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.

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 92 (3) ◽  
pp. 390-400 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Healthy Volunteers ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Plasma Concentrations ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Content Type ◽  
History Of ◽  
Fine Print

Object. The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH.Methods. Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique.On the whole, mean plasma ET concentrations in patients with SAH (mean ± standard error of mean, 2.1 ± 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 ± 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml compared with 2.1 ± 0.2 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml compared with 1.9 ± 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0–5, 3.2 ± 0.8 pg/ml; post-SAH Days 6–14, 2.7 ± 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 ± 0.3 compared with 1.9 ± 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others.Conclusions. Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.

Plasma endothelin and big endothelin concentrations and serum endothelin-converting enzyme activity following aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1287-1293 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Plasma Concentrations ◽  
Delayed Cerebral Ischemia ◽  
Magnetic Resonance Images ◽  
Converting Enzyme ◽  
Content Type ◽  
Endothelin Converting Enzyme ◽  
Fine Print

Object. Pathogenesis of delayed ischemia after aneurysmal subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET)-1 with its powerful and long-lasting vasoconstricting activity. In this prospective study the author investigated the correlations between serial plasma concentrations of ET-1 and big ET-1 as well as the ET-1/big ET-1 molar concentration ratio and serum endothelin-converting enzyme (ECE)-1 activity, and ischemic complications after SAH. Methods. To measure plasma ET-1 (51 patients), big ET-1 immunoreactivity (22 patients), and serum ECE-1 activity (13 patients), blood samples were obtained on admission, in the morning after aneurysm surgery, and during the 2nd week after hemorrhage in 51 consecutive patients (28 men and 23 women, with a mean age of 50.8 years) with aneurysmal SAH. Mean plasma concentrations of ET-1 in patients with SAH (mean ± standard deviation: on admission, 4.2 ± 2 pg/ml; after surgery, 4.3 ± 2.2 pg/ml; and during the 2nd week after SAH, 3.7 ± 1.9 pg/ml) differed from those in healthy volunteers (2.9 ± 1.2 pg/ml; p < 0.01). Plasma concentrations of ET-1 and big ET-1 as well as the ET-1/big ET-1 ratio did not change significantly with elapsed time following SAH; however, serum ECE-1 activity during the 2nd week after SAH was higher in patients with SAH than that in controls (162 ± 43 compared with 121 ± 56 pg/ml, respectively; p = 0.028). Plasma ET-1 concentrations (p < 0.05) and the ET-1/big ET-1 ratios (p = 0.063) were higher but plasma big ET-1 concentrations were lower (p < 0.05) in patients who experienced symptomatic delayed cerebral ischemia, compared with other patients with SAH. In addition, in cases in which follow-up computerized tomography scans or magnetic resonance images demonstrated permanent ischemic lesions attributable to vasospasm, patients had higher ET-1 concentrations than did other patients with SAH. Conclusions. The plasma ET-1 concentration correlates with delayed cerebral ischemia after SAH, suggesting that an increased ET conversion rate in the endothelium predicts ischemic symptoms. Increased serum ECE-1 activity during the 2nd week may reflect the severity of endothelial injury to cerebral arteries.

Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 93 (5) ◽  
pp. 808-814 ◽  
Author(s):  
Mette K. Schulz ◽  
Lars Peter Wang ◽  
Mogens Tange ◽  
Per Bjerre
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Delayed Cerebral Ischemia ◽  
Neuronal Injury ◽  
Low Flow ◽  
Cerebral Microdialysis ◽  
Intracerebral Microdialysis ◽  
Content Type ◽  
Wide Range ◽  
Fine Print

Object. The success of treatment for delayed cerebral ischemia is time dependent, and neuronal monitoring methods that can detect early subclinical levels of cerebral ischemia may improve overall treatment results. Cerebral microdialysis may represent such a method. The authors' goal was to characterize patterns of markers of energy metabolism (glucose, pyruvate, and lactate) and neuronal injury (glutamate and glycerol) in patients with subarachnoid hemorrhage (SAH), in whom ischemia was or was not suspected.Methods. By using low-flow intracerebral microdialysis monitoring, central nervous system extracellular fluid concentrations of glucose, pyruvate, lactate, glutamate, and glycerol were determined in 46 patients suffering from poor-grade SAH. The results in two subgroups were analyzed: those patients with no clinical or radiological signs of cerebral ischemia (14 patients) and those who succumbed to brain death (five patients).Significantly lower levels of energy substrates and significantly higher levels of lactate and neuronal injury markers were observed in patients with severe and complete ischemia when compared with patients without symptoms of ischemia (glucose 0 compared with 2.12 ± 0.15 mmol/L; pyruvate 0 compared with 151 ± 11.5 µmol; lactate 6.57 ± 1.07 compared with 3.06 ± 0.32 mmol/L; glycerol 639 ± 91 compared with 81.6 ± 12.4 µmol; and glutamate 339 ± 53.4 compared with 14 ± 3.33 µmol). Immediately after catheter placement, glutamate concentrations declined over the first 4 to 6 hours to reach stable values. The remaining parameters exhibited stable values after 1 to 2 hours.Conclusions. The results confirm that intracerebral microdialysis monitoring of patients with SAH can be used to detect patterns of cerebral ischemia. The wide range from normal to severe ischemic values calls for additional studies to characterize further incomplete and possible subclinical levels of ischemia.

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Platelet Function ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Content Type ◽  
Reduced Risk ◽  
Fine Print

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

Detection of delayed cerebral ischemia using objective pupillometry in patients with aneurysmal subarachnoid hemorrhage

2020 ◽  
Vol 132 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Salah G. Aoun ◽  
Sonja E. Stutzman ◽  
Phuong-Uyen N. Vo ◽  
Tarek Y. El Ahmadieh ◽  
Mohamed Osman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Medical Center ◽  
Delayed Cerebral Ischemia ◽  
Final Analysis ◽  
Neurological Injury ◽  
University Of Texas ◽  
The University

OBJECTIVECerebral vasospasm causing delayed cerebral ischemia (DCI) is a source of significant morbidity after subarachnoid hemorrhage (SAH). Transcranial Doppler is used at most institutions to detect sonographic vasospasm but has poor positive predictive value for DCI. Automated assessment of the pupillary light reflex has been increasingly used as a reliable way of assessing pupillary reactivity, and the Neurological Pupil Index (NPi) has been shown to decrease hours prior to the clinical manifestation of ischemic injury or herniation syndromes. The aim of this study was to investigate the role of automated pupillometry in the setting of SAH, as a potential adjunct to TCD.METHODSOur analysis included patients that had been diagnosed with aneurysmal SAH and admitted to the neuro–intensive care unit of the University of Texas Southwestern Medical Center between November 2015 and June 2017. A dynamic infrared pupillometer was used for all pupillary measurements. An NPi value ranging from 3 to 5 was considered normal, and from 0 to 2.9 abnormal. Sonographic vasospasm was defined as middle cerebral artery velocities greater than 100 cm/sec with a Lindegaard ratio greater than 3 on either side on transcranial Doppler. Most patients had multiple NPi readings daily and we retained the lowest value for our analysis. We aimed to study the association between DCI and sonographic vasospasm, and DCI and NPi readings.RESULTSA total of 56 patients were included in the final analysis with 635 paired observations of daily TCD and NPi data. There was no statistically significant association between the NPi value and the presence of sonographic vasospasm. There was a significant association between DCI and sonographic vasospasm, χ2(1) = 6.4112, p = 0.0113, OR 1.6419 (95% CI 1.1163–2.4150), and between DCI and an abnormal decrease in NPi, χ2(1) = 38.4456, p < 0.001, OR 3.3930 (95% CI 2.2789–5.0517). Twelve patients experienced DCI, with 7 showing a decrease of their NPi to an abnormal range. This change occurred > 8 hours prior to the clinical decline 71.4% of the time. The NPi normalized in all patients after treatment of their vasospasm.CONCLUSIONSIsolated sonographic vasospasm does not seem to correlate with NPi changes, as the latter likely reflects an ischemic neurological injury. NPi changes are strongly associated with the advent of DCI and could be an early herald of clinical deterioration.

Abstract P350: Early Transcranial Doppler Velocity Changes as a Predictor for Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Matthew Triano ◽  
Maite J Corbin ◽  
Sameer Desale ◽  
Ai-Hsi Liu ◽  
Daniel R Felbaum ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Delayed Cerebral Ischemia ◽  
Multivariate Logistic Regression Analysis ◽  
Absolute Velocity ◽  
Doppler Velocity ◽  
Velocity Change

Introduction: Although transcranial Doppler (TCD) evaluation for vasospasm remains an important study in aneurysmal subarachnoid hemorrhage (aSAH) management, its precise role in predicting delayed cerebral ischemia (DCI) remains unclear. Hypothesis: We evaluated optimal measures for evaluating TCD velocities and hypothesized that TCD velocity change would be the best predictor for DCI in patients with aSAH. Methods: Patients with aSAH over a two-year period were retrospectively analyzed. Baseline characteristics, outcomes, and TCD velocities in bilateral middle cerebral arteries (MCA) for hospital days 2 to14 were recorded. TCD variables, including absolute velocity and change in velocity, were obtained by creating a smoothing curve. A variable representing change in TCD velocity was then created through a linear regression model that confirmed greatest change in velocity associated with DCI occurred at days 2-7. Multivariate logistic regression analysis using DCI as outcome was then completed. Results: 95 patients with aSAH were evaluated. Increased TCD velocity at days 2-7 proved to be a better predictor for DCI than absolute velocity with an optimal cutoff of 8.9 cm/sec/day ( p = 0.019) and AUC 0.651. Multivariate logistic analysis using DCI as the outcome showed that poor admission Hunt-Hess scores (OR 5.02, 95%CI 1.22-22.67, p = 0.028) and increase in TCD velocity during days 2-7 (OR 5.32, 95%CI 1.41-23.33, p = 0.018) were independently associated with DCI. Conclusions: We found that relative increases in TCD velocities in the MCAs during the first 7 days (threshold increase of 8.9 cm/sec/day or 53.4 cm/sec from days 2-7) after aSAH were independently associated with DCI. Our findings suggest that vasospasm should be confirmed and treated aggressively when detected via increased TCD velocities during the first seven days in order to minimize DCI. This association requires independent confirmation.

scholarly journals Body mass index and leptin levels in serum and cerebrospinal fluid in relation to delayed cerebral ischemia and outcome after aneurysmal subarachnoid hemorrhage

2021 ◽  
Author(s):  
Michael Veldeman ◽  
Miriam Weiss ◽  
Tim Philipp Simon ◽  
Anke Hoellig ◽  
Hans Clusmann ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Outcome ◽  
Body Mass ◽  
Ct Perfusion ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Overweight And Obesity ◽  
Protective Effects

AbstractAneurysmal subarachnoid hemorrhage (SAH) is associated with a high mortality rate and may leave surviving patients severely disabled. After the initial hemorrhage, clinical outcome is further compromised by the occurrence of delayed cerebral ischemia (DCI). Overweight and obesity have previously been associated with protective effects in the post-bleeding phase. The aim of this study was to assess the effects of a patient’s body mass index (BMI) and leptin levels on the occurrence of DCI, DCI-related cerebral infarction, and clinical outcome. In total, 263 SAH patients were included of which leptin levels were assessed in 24 cases. BMI was recorded along disease severity documented by the Hunt and Hess and modified Fisher scales. The occurrence of clinical or functional DCI (neuromonitoring, CT Perfusion) was assessed. Long-term clinical outcome was documented after 12 months (extended Glasgow outcome scale). A total of 136 (51.7%) patients developed DCI of which 72 (27.4%) developed DCI-related cerebral infarctions. No association between BMI and DCI occurrence (P = .410) or better clinical outcome (P = .643) was identified. Early leptin concentration in serum (P = .258) and CSF (P = .159) showed no predictive value in identifying patients at risk of unfavorable outcomes. However, a significant increase of leptin levels in CSF occurred from 326.0 pg/ml IQR 171.9 prior to DCI development to 579.2 pg/ml IQR 211.9 during ongoing DCI (P = .049). In our data, no association between obesity and clinical outcome was detected. After DCI development, leptin levels in CSF increased either by an upsurge of active transport or disruption of the blood-CSF barrier. This trial has been registered at ClinicalTrials.gov (NCT02142166) as part of a larger-scale prospective data collection. BioSAB: https://clinicaltrials.gov/ct2/show/NCT02142166

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