nor were World Federation of Neurosurgical Societies grades. Hypertension was inversely correlated with DIND (P = 0.0233). Eighty-six patients (89%) had an independent status at 3 months. Logistic regression analysis demonstrated that age (odds ratio [OR], 6.836; P = 0.034), World Federation of Neurosurgical Societies grade (OR, 23.317; P = 0.001), intraventricular hemorrhage on admission CT scans (OR, 6.332; P = 0.024), and surgical complications (OR, 32.861; P = 0.003) were independent risk factors influencing an unfavorable outcome. CT grouping on admission and DIND were not. Our findings suggest that the incidence of DIND may decrease and, therefore, an unfavorable outcome may improve if NPRIs are applied for patients with thick clots (Fisher Group 3) during surgery.

重症くも膜下出血の治療―ニカルジピン徐放剤を用いて―

Nicardipine prolonged-release pellets (NP) are made for implantation during surgery to prevent cerebral vasospasm. We retrospectively analyzed patients with a poor-grade subarachnoid hemorrhage (SAH) between October 1999 and September 2004. Among 125 surgically treated SAH patients, 34 belonged to WFNS grades 4 and 5 (male/female 13/21, the average age was 63, the ratio craniotomy/coil 26/8). Four to 12 NPs (16-48 mg of nicardipine) were placed along the respective artery (IC, A1, A2, A3, M1, M2, and M3) after clipping the aneurysm, where there was thick clot and therefore subsequent vasospasm was highly likely. The intracranial pressure was monitored and treated with glycerin, ventricular drainage, external decompression, and/or barbiturate administration. Neither induced hypervolemia nor induced hypertension was used. A delayed ischemic neurological deficit was seen in 1 patient, but there were no cerebral infarctions due to cerebral vasospasm. Angiography performed on days 7-12 revealed no vasospasm in any arteries close to where the NPs were placed. The outcome after 3 months was good in 7, moderately disabled in 13, severely disabled in 7, vegetative state in 2, and 5 patients had deceased. The NP is an effective, simple, and safe prophylactic treatment to prevent vasospasm when a surgical procedure is chosen to treat ruptured aneurysms of poor-grade SAH patients.

Denver by Morning

On the last day in June, had you been driving northbound on I-25, the piebald peaks of the Rockies flanking the horizon, you might have been diverted on the stretch just south of Denver. The cause: an early-morning, single-vehicle accident. If you got there before the detour was in place, you might have seen the six-horse goose neck trailer flipped over in the drainage ditch, the cab of the truck so smashed in that it would be hard to believe when you heard later that the driver and passenger both walked away unscratched. Depending how soon after sunrise you passed that way, you might have seen two frantic women pulling at the door to the trailer, wait ing for someone to come, or you might have seen the firefighters reaching into the mangled heap of metal with the jaws of life. You would have encountered a delay throughout the day, though later on, you might only have been able to see the row of uprooted guard rails leading to the scene, then a thick clot of highway patrol cars and camera crews and caution tape. Perhaps you would have called your wife, to say I'll be late, and lit up a cigarette to pass the time, tapping the ashes out the driver side window into the violently blue Colorado summer.

Application of Nicardipine Prolonged-release Implants: Analysis of 97 Consecutive Patients with Acute Subarachnoid Hemorrhage

Since October 1999, nicardipine prolonged-release implants (NPRIs) have been used to prevent vasospasm in patients with subarachnoid hemorrhage. This study was conducted to examine the incidence of cerebral vasospasm and outcome after the application of NPRIs. Ninety-seven consecutive patients among 125 patients with subarachnoid hemorrhage who were surgically treated within 72 hours were analyzed. NPRIs were applied principally to patients with thick clots (Fisher Group 3) through a frontotemporal or frontal craniotomy. Sixty-nine patients, including five in Fisher Group 2, were treated with NPRIs, and 28 were not. NPRIs were placed in the cisterns of thick clots where vasospasm was highly probable. Four (6%) of the 69 patients treated with NPRIs and 3 (11%) of the 28 patients not treated with NPRIs developed delayed ischemic neurological deficits (DINDs). Of these patients, clinical deterioration with infarction occurred in two patients (3%). Current smoking (P = 0.0088) and intraventricular hemorrhage on admission computed tomographic (CT) scans (P = 0.0077) were correlated with DIND. CT groupings on admission and postoperatively were not correlated, nor were World Federation of Neurosurgical Societies grades. Hypertension was inversely correlated with DIND (P = 0.0233). Eighty-six patients (89%) had an independent status at 3 months. Logistic regression analysis demonstrated that age (odds ratio [OR], 6.836; P = 0.034), World Federation of Neurosurgical Societies grade (OR, 23.317; P = 0.001), intraventricular hemorrhage on admission CT scans (OR, 6.332; P = 0.024), and surgical complications (OR, 32.861; P = 0.003) were independent risk factors influencing an unfavorable outcome. CT grouping on admission and DIND were not. Our findings suggest that the incidence of DIND may decrease and, therefore, an unfavorable outcome may improve if NPRIs are applied for patients with thick clots (Fisher Group 3) during surgery.

Grading of Subarachnoid Hemorrhage: Modification of the World Federation of Neurosurgical Societies Scale on the Basis of Data for a Large Series of Patients.

Abstract OBJECTIVE The goals of this study were to use a large, prospectively collected, multicenter database for patients with aneurysmal subarachnoid hemorrhage (SAH) who were treated between 1991 and 1997 to determine the prognostic significance of clinical and radiological factors for outcomes and to use those factors to develop a grading scale to predict outcomes. METHODS A total of 3567 patients with SAH who were entered into four randomized clinical trials of tirilazad were studied. Outcomes were assessed 3 months after SAH, with the Glasgow Outcome Scale. Twenty clinical and radiological factors were entered into univariate and multivariate analyses, to determine factors prognostic for outcomes. Grading scales based on the most powerful prognostic parameters were statistically derived and validated and were compared with the World Federation of Neurosurgical Societies (WFNS) grading scale. RESULTS Factors predictive of outcomes included age, WFNS grade, history of hypertension, systolic blood pressure at admission, ruptured aneurysm location and size, blood clot thickness on computed tomographic scans, and angiographic vasospasm at admission. A grading scale using these factors could be derived; it predicted outcomes more accurately than did the WFNS scale, although it would be more complex to use. CONCLUSION Outcome prediction after SAH can be improved by adding additional clinical and radiological factors to the WFNS scale, albeit with added complexity.

Symptomatic vasospasm diagnosis after subarachnoid hemorrhage: evaluation of transcranial Doppler ultrasound and cerebral angiography as related to compromised vascular distribution.

To evaluate the reliability of transcranial Doppler ultrasound in detecting symptomatic vasospasm in patients after aneurysmal subarachnoid hemorrhage and monitoring response after hypertensive and endovascular treatments. Retrospective chart review. Neurosciences critical care unit in a tertiary-care university hospital. All patients admitted to a neurosciences critical care unit with the diagnosis of subarachnoid hemorrhage between January 1990 and June 1997. None We reviewed transcranial Doppler ultrasound data of 199 patients; 55 had symptomatic vasospasm. Clinical symptoms and corresponding vascular distributions were identified, as was angiographic vasospasm (n = 35). The sensitivity and specificity of transcranial Doppler ultrasound for anterior circulation vessels were calculated by using a mean cerebral blood flow velocity criterion of >120 cm/sec. Clinical diagnosis of symptomatic vasospasm was used as the standard to determine sensitivity and specificity of transcranial Doppler ultrasound and cerebral angiography. The sensitivity of transcranial Doppler ultrasound for anterior circulation in patients with symptomatic vasospasm was 73% with a specificity of 80%. The sensitivity of cerebral angiography was 80%. For individual vessels, the sensitivity and specificity of transcranial Doppler ultrasound were middle cerebral artery, 64% and 78%; anterior cerebral artery, 45% and 84%; and internal carotid artery, 80% and 77%, respectively. The mean times for symptomatic and transcranial Doppler ultrasound signs of vasospasm presentation were 6.4 +/- 2 and 6.1 +/- 3 days, respectively. In patients without symptomatic vasospasm, the mean time for mean cerebral blood flow velocities >120 cm/sec was 7.0 +/- 3 days (p <.05). Symptomatic vasospasm also was associated with thickness of clot on head computed tomography scan and rapidly increasing mean cerebral blood flow velocities. Transcranial Doppler ultrasound signs of vasospasm improved after endovascular treatment in 30 patients. The reliability of transcranial Doppler ultrasound was better at detecting high mean cerebral blood flow velocities in patients with symptomatic vasospasm related to middle cerebral and internal carotid artery distributions than for anterior cerebral artery distribution. Transcranial Doppler ultrasound was as sensitive as cerebral angiography at detecting symptomatic vasospasm. High mean cerebral blood flow velocities can be apparent before the presence of symptomatic vasospasm. Daily transcranial Doppler ultrasound monitoring could provide early identification of patients with aneurysmal subarachnoid hemorrhage who are at high risk for symptomatic vasospasm and may be helpful at following success of endovascular treatment.