Decompressive Craniectomy for Stroke: Who, When, and How.

Malignant cerebral edema after large hemispheric infarct is a highly morbid condition, and major, randomized trials over the last 2 decades have affirmed the beneficial effect of surgical intervention in the form of decompressive craniectomy. Early (<48 hours) decompressive craniectomy increases good functional outcomes (mRS 0-3) and reduces mortality. Additionally, trials have found the benefit of surgery to persist in those patients more than 60 years, though the apparent benefit is of lesser magnitude. A summary table of the major randomized trials of decompressive craniectomy is included. A detailed description and figures of the decompressive craniectomy procedure is included. The complications of decompressive craniectomy are also discussed, and recent literature on promising alternatives, both surgical and medical, is reviewed.

Initial Stress Hyperglycemia Is Associated With Malignant Cerebral Edema, Hemorrhage, and Poor Functional Outcome After Mechanical Thrombectomy.

BACKGROUND: Malignant cerebral edema (MCE) and intracranial hemorrhage (ICH) are associated with poor neurological outcomes despite revascularization after mechanical thrombectomy (MT). The factors associated with the development of MCE and ICH after MT are not well understood. OBJECTIVE: To determine periprocedural factors associated with MCE, ICH, and poor functional outcome. METHODS: We retrospectively analyzed anterior cerebral circulation large vessel occlusion cases that underwent MT from 2012 to 2019 at a single Comprehensive Stroke Center. Multivariate logistic regression analyses were performed to determine significant predictors of MCE, ICH, and poor functional outcome (modified Rankin Scale, 3-6) at 90 d. RESULTS: Four hundred patients were included. Significant independent predictors of MCE after MT included initial stress glucose ratio (iSGR) (odds ratio [OR], 14.26; 95% CI, 3.82-53.26; P < .001), National Institutes of Health Stroke Scale (NIHSS) (OR, 1.10; 95% CI, 1.03-1.18; P = .008), internal carotid artery compared with M1 or M2 occlusion, and absence of successful revascularization (OR, 0.16; 95% CI, 0.06-0.44; P < .001). Significant independent predictors of poor functional outcome included MCE (OR, 7.47; 95% CI, 2.20-25.37; P = .001), iSGR (OR, 5.15; 95% CI, 1.82-14.53; P = .002), ICH (OR, 4.77; 95% CI, 1.20-18.69; P = .024), NIHSS (OR, 1.10; 95% CI, 1.05-1.16; P < .001), age (OR, 1.04; 95% CI, 1.03-1.07; P < .001), and thrombolysis in cerebral infarction 2C/3 recanalization (OR, 0.12; 95% CI, 0.05-0.29; P < .001). CONCLUSION: Elevated iSGR significantly increases the risk of MCE and ICH and is an independent predictor of poor functional outcome. Thrombolysis in cerebral infarction 2C/3 revascularization is associated with reduced risk of MCE, ICH, and poor functional outcome. Whether stress hyperglycemia represents a modifiable risk factor is uncertain, and further investigation is warranted.

When the Blood Hits Your Brain: The Neurotoxicity of Extravasated Blood.

Hemorrhage in the central nervous system (CNS), including intracerebral hemorrhage (ICH), intraventricular hemorrhage (IVH), and aneurysmal subarachnoid hemorrhage (aSAH), remains highly morbid. Trials of medical management for these conditions over recent decades have been largely unsuccessful in improving outcome and reducing mortality. Beyond its role in creating mass effect, the presence of extravasated blood in patients with CNS hemorrhage is generally overlooked. Since trials of surgical intervention to remove CNS hemorrhage have been generally unsuccessful, the potent neurotoxicity of blood is generally viewed as a basic scientific curiosity rather than a clinically meaningful factor. In this review, we evaluate the direct role of blood as a neurotoxin and its subsequent clinical relevance. We first describe the molecular mechanisms of blood neurotoxicity. We then evaluate the clinical literature that directly relates to the evacuation of CNS hemorrhage. We posit that the efficacy of clot removal is a critical factor in outcome following surgical intervention. Future interventions for CNS hemorrhage should be guided by the principle that blood is exquisitely toxic to the brain.

Low-Dose Intravenous Heparin Infusion After Aneurysmal Subarachnoid Hemorrhage is Associated With Decreased Risk of Delayed Neurological Deficit and Cerebral Infarction.

BACKGROUND: Patients who survive aneurysmal subarachnoid hemorrhage (aSAH) are at risk for delayed neurological deficits (DND) and cerebral infarction. In this exploratory cohort comparison analysis, we compared in-hospital outcomes of aSAH patients administered a low-dose intravenous heparin (LDIVH) infusion (12 U/kg/h) vs those administered standard subcutaneous heparin (SQH) prophylaxis for deep vein thrombosis (DVT; 5000 U, 3 × daily). OBJECTIVE: To assess the safety and efficacy of LDIVH in aSAH patients. METHODS: We retrospectively analyzed 556 consecutive cases of aSAH patients whose aneurysm was secured by clipping or coiling at a single institution over a 10-yr period, including 233 administered the LDIVH protocol and 323 administered the SQH protocol. Radiological and outcome data were compared between the 2 cohorts using multivariable logistic regression and propensity score-based inverse probability of treatment weighting (IPTW). RESULTS: The unadjusted rate of cerebral infarction in the LDIVH cohort was half that in SQH cohort (9 vs 18%; P = .004). Multivariable logistic regression showed that patients in the LDIVH cohort were significantly less likely than those in the SQH cohort to have DND (odds ratio (OR) 0.53 [95% CI: 0.33, 0.85]) or cerebral infarction (OR 0.40 [95% CI: 0.23, 0.71]). Analysis following IPTW showed similar results. Rates of hemorrhagic complications, heparin-induced thrombocytopenia and DVT were not different between cohorts. CONCLUSION: This cohort comparison analysis suggests that LDIVH infusion may favorably influence the outcome of patients after aSAH. Prospective studies are required to further assess the benefit of LDIVH infusion in patients with aSAH.

Utility of the Hijdra Sum Score in Predicting Risk of Aneurysm in Patients With Subarachnoid Hemorrhage: A Single-Center Experience With 550 Patients.

BACKGROUND: Subarachnoid hemorrhage (SAH) is most commonly caused by a ruptured vascular lesion. A significant number of patients presenting with SAH have no identifiable cause despite extensive cerebrovascular imaging at presentation. Significant neurological morbidity or mortality can result from misdiagnosis of aneurysm. OBJECTIVE: To generate a model to assist in predicting the risk of aneurysm in this patient population. METHODS: We conducted a retrospective study of all patients aged ≥18 yr admitted to a single center from March 2008 to March 2018 with nontraumatic SAH (n = 550). Patient information was compared between those with and without aneurysm to identify potential predictors. Odds ratios obtained from a logistic regression model were converted into scores which were summed and tested for predictive ability. RESULTS: Female sex, higher modified Fisher or Hijdra score, nonperimesencephalic location, presence of intracerebral hemorrhage, World Federation of Neurosurgical Societies (WFNS) score ≥3, need for cerebrospinal fluid diversion on admission, and history of tobacco use were all entered into multivariable analysis. Greater modified Fisher, greater Hijdra score, WFNS ≥3, and hydrocephalus present on admission were significantly associated with the presence of an aneurysm. A model based on the Hijdra score and SAH location was generated and validated. CONCLUSION: We show for the first time that the Hijdra score, in addition to other factors, may assist in identifying patients at risk for aneurysm on cerebrovascular imaging. A simple scoring tool based on patient sex, SAH location, and SAH burden can assist in predicting the presence of an aneurysm in patients with nontraumatic SAH.