Early Circulating Lactate and Glucose Levels After Aneurysmal Subarachnoid Hemorrhage Correlate With Poor Outcome and Delayed Cerebral Ischemia

2016 ◽  
Vol 44 (5) ◽  
pp. 966-972 ◽  
Author(s):  
Carlina E. van Donkelaar ◽  
Simone A. Dijkland ◽  
Walter M. van den Bergh ◽  
Jan Bakker ◽  
Diederik W. Dippel ◽  
...  
1993 ◽  
Vol 79 (6) ◽  
pp. 885-891 ◽  
Author(s):  
Giuseppe Lanzino ◽  
Neal F. Kassell ◽  
Teresa Germanson ◽  
Laura Truskowski ◽  
Wayne Alves

✓ Plasma glucose levels were studied in 616 patients admitted within 72 hours after subarachnoid hemorrhage (SAH). Glucose levels measured at admission showed a statistically significant association with Glasgow Coma Scale scores, Botterell grade, deposition of blood on computerized tomography (CT) scans, and level of consciousness at admission. Elevated glucose levels at admission predicted poor outcome. A good recovery, as assessed by the Glasgow Outcome Scale at 3 months, occurred in 70.2% of patients with normal glucose levels (≤ 120 mg/dl) and in 53.7% of patients with hyperglycemia (> 120 mg/dl) (p = 0.002). The death rates for these two groups were 6.7% and 19.9%, respectively (p = 0.001). The association was still maintained after adjusting for age (> or ≤ 50 years) and thickness of clot on CT scans (thin or thick) in the subset of patients who were alert/drowsy at admission. Increased mean glucose levels between Days 3 and 7 also predicted a worse outcome; good recovery was observed in 132 (73.7%) of 179 patients who had normal mean glucose levels (≤ 120 mg/dl) and 160 (49.7%) of 322 who had elevated mean glucose levels (> 120 mg/dl) (p < 0.0001). Death occurred in 6.7% and 20.8% of the two groups, respectively (p < 0.0001). It is concluded that admission plasma glucose levels can serve as an objective prognostic indicator after SAH. Elevated glucose levels during the 1st week after SAH also predict a poor outcome. However, a causal link between hyperglycemia and outcome after delayed cerebral ischemia, although suggested by experimental data, cannot be established on the basis of this study.


2020 ◽  
Vol 133 (2) ◽  
pp. 360-368
Author(s):  
Victor M. Lu ◽  
Christopher S. Graffeo ◽  
Avital Perry ◽  
Lucas P. Carlstrom ◽  
Leonardo Rangel-Castilla ◽  
...  

OBJECTIVEDelayed cerebral ischemia (DCI) and aneurysm rebleeding contribute to morbidity and mortality in aneurysmal subarachnoid hemorrhage (aSAH); however, the relationship between their impacts on overall functional outcome is incompletely understood.METHODSThe authors conducted a cohort study of all aSAH during the study period from 2001 to 2016. Primary end points were overall functional outcome and ischemic aSAH sequelae, defined as delayed cerebral ischemia (DCI), DCI with infarction, symptomatic vasospasm (SV), and global cerebral edema (GCE). Outcomes were compared between the rebleed and nonrebleed cohorts overall and after propensity-score matching (PSM) for risk factors and treatment modality. Univariate and multivariate ordered logistic regression analyses for functional outcomes were performed in the PSM cohort to identify predictors of poor outcome.RESULTSFour hundred fifty-five aSAH cases admitted within 24 hours of aneurysm rupture were included, of which 411 (90%) experienced initial aneurysm ruptures only, while 44 (10%) had clinically confirmed rebleeding. In the overall cohort, rebleeding was associated with significantly worse functional outcome, longer intensive care unit length of stay (LOS), and GCE (all p < 0.01); treatment modality, overall LOS, DCI, DCI with infarction, and SV were nonsignificant. In the PSM analysis of 43 matched rebleed and 43 matched nonrebleed cases, only poor functional outcome and GCE remained significantly associated with rebleeding (p < 0.01 and p = 0.02, respectively). Multivariate regression identified that both rebleeding (HR 21.5, p < 0.01) and DCI (HR 10.1, p = 0.01) independently predicted poor functional outcome.CONCLUSIONSRebleeding and DCI after aSAH are highly morbid and potentially deadly events after aSAH, which appear to have independent negative impacts on overall functional outcome. Early rebleeding did not significantly affect the risk of delayed ischemic complications.


2019 ◽  
pp. 1-8 ◽  
Author(s):  
Shinya Fukuda ◽  
Yasutaka Koga ◽  
Motoki Fujita ◽  
Eiichi Suehiro ◽  
Kotaro Kaneda ◽  
...  

OBJECTIVEThe harmful effects of hyperoxemia have been reported in critically ill patients with various disorders, including those with brain injuries. However, the effect of hyperoxemia on aneurysmal subarachnoid hemorrhage (aSAH) patients is unclear. In this study the authors aimed to determine whether hyperoxemia during the hyperacute or acute phase in patients with aSAH is associated with delayed cerebral ischemia (DCI) and poor neurological outcome.METHODSIn this single-center retrospective study, data from patients with aSAH treated between January 2011 and June 2017 were reviewed. The patients were classified into groups according to whether they experienced DCI (DCI group and non-DCI group) and whether they had a poor outcome at discharge (poor outcome group and favorable outcome group). The background characteristics and time-weighted average (TWA) PaO2 during the first 24 hours after arrival at the treatment facility (TWA24h-PaO2) and between the first 24 hours after arrival and day 6 (TWA6d-PaO2), the hyperacute and acute phases, respectively, were compared between the groups. Factors related to DCI and poor outcome were evaluated with logistic regression analyses.RESULTSOf 197 patients with aSAH, 42 patients experienced DCI and 82 patients had a poor outcome at discharge. TWA24h-PaO2 was significantly higher in the DCI group than in the non-DCI group (186 [141–213] vs 161 [138–192] mm Hg, p = 0.029) and in the poor outcome group than in the favorable outcome group (176 [154–205] vs 156 [136–188] mm Hg, p = 0.004). TWA6d-PaO2 did not differ significantly between the groups. Logistic regression analyses revealed that higher TWA24h-PaO2 was an independent risk factor for DCI (OR 1.09, 95% CI 1.01–1.17, p = 0.037) and poor outcome (OR 1.17, 95% CI 1.06–1.29, p = 0.002).CONCLUSIONSHyperoxemia during the first 24 hours was associated with DCI and a poor outcome in patients with aSAH. Excessive oxygen therapy might have an adverse effect in the hyperacute phase of aSAH.


2009 ◽  
Vol 110 (5) ◽  
pp. 989-995 ◽  
Author(s):  
Seppo Juvela ◽  
Jari Siironen ◽  
Jaakko Lappalainen

Object After aneurysmal subarachnoid hemorrhage (SAH), conflicting results concerning an association between the APOE genotype and impaired outcome have been reported. The authors tested prospectively whether APOE ε2 or ε4 allele–containing genotypes (ε2+ and ε4+) affect outcome after SAH. Methods Previous disease histories and clinical and radiological variables were recorded for 105 patients who were admitted within 48 hours after SAH. Fifteen patients (14%) had the ε2+ genotype and 31 (17%) had ε4+ genotypes. Factors predicting poor outcome according to the Glasgow Outcome Scale and cerebral infarction visible on CT scans obtained at 3 months after SAH were tested with multiple logistic regression analyses. Results Apolipoprotein E ε2 or ε4–containing genotypes were not associated with outcome, occurrence of cerebral infarction, or with any of their predictors, either in univariate or multivariate analysis. Poor outcome was predicted independently by the occurrence of intraventricular bleeding and intracerebral hematoma as well as by elevated levels of both plasma glucose and D-dimer, and delayed cerebral ischemia (p < 0.05 for each factor), and in univariate analysis only by clinical condition on admission and patient age. Cerebral infarction was predicted independently according to clinical condition on admission (p < 0.05), amount of subarachnoid blood (p < 0.01), duration of intraoperative parent artery clipping (p < 0.01), and body mass index (p < 0.05). In the univariate analysis only cerebral infarction was also predicted by patient age, intracerebral hematoma, and delayed cerebral ischemia. Conclusions Severity of bleeding for the most part predicts outcome after SAH; APOE polymorphisms seem to have no prognostic value for outcome after SAH. This result was in accordance with the findings from the largest ischemic stroke studies.


2011 ◽  
Vol 31 (6) ◽  
pp. 1443-1451 ◽  
Author(s):  
Nima Etminan ◽  
Mervyn DI Vergouwen ◽  
Don Ilodigwe ◽  
R Loch Macdonald

As it is often assumed that delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is caused by vasospasm, clinical trials often focus on prevention of vasospasm with the aim to improve clinical outcome. However, the role of vasospasm in the pathogenesis of DCI and clinical outcome is possibly smaller than previously assumed. We performed a systematic review and meta-analysis on all randomized, double-blind, placebo-controlled trials that studied the effect of pharmaceutical preventive strategies on vasospasm, DCI, and clinical outcome in SAH patients to further investigate the relationship between vasospasm and clinical outcome. Effect sizes were expressed in pooled risk ratio (RR) estimates with corresponding 95% confidence intervals (CI). A total of 14 studies randomizing 4,235 patients were included. Despite a reduction of vasospasm (RR 0.80 (95% CI 0.70 to 0.92)), no statistically significant effect on poor outcome was observed (RR 0.93 (95% CI 0.85 to 1.03)). The variety of DCI definitions did not justify pooling the DCI data. We conclude that pharmaceutical treatments have significantly decreased the incidence of vasospasm, but not of poor clinical outcome. This dissociation between vasospasm and clinical outcome could result from methodological problems, sample size, insensitivity of clinical outcome measures, or from mechanisms other than vasospasm that also contribute to poor outcome.


2016 ◽  
Vol 125 (6) ◽  
pp. 1383-1389 ◽  
Author(s):  
Paul M. Foreman ◽  
Michelle Chua ◽  
Mark R. Harrigan ◽  
Winfield S. Fisher ◽  
Nilesh A. Vyas ◽  
...  

OBJECTIVE Delayed cerebral ischemia (DCI) is a recognized complication of aneurysmal subarachnoid hemorrhage (aSAH) that contributes to poor outcome. This study seeks to determine the effect of nosocomial infection on the incidence of DCI and patient outcome. METHODS An exploratory analysis was performed on 156 patients with aSAH enrolled in the Cerebral Aneurysm Renin Angiotensin System study. Clinical and radiographic data were analyzed with univariate analysis to detect risk factors for the development of DCI and poor outcome. Multivariate logistic regression was performed to identify independent predictors of DCI. RESULTS One hundred fifty-three patients with aSAH were included. DCI was identified in 32 patients (20.9%). Nosocomial infection (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.09–11.2, p = 0.04), ventriculitis (OR 25.3, 95% CI 1.39–458.7, p = 0.03), aneurysm re-rupture (OR 7.55, 95% CI 1.02–55.7, p = 0.05), and clinical vasospasm (OR 43.4, 95% CI 13.1–143.4, p < 0.01) were independently associated with the development of DCI. Diagnosis of nosocomial infection preceded the diagnosis of DCI in 15 (71.4%) of 21 patients. Patients diagnosed with nosocomial infection experienced significantly worse outcomes as measured by the modified Rankin Scale score at discharge and 1 year (p < 0.01 and p = 0.03, respectively). CONCLUSIONS Nosocomial infection is independently associated with DCI. This association is hypothesized to be partly causative through the exacerbation of systemic inflammation leading to thrombosis and subsequent ischemia.


Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Paul M Foreman ◽  
Michelle Chua ◽  
Mark R Harrigan ◽  
Winfield S Fisher ◽  
Nilesh A Vyas ◽  
...  

Background and Purpose: Delayed cerebral ischemia (DCI) is a recognized complication of aneurysmal subarachnoid hemorrhage (aSAH) that contributes to poor outcome. This study seeks to determine the effect of nosocomial infection on the incidence of DCI and patient outcome. Methods and Subjects: An exploratory analysis was performed on 156 aSAH patients enrolled in the Cerebral Aneurysm Renin Angiotensin System (CARAS) study. Clinical and radiographic data were analyzed with univariate analysis to detect risk factors for the development of DCI and poor outcome. Multivariate logistic regression was performed to identify independent predictors of DCI. Results: One hundred and fifty three patients with aSAH were included. Delayed cerebral ischemia was identified in 32 (20.9%) patients. Nosocomial infection, ventriculitis, aneurysm rerupture, and clinical vasospasm were independently associated with the development of DCI [3.5 (1.93 - 6.35), p < 0.00; 25.3 (4.39 - 110.9), p = 0.03; 7.55 (2.72 - 20.9), p = 0.05; 43.4 (23.6 - 79.8), p < 0.00; respectively]. Diagnosis of nosocomial infection preceded the diagnosis of DCI in 15 of 21 (71.4%) patients. Patients diagnosed with nosocomial infection experienced significantly worse outcomes as measured by mRS at discharge and 1 year (p < 0.00 and p = 0.03, respectively). Conclusions: Nosocomial infection is independently associated with DCI. This association is hypothesized to be partly causative through the exacerbation of systemic inflammation leading to thrombosis and subsequent ischemia.


2021 ◽  
pp. 0271678X2110454
Author(s):  
Masato Naraoka ◽  
Naoya Matsuda ◽  
Norihito Shimamura ◽  
Hiroki Ohkuma

Early brain injury (EBI) is considered an important cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). As a factor in EBI, microcirculatory dysfunction has become a focus of interest, but whether microcirculatory dysfunction is more important than angiographic vasospasm (aVS) remains unclear. Using data from 128 cases, we measured the time to peak (TTP) in several regions of interest on digital subtraction angiography. The intracerebral circulation time (iCCT) was obtained between the TTP in the ultra-early phase (the baseline iCCT) and in the subacute phase and/or at delayed cerebral ischemia (DCI) onset (the follow-up iCCT). In addition, the difference in the iCCT was calculated by subtracting the baseline iCCT from the follow-up iCCT. Univariate analysis showed that DCI was significantly increased in those patients with a prolonged baseline iCCT, prolonged follow-up iCCT, increased differences in the iCCT, and with severe aVS. Poor outcome was significantly increased in patients with prolonged follow-up iCCT and increased differences in the iCCT. Multivariate analysis revealed that increased differences in the iCCT were a significant risk factor that increased DCI and poor outcome. The results suggest that the increasing microcirculatory dysfunction over time, not aVS, causes DCI and poor outcome after aneurysmal aSAH.


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