The Role of Consecutive Plasma Copeptin Levels in the Screening of Delayed Cerebral Ischemia in Poor-Grade Subarachnoid Hemorrhage.
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SUBMITTER: Rhim JK
PROVIDER: S-EPMC8066417 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:AimsTo assess differences in the clinical prognosis between different treatment timings in poor-grade (Hunt and Hess grade 4-5) aneurysmal subarachnoid hemorrhage patients.MethodsThe treated 127 poor-grade aneurysmal subarachnoid hemorrhage patients were divided into three groups: early treatment within 2 days, treatment on days 3 to 10, and treatment for more than 10 days after the hemorrhage. Odd ratios with a 95% confidence interval were calculated in logistic regression for different timing strategies regarding delayed cerebral ischemia and poor prognosis at 3 months. Subgroup analyses were conducted to determine whether the different timing strategies affect the prognosis.ResultsPatients who received the treatment on days 3 to 10 were prone to develop delayed cerebral ischemia and poor prognosis at 3 months. Postponing treatment in patients older than 55 years or diagnosed with an intraventricular hematoma on the initial computed tomography scan may lead to poor prognosis, with the early intervention group as a reference.ConclusionsEarly intervention in poor-grade aneurysmal subarachnoid hemorrhage is suggested to be implemented. The treatment on 3 to 10 days harbored the highest risk of poor prognosis; patients might benefit more from early intervention, especially for ones older than 55 years or diagnosed with an intraventricular hematoma.
| S-EPMC10018093 | biostudies-literature
Project description:Delayed cerebral ischemia (DCI) is a serious complication of aneurysmal subarachnoid hemorrhage (SAH). Matricellular protein periostin (POSTN) has been found to be upregulated and linked with early brain injury after experimental SAH. The aim of the present study was to investigate the relationship between plasma POSTN levels and various clinical factors including serum levels of C-reactive protein (CRP), an inflammatory marker, in 109 consecutive SAH patients whose POSTN levels were measured at days 1-12 after aneurysmal obliteration. DCI developed in 16 patients associated with higher incidence of angiographic vasospasm, cerebral infarction, and 90-day worse outcomes. POSTN levels peaked at days 4-6 before DCI development. Cerebrospinal fluid (CSF) drainage was associated with reduced POSTN levels, but did not influence CRP levels. There was no correlation between POSTN levels and other treatments or CRP levels. To predict DCI development, receiver-operating characteristic curves indicated that the most reasonable cutoff POSTN levels were obtained at days 1-3 in patients without CSF drainage (80.5 ng/ml; specificity, 77.6%; sensitivity, 85.7%). Multivariate analyses using variables obtained by day 3 revealed that POSTN level was an independent predictor of DCI. POSTN levels over the cutoff value were associated with higher incidence of DCI, but not angiographic vasospasm. This study shows for the first time that CSF drainage may reduce plasma POSTN levels, and that POSTN levels may increase prior to the development of DCI with and without vasospasm irrespective of systemic inflammatory reactions in clinical settings. These findings suggest POSTN as a new therapeutic molecular target against post-SAH DCI.
| S-EPMC6554464 | biostudies-literature
Project description:BackgroundThe objective of this study was to investigate the clinical feasibility of near-infrared spectroscopy (NIRS) for the detection of delayed cerebral ischemia (DCI) in patients with poor-grade subarachnoid hemorrhage (SAH) treated with coil embolization.MethodsCerebral regional oxygen saturation (rSO2) was continuously monitored via two-channel NIRS for 14 days following SAH. The rSO2 levels according to DCI were analyzed by using the Mann-Whitney U-test. A receiver operating characteristic curve was generated on the basis of changes in rSO2 by using the rSO2 level on day 1 as a reference value to determine the optimal cutoff value for identifying DCI.ResultsTwenty-four patients with poor-grade SAH were included (DCI, n = 8 [33.3%]; non-DCI, n = 16 [66.7%]). The rSO2 levels of patients with DCI were significantly lowered from 6 to 9 days compared with those in without DCI. The rSO2 level was 62.55% (58.30-63.40%) on day 6 in patients with DCI versus 65.40% (60.90-68.70%) in those without DCI. By day 7, it was 60.40% (58.10-61.90%) in patients with DCI versus 64.25% (62.50-67.10%) those without DCI. By day 8, it was 58.90% (56.50-63.10%) in patients with DCI versus 66.05% (59.90-69.20%) in those without DCI, and by day 9, it was 60.85% (58.40-65.20%) in patients with DCI versus 65.80% (62.70-68.30%) in those without DCI. A decline of greater than 14.5% in the rSO2 rate yielded a sensitivity of 92.86% (95% confidence interval: 66.1-99.8%) and a specificity of 88.24% (95% confidence interval: 72.5-96.7%) for identifying DCI. A decrease by more than 14.7% of the rSO2 level indicates a sensitivity of 85.7% and a specificity of 85.7% for identifying DCI.ConclusionsNear-infrared spectroscopy shows some promising results for the detection of DCI in patients with poor-grade SAH. Further studies involving a large cohort of the SAH population are required to confirm our results.
| S-EPMC8104035 | biostudies-literature
Project description:BackgroundWe investigated the proportion of patients in an initial good clinical condition who developed devastating DCI, and aimed to characterize these patients by aneurysm location, blood pressure instability prior to DCI, and the extent of cerebral ischemia.MethodsWe included aSAH patients admitted between 2010 and 2021 with a Glasgow Coma Scale of 11 or higher 24 h after aneurysm treatment, who developed devastating DCI, defined as DCI leading to coma for at least 48 h with cerebral infarction on the subsequent scan. Blood pressure instability was defined as nimodipine-induced blood pressure drops, dosage adjustments, or the use of blood pressure drugs before onset of DCI. Descriptive statistics were used to summarize the data.ResultsOut of 1,211 consecutive aSAH patients, 617 patients had a good clinical condition after aneurysm treatment of whom 16 (3%) patients [14 (88%) women] were included in this study. Thirteen (81%) patients had an aneurysm in the anterior circulation. Thirteen patients (81%) had blood pressure instability: twelve (75%) had nimodipine-induced blood pressure drops, eleven (69%) received antihypertensive drugs, and 7 (44%) received hypertension induction before onset of DCI. Thirteen (81%) patients had bilateral ischemia, mainly in the anterior circulation (56%).ConclusionsThe proportion of aSAH patients with a good clinical condition after aneurysm treatment who develop devastating DCI is small. The vast majority of these patients had blood pressure instability. Future studies are needed to investigate if a reduction in the number and extent of blood pressure fluctuations decreases the incidence of devastating DCI.
| S-EPMC9606612 | biostudies-literature
Project description:Background A subset of good-grade patients with aneurysmal subarachnoid hemorrhage (aSAH) develop delayed cerebral ischemia (DCI) that may cause permanent disabilities after aSAH. However, little is known about the risk factors of DCI among this specific patient group. Methods and Results We obtained a multinational cohort of good-grade (Glasgow Coma Scale 13-15 on admission) patients with aSAH by pooling patient data from 4 clinical trials and 2 prospective cohort studies. We collected baseline data on lifestyle-related factors and the clinical characteristics of aSAHs. By calculating fully adjusted risk estimates for DCI and DCI-related poor outcome, we identified the most high-risk patient groups. The pooled study cohort included 1918 good-grade patients with aSAH (median age, 51 years; 64% women), of whom 21% and 7% experienced DCI and DCI-related poor outcome, respectively. Among men, patients with obesity and (body mass index ≥30 kg/m2) thick aSAH experienced most commonly DCI (33%) and DCI-related poor outcome (20%), whereas none of the normotensive or young (aged <50 years) men with low body mass index (body mass index <22.5 kg/m2) had DCI-related poor outcome. In women, the highest prevalence of DCI (28%) and DCI-related poor outcome (13%) was found in patients with preadmission hypertension and thick aSAH. Conversely, the lowest rates (11% and 2%, respectively) were observed in normotensive women with a thin aSAH. Conclusions Increasing age, thick aSAH, obesity, and preadmission hypertension are risk factors for DCI in good-grade patients with aSAH. These findings may help clinicians to consider which good-grade patients with aSAH should be monitored carefully in the intensive care unit.
| S-EPMC9851459 | biostudies-literature
Project description:BackgroundGood-grade aneurysmal subarachnoid hemorrhage (Hunt and Hess 1-2) is generally associated with a favorable prognosis. Nonetheless, patients may still experience secondary deterioration due to delayed cerebral ischemia (DCI), contributing to poor outcome. In those patients, neurological assessment is challenging and invasive neuromonitoring (INM) may help guide DCI treatment.MethodsAn observational analysis of 135 good-grade SAH patients referred to a single tertiary care center between 2010 and 2018 was performed. In total, 54 good-grade SAH patients with secondary deterioration evading further neurological assessment, were prospectively enrolled for this analysis. The cohort was separated into two groups: before and after introduction of INM in 2014 (pre-INMSecD: n = 28; post-INMSecD: n = 26). INM included either parenchymal oxygen saturation measurement (ptiO2), cerebral microdialysis or both. Episodes of DCI (ptiO2 < 10 mmHg or lactate/pyruvate > 40) were treated via induced hypertension or in refractory cases by endovascular means. The primary outcome was defined as the extended Glasgow outcome scale after 12 months. In addition, we recorded the amount of imaging studies performed and the occurrence of silent and overall DCI-related infarction.ResultsSecondary deterioration, impeding neurological assessment, occurred in 54 (40.0%) of all good-grade SAH patients. In those patients, a comparable rate of favorable outcome at 12 months was observed before and after the introduction of INM (pre-INMSecD 14 (50.0%) vs. post-INMSecD 16, (61.6%); p = 0.253). A significant increase in good recovery (pre-INMSecD 6 (50.0%) vs. post-INMSecD 14, (61.6%); p = 0.014) was observed alongside a reduction in the incidence of silent infarctions (pre-INMSecD 8 (28.6%) vs. post-INMSecD 2 (7.7%); p = 0.048) and of overall DCI-related infarction (pre-INMSecD 12 (42.8%) vs. post-INMSecD 4 (23.1%); p = 0.027). The number of CT investigations performed during the DCI time frame decreased from 9.8 ± 5.2 scans in the pre-INMSecD group to 6.1 ± 4.0 (p = 0.003) in the post-INMSecD group.ConclusionsA considerable number of patients with good-grade SAH experiences secondary deterioration rendering them neurologically not assessable. In our cohort, the introduction of INM to guide DCI treatment in patients with secondary deterioration increased the rate of good recovery after 12 months. Additionally, a significant reduction of CT scans and infarction load was recorded, which may have an underestimated impact on quality of life and more subtle neuropsychological deficits common after SAH.
| S-EPMC8285339 | biostudies-literature
Project description:Delayed cerebral ischemia (DCI) continues to be a sequela of aneurysmal subarachnoid hemorrhage (aSAH) that carries significant morbidity and mortality. Aside from nimodipine, no therapeutic agents are available to reduce the incidence of DCI. Pathophysiologic mechanisms contributing to DCI are poorly understood, but accumulating evidence over the years implicates several factors. Those have included microvessel vasoconstriction, microthrombosis, oxidative tissue damage, and cortical spreading depolarization as well as large vessel vasospasm. Common to these processes is red blood cell leakage into the cerebrospinal fluids (CSF) and subsequent lysis which releases hemoglobin, a central instigator in these events. This has led to the hypothesis that early blood removal may improve clinical outcome and reduce DCI. This paper will provide a narrative review of the evidence of hemoglobin as an instigator of DCI. It will also elaborate on available human data that discuss blood clearance and CSF drainage as a treatment of DCI. Finally, we will address a recent novel device that is currently being tested, the Neurapheresis CSF Management System™. This is an automated dual-lumen lumbar drainage system that has an option to filter CSF and return it to the patient.
| S-EPMC9375776 | biostudies-literature
Project description:BackgroundDelayed cerebral ischemia (DCI), a complication of subarachnoid hemorrhage (SAH), is linked to cerebral vasospasm and associated with poor long-term outcome. We implemented a structured cerebral microdialysis (CMD) based protocol using the lactate/pyruvate ratio (LPR) as an indicator of the cerebral energy metabolic status in the neurocritical care decision making, using an LPR ≥ 30 as a cutoff suggesting an energy metabolic disturbance. We hypothesized that CMD monitoring could contribute to active, protocol-driven therapeutic interventions that may lead to the improved management of patients with SAH.MethodsBetween 2018 and 2020, 49 invasively monitored patients with SAH, median Glasgow Coma Scale 11 (range 3-15), and World Federation of Neurosurgical Societies scale 4 (range 1-5) on admission receiving CMD were included. We defined a major CMD event as an LPR ≥ 40 for ≥ 2 h and a minor CMD event as an LPR ≥ 30 for ≥ 2 h.ResultsWe analyzed 7,223 CMD samples over a median of 6 days (5-8). Eight patients had no CMD events. In 41 patients, 113 minor events were recorded, and in 23 patients 42 major events were recorded. Our local protocols were adhered to in 40 major (95%) and 98 minor events (87%), with an active intervention in 32 (76%) and 71 (63%), respectively. Normalization of energy metabolic status (defined as four consecutive samples with LPR < 30 for minor and LPR < 40 for major events) was seen after 69% of major and 59% of minor events. The incidence of DCI-related infarcts was 10% (five patients), with only two observed in a CMD-monitored brain region.ConclusionsActive interventions were initiated in a majority of LPR events based on CMD monitoring. A low DCI incidence was observed, which may be associated with the active interventions. The potential aid of CMD in the clinical decision-making targeting DCI needs confirmation in additional SAH studies.
| S-EPMC9283139 | biostudies-literature
Project description:Delayed cerebral ischemia (DCI) is a major determinant of patient outcome following aneurysmal subarachnoid hemorrhage. Although the exact mechanisms leading to DCI are not fully known, inflammation, cerebral vasospasm, and microthrombi may all function together to mediate the onset of DCI. Indeed, inflammation is tightly linked with activation of coagulation and microthrombi formation. Thromboinflammation is the intersection at which inflammation and thrombosis regulate one another in a feedforward manner, potentiating the formation of thrombi and pro-inflammatory signaling. In this review, we will explore the role(s) of inflammation and microthrombi in subarachnoid hemorrhage (SAH) pathophysiology and DCI, and discuss the potential of targeting thromboinflammation to prevent DCI after SAH.
| S-EPMC5660311 | biostudies-literature
Project description:Delayed cerebral ischemia (DCI) is a common secondary complication and an important cause of disability and mortality among patients who survive aneurysmal subarachnoid hemorrhage (aSAH). Knowledge on DCI pathogenesis, risk factors, and biomarkers are essential for early detection and improved prognosis. To investigate the role of DNA methylation in DCI risk, we conducted an epigenome-wide association study (EWAS) in 68 patients followed up to 1 year after the initial aneurysm rupture. Blood samples were collected within 48 h post hemorrhage and used for DNA methylation profiling at ~ 450k CpG sites. A separate cohort of 175 patients was sequenced for the top CpG sites from the discovery analysis for a replication of the EWAS findings. EWAS did not identify any epigenome-wide significant CpGs. The top signal, cg18031596, was annotated to ANGPT1, a gene with critical functions in angiogenesis after vascular injury. Post hoc power calculations indicated a well-powered discovery analysis for cg18031596. Analysis of the replication cohort showed that four out of the five CpG sites sequenced at the ANGPT1 locus passed a Bonferroni-adjusted significance threshold. In a pooled analysis of the entire sample, three out of five yielded a significant p-value, and the top association signal (p-value = 0.004) was seen for a CpG that was not originally measured in the discovery EWAS. However, four ANGPT1 CpG sites had an opposite effect direction in the replication analysis compared to the discovery EWAS, marking a failure of replication. We carefully examined this observed flip in directions and propose several possible explanations in addition to that it was a random chance that ANGPT1 ranked at the top in the discovery EWAS. We failed to demonstrate a significant and consistent effect of ANGPT1 methylation in DCI risk in two cohorts. Though the replication attempt to weaken the overall support of this gene, given its relevant function and top rank of significance in the EWAS, our results call for future studies of larger aSAH cohorts to determine its relevance for the occurrence of DCI.
| S-EPMC8967216 | biostudies-literature