Abstract:Background and Purpose
Rapid recognition of those at high-risk for malignant edema after stroke would facilitate triage for monitoring and potential surgery. Admission data may be insufficient for accurate triage decisions. We developed a risk prediction score using clinical and radiographic variables within 24 hours of ictus to better predict potentially lethal malignant edema (PLME).
Methods
Patients admitted with diagnosis codes of “Cerebral Edema” and “Ischemic Stroke,” NIHSS ≥ 8, and head CTs within 24 … Show more
“…We identi ed four independent predictors of MCE in this study, The three of which were consistent with previous studies, including NIHSS, MLS and ACA territory involvement (17,18). The association between KAF and MCE is still controversial.…”
Section: Discussionsupporting
confidence: 85%
“…Furthermore, traditional scoring model of MCE enrolled NHISS and MLS as categorical variables for the convenience of clinical use, which may end up degrading the precision (15)(16)(17)(18). Nomogram can get rid of that limitation but is not as clinically accessible as scoring model.…”
Background: For large hemispheric infarction (LHI), malignant cerebral edema (MCE) is a life-threatening complication with a mortality rate approaching 80%. Establishing a convenient prediction model of MCE after LHI is vital for the rapid identification of high-risk patients as well as for a better understanding of the potential mechanism underlying MCE.Methods: 142 consecutive patients with LHI within 24h of onset from January 1, 2016 to August 31, 2019 were retrospectively collected. MCE was defined as patient death or received decompressive hemicraniectomy (DHC) with obvious mass effect (≥ 5mm midline shift or Basal cistern effacement). Binary logistic regression was performed to identify independent predictors of MCE. Independent prognostic factors were incorporated to build a dynamic nomogram for MCE prediction. Results: After adjustment for confounders, four independent factors were identified, including previously known atrial fibrillation (KAF), midline shift (MLS), National Institutes of Health Stroke Scale (NIHSS) and anterior cerebral artery (ACA) territory involvement. To facilitate the use of nomogram for clinicians, we use “Dynnom” package to build dynamic MANA (acronym for MLS, ACA territory involvement, NIHSS and KAF) nomogram on web page (http://www.MANA-nom.com) to calculate the exact probability of developing MCE. The c-statistic of MANA nomogram was up to 0.887 ± 0.041 and AUC-ROC value in this cohort was 0.887 (95%CI, 0.828~0.934).Conclusions: Independent predictors of MCE included KAF, MLS, NIHSS, and ACA territory involvement. The dynamic MANA nomogram is a convenient, practical and effective clinical decision-making tool for predicting MCE after LHI in Chinese patients.
“…We identi ed four independent predictors of MCE in this study, The three of which were consistent with previous studies, including NIHSS, MLS and ACA territory involvement (17,18). The association between KAF and MCE is still controversial.…”
Section: Discussionsupporting
confidence: 85%
“…Furthermore, traditional scoring model of MCE enrolled NHISS and MLS as categorical variables for the convenience of clinical use, which may end up degrading the precision (15)(16)(17)(18). Nomogram can get rid of that limitation but is not as clinically accessible as scoring model.…”
Background: For large hemispheric infarction (LHI), malignant cerebral edema (MCE) is a life-threatening complication with a mortality rate approaching 80%. Establishing a convenient prediction model of MCE after LHI is vital for the rapid identification of high-risk patients as well as for a better understanding of the potential mechanism underlying MCE.Methods: 142 consecutive patients with LHI within 24h of onset from January 1, 2016 to August 31, 2019 were retrospectively collected. MCE was defined as patient death or received decompressive hemicraniectomy (DHC) with obvious mass effect (≥ 5mm midline shift or Basal cistern effacement). Binary logistic regression was performed to identify independent predictors of MCE. Independent prognostic factors were incorporated to build a dynamic nomogram for MCE prediction. Results: After adjustment for confounders, four independent factors were identified, including previously known atrial fibrillation (KAF), midline shift (MLS), National Institutes of Health Stroke Scale (NIHSS) and anterior cerebral artery (ACA) territory involvement. To facilitate the use of nomogram for clinicians, we use “Dynnom” package to build dynamic MANA (acronym for MLS, ACA territory involvement, NIHSS and KAF) nomogram on web page (http://www.MANA-nom.com) to calculate the exact probability of developing MCE. The c-statistic of MANA nomogram was up to 0.887 ± 0.041 and AUC-ROC value in this cohort was 0.887 (95%CI, 0.828~0.934).Conclusions: Independent predictors of MCE included KAF, MLS, NIHSS, and ACA territory involvement. The dynamic MANA nomogram is a convenient, practical and effective clinical decision-making tool for predicting MCE after LHI in Chinese patients.
“…This novel action of GBC has been attributed to the blockage of the Sur1-Trpm4 channel, which, when activated, allows ingress of cations into affected cells, resulting in cytotoxic edema, cell lysis, and blood-brain barrier disruption. 17 As expected, oral GBC treatment seemed to prevent the development of brain edema, as reflected in decrease in CED scores. 28 Retrospective studies in diabetics with acute ischemic stroke and used sulfonylurea around the onset have suggested a protective role of sulfonylurea in blood-brain barrier.…”
Section: Discussionsupporting
confidence: 64%
“…After matching, the subjects in these two groups had comparable EDEMA score at baseline, indicating that they had similar risks in developing malignant edema. 17 As expected, oral GBC treatment seemed to prevent the development of brain edema, as reflected in decrease in CED scores. Moreover, we observed a slight trend toward less severe disability and death (mRS of 5 and 6) after GBC treatment, which might partly be attributed to the prevention of brain edema.…”
Section: Discussionsupporting
confidence: 64%
“…20 The stroke subtypes for TOAST and Enhanced Detection of Edema in Malignant Anterior Circulation Stroke (EDEMA) score at admission were obtained to help identifying risk of developing malignant edema at baseline. 17 The severity of brain edema, if presented within 96 hours of admission, was classified into three types based on the radiological appearance: CED 1 (focal edema up to one third of the hemisphere), CED 2 (focal edema greater than one third of the hemisphere), and CED 3 (edema with midline shift). 21 The number of patients receiving antiplatelet and/ or anticoagulant treatment, vasopressor, and mechanical ventilation during hospitalization was also recorded.…”
Objectives
Intravenous glibenclamide (GBC) exerts neuroprotection in both preclinical and preliminary clinical studies. This study explored the safety and potential efficacy of oral GBC in patients with acute hemispheric infarction.
Materials & Methods
During January 2017 and August 2017, adult volunteers were recruited to receive oral GBC treatment, if they presented with an acute anterior ischemic stroke and a National Institute of Health Stroke Score of ≥8. Controls were those who met the above inclusion criteria and had not been on GBC or other sulfonylureas prior to stroke or after hospitalization. Propensity score matching (PSM) was performed to balance baseline characteristics. The primary endpoint was the score on the modified Rankin Scale (mRS) at 6 months.
Results
We included 213 patients in the unmatched cohort (20 in the GBC group and 193 in the control group) and 40 patients (20 in each group) in the matched cohort. In both cohorts, GBC treatment did not increase the risks of early death, hypoglycemia, and early neurological deterioration. Although GBC did not substantially improve 6‐month functional outcome that measured in shift analysis of mRS, a slight trend toward less severe disability and death (mRS 5‐6) was observed. In the matched cohort, GBC treatment was associated with lighter brain edema, when CED score was used for evaluation.
Conclusions
In this study, oral GBC is safe in treating acute hemispheric infarction and might have potential in preventing brain edema and consequential severe disability and death. An adequately powered and randomized trial is warranted.
Objectives To produce a scoring system for predicting the development of edema in ischemic stroke patients without edema on admission. Methods This retrospective study included 572 ischemic stroke patients (73.3 ± 13.0 years, 300 male) without signs of cerebral edema on the first CT scan, which was performed on admission. Another scan was normally performed 3 days later, and subsequently whenever needed. Edema was defined as cerebral hypodensity with compression of lateral ventricles. The main clinical, laboratory, and instrumental variables obtained during the first 24 h were related to the appearance of edema on the CT scans performed after the first one. Results Cerebral edema occurred in 158 patients (27.6%) after a median time of 4 days. The variables independently associated with edema development were (odds ratio, 95% CI) the following: (1) total anterior circulation syndrome (4.20, 2.55-6.93; P < 0.0001), (2) hyperdense appearance of middle cerebral artery (4.12, 2.03-8.36; P = 0.0001), (3) closed eyes (2.53, 1.39-4.60; P = 0.002), ( 4) vomiting (3.53, 1.45-8.60; P = 0.006), ( 5) lacunar cerebral syndrome (0.36, 0.17-0.77; P = 0.008); and (6) white matter lesions (0.53, 0.33-0.86; P = 0.01). Counting one positive point for the first four variables and one negative point for the last two variables, a scoring system (E-score) was built. Cerebral edema could be predicted when the score was ≥ 1 (positive predictive value 61.6%, specificity 85.3%, sensitivity 62.0%). The area under the receiver operating characteristic curve was 0.78. Conclusions In ischemic stroke patients, six variables obtained during the first 24 h of hospitalization were predictive of subsequent cerebral edema development.
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