Hematoma Volume Change Research Articles

Aquaporin 2 in Cerebral Edema: Potential Prognostic Marker in Craniocerebral Injuries.

Despite continuous medical advancements, traumatic brain injury (TBI) remains a leading cause of death and disability worldwide. Consequently, there is a pursuit for biomarkers that allow non-invasive monitoring of patients after cranial trauma, potentially improving clinical management and reducing complications and mortality. Aquaporins (AQPs), which are crucial for transmembrane water transport, may be significant in this context. This study included 48 patients, with 27 having acute (aSDH) and 21 having chronic subdural hematoma (cSDH). Blood plasma samples were collected from the participants at three intervals: the first sample before surgery, the second at 15 h, and the third at 30 h post-surgery. Plasma concentrations of AQP1, AQP2, AQP4, and AQP9 were determined using the sandwich ELISA technique. CT scans were performed on all patients pre- and post-surgery. Correlations between variables were examined using Spearman's nonparametric rank correlation coefficient. A strong correlation was found between aquaporin 2 levels and the volume of chronic subdural hematoma and midline shift. However, no significant link was found between aquaporin levels (AQP1, AQP2, AQP4, and AQP9) before and after surgery for acute subdural hematoma, nor for AQP1, AQP4, and AQP9 after surgery for chronic subdural hematoma. In the chronic SDH group, AQP2 plasma concentration negatively correlated with the midline shift measured before surgery (Spearman's ρ -0.54; p = 0.017) and positively with hematoma volume change between baseline and 30 h post-surgery (Spearman's ρ 0.627; p = 0.007). No statistically significant correlation was found between aquaporin plasma levels and hematoma volume for AQP1, AQP2, AQP4, and AQP9 in patients with acute SDH. There is a correlation between chronic subdural hematoma volume, measured radiologically, and serum AQP2 concentration, highlighting aquaporins' potential as clinical biomarkers.

122 Use of Automated Active and Continuous CSF Irrigation and Drainage for Treatment of Intraventricular Hemorrhage a Retrospective Comparative Study With Volumetric Analysis

INTRODUCTION: Intraventricular hemorrhage (IVH) is a common neurosurgical pathological conditon that can occur in isolation or along with intraparenchymal and subarachnoid hemorrhage and is associated with poor outcome. Hydrocephalus associated with IVH is often treated with external ventricular drain (EVD) placement, although occlusion and replacement of the drain are common. METHODS: A prospectively maintained database was retrospectively searched for consecutive patients who presented with IVH between September 2020 and Febuary 2023 who were treated with an EVD or the IRRAflow. Pretreatment and posttreatment noncontrast computed tomography scans were segmented to determine IVH volumes. Change in hematoma volume, catheter related conversion and infections, in-hospital mortality, shunt dependency, and symptom resolution or improvement were recorded for outcome assessment. RESULTS: A total of 51 patients were included (21 in the active irrigation and drainage [IRRAflow] group vs. 30 in the passive EVD group. Demographic, disease severity, and presenting variables betweeen the groups were statistically similar. Mean hematoma volume change (8.8 ± 11.3 vs. 17.7 ± 19.4 mL, p = 0.0459) of IVH was significantly lower in the EVD group than the IRRAflow group. No. of days catheter was put in was longer in the EVD group compared to IRRAflow (15.2 ± 10.0 vs. 9.4 ± 4.5; p = 0.0019). On multivaritate logistic regression, shunt dependency on follow-up was higher in the passive EVD group compared to active irrigation and drainage group (p = 0.0215). CONCLUSIONS: Active irrigation with drainage along with CSF exchange for IVH patients appears to be superor to passive drainage alone using EVD.

Development and validation of a random forest model to predict functional outcome in patients with intracerebral hemorrhage.

To develop and validate a machine learning (ML)-based model to predict functional outcome in Chinese patients with intracerebral hemorrhage (ICH). This retrospective cohort study enrolled patients with ICH between November 2017 and November 2020. The follow-up period ended in February 2021. The study population was divided into training and testing sets with a ratio of 7:3. All variables were included in the least absolute shrinkage and selection operator (LASSO) regression for feature selection. The selected variables were incorporated into the random forest algorithm to construct the prediction model. The predictive performance of the model was evaluated via the area under the curve (AUC), accuracy, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and calibration curve. A total of 412 ICH patients were included, with 288 in the training set, and 124 in the testing set. Twelve attributes were selected: neurological deterioration, Glasgow Coma Scale (GCS) score at 24 h, baseline GCS score, time from onset to the emergency room, blood glucose, diastolic blood pressure (DBP) change in 24 h, hematoma volume change in 24 h, systemic immune-inflammatory index (SII), systolic blood pressure (SBP) change in 24 h, serum creatinine, serum sodium, and age. In the testing set, the accuracy, AUC, sensitivity, specificity, PPV, and NPV of the model were 0.895, 0.964, 0.872, 0.906, 0.810, and 0.939, respectively. The calibration curves showed a good calibration capability of the model. This developed random forest model performed well in predicting 3-month poor functional outcome for Chinese ICH patients.

Abstract TP130: Effect Of Antifibrinolytic Medication On Hematoma Expansion In Acute Ischemic Stroke Patients With Post Thrombolytic Intracerebral Hemorrhages

Background and Purpose: Antifibrinolytic medications such as the synthetic lysine analogs tranexamic acid and ε-aminocaproic acid inhibit fibrinolysis by attaching to the lysine-binding site of the plasminogen molecule. However, the efficacy of intravenous (IV) antifibrinolytic medication in the prevention of hematoma expansion in acute ischemic stroke patients who develop post thrombolytic intracerebral hemorrhage (ICH) is unclear. Methods: We analyzed the effect of antifibrinolytic medication in acute ischemic stroke patients with post thrombolytic ICH on hematoma expansion over an 8-year period. The Region-of-Interest; method on a Horos Medical Image Viewer (Version 3.3.6) was utilized for hematoma volume measurement on serial computed tomographic scans. We compared changes in hemorrhage volume in patients who did and did not receive IV antifibrinolytic medication. Results: A total of 53 patients (mean age 69.7±14.3, 53% were men) with post thrombolytic ICH were analyzed. Twenty-six patients received antifibrinolytic treatment: 20 and 6 patients received a single IV dose of ε-aminocaproic acid (5 g) or tranexamic acid (1 g), respectively. Ten patients (38%) had a reduction or stabilization in hematoma volume (overall pre and post-treatment volumes were 17.43±16.23 cm3 and 25.14±26.57 cm3 respectively). Mean fibrinogen level in the antifibrinolytic medication group was 277 mg/dL; 3 patients had levels <200 mg/dL. In patients that did not receive antifibrinolytics, 16 (59%) out of 27 patients had a reduction or stabilization in hematoma volume (overall pre and post-treatment volumes were 19.74±32.32 cm3 and 27.15±52.58 cm3 respectively). The mean percent change in hematoma volume with antifibrinolytic medication treatment was 48% and without was 27%. [Figure 1] Conclusion: We did not identify any reduction in any of the measures of hematoma expansion with antifibrinolytic treatment in acute ischemic stroke patients with post thrombolytic ICH.

Abstract WMP23: Dynamic Imaging Of Blood Coagulation Within The Hematoma Of Patients With Acute Intracerebral Hemorrhage

Objective: To serially quantify the blood coagulation within hematoma of patients with hyper-acute intracerebral hemorrhagic (ICH) stroke using non-invasive quantitative susceptibility mapping (QSM) MRI. Introduction: A blood clot is a combination of aggregated red blood cells, fibrin, platelets, hemosiderin, and other cell debris. An accurate evaluation of clot formation within hematoma could advance the clinical management of hematoma expansion, blood pressure management, and reversal of anticoagulants. Post-ICH hemolysis changes the heme iron oxidation state from oxy to deoxyhemoglobin (deoxy-Hb) resulting in unpaired iron electrons on aggregated RBC’s deoxy-Hb inducing magnetic susceptibility (χ). Therefore, a region with a higher number of aggregated RBC deoxy-Hb molecules, the dominant component of clots, will exhibit a higher positive χ susceptibility. We hypothesized that coagulated blood within hematoma will exhibit a higher positive χ in comparison to the non-clotted which can be quantified using quantitative susceptibility mapping (QSM), which is an advanced MRI image-processing algorithm. Methods: For proof of concept, we measured susceptibilities of 5 human blood phantoms with various percentages of the clot. Twenty-four patients with acute spontaneous ICH were enrolled and serially imaged 3 times within 12-24 (T1), 36-48 (T2), and 60-72(T3) hours of last known well (LNW). A 3D anatomical and multi-echo gradient echo images were obtained using a 3T MRI system. Hematoma and edema volumes were segmented and used as a region of interest (ROI). The rate of coagulation was assessed by measuring the change in susceptibilities within the hematoma. Results: The blood phantom exhibited a linear relationship between the percent coagulation and χ (R 2 =0.91). The QSM maps showed a significant increased in hematoma susceptibility over time (T1=0.29 ± 0.04, T2=0.36 ± 0.04, T3= 0.45 ± 0.04 ppm, p<0.0001). The overall average rate of coagulation was 0.00290 ± 0.0029 ppm per hour. No significant change in hematoma volume (18.9 ±3.1 cc) over time. A significant edema growth over time (T1=25.3 ± 3.6, T2= 28.1 ± 3, T3= 32.37 cc, p<0.05). Conclusion: In conclusion, we present novel surrogate imaging markers of coagulation within the hematoma of ICH.

Time Course and Clinical Significance of Hematoma Expansion in Moderate-to-Severe Traumatic Brain Injury: An Observational Cohort Study

BackgroundPreventing intracranial hematoma expansion has been advertised as a possible treatment opportunity in traumatic brain injury (TBI). However, the time course of hematoma expansion, and whether the expansion affects outcome, remains poorly understood. In light of this, the aim of this study was to use 3D volume rendering to determine how traumatic intracranial hematomas expand over time and evaluate its impact on outcome.MethodsSingle-center, population-based, observational cohort study of adults with moderate-to-severe TBI. Hematoma expansion was defined as the change in hematoma volume from the baseline computed tomography scan until the lesion had stopped progressing. Volumes were calculated by using semiautomated volumetric segmentation. Functional outcome was measured by using the 12 month Glasgow outcome scale (GOS).ResultsIn total, 643 patients were included. The mean baseline hematoma volume was 4.2 ml, and the subsequent mean hematoma expansion was 3.8 ml. Overall, 33% of hematomas had stopped progressing within 3 h, and 94% of hematomas had stopped progressing within 24 h of injury. Contusions expanded significantly more, and for a longer period of time, than extra-axial hematomas. There was a significant dose–response relationship between hematoma expansion and 12 month GOS, even after adjusting for known outcome predictors, with every 1-ml increase in hematoma volume associated with a 6% increased risk of 1-point GOS deduction.ConclusionsHematoma expansion is a driver of unfavorable outcome in TBI, with small changes in hematoma volume also impacting functional outcome. This study also proposes a wider window of opportunity to prevent lesion progression than what has previously been suggested.

Tranexamic Acid for Adult Patients with Spontaneous Intracerebral Hemorrhage: A Systematic Review with Meta-analysis.

The effects of tranexamic acid on spontaneous intracerebral hemorrhage in reducing hematoma expansion and mortality as well as its role in thromboembolic complications and in the improvement of functional outcomes remain substantially uncertain. The objective of this systematic review was to evaluate the efficacy and safety of tranexamic acid in patients with spontaneous intracerebral hemorrhage. Several databases were searched from inception up to 20 June, 2021. We included randomized controlled trials that compared tranexamic acid with placebo or no treatment for the management of intracerebral hemorrhage. The primary outcomes were hematoma expansion and 90-day mortality. The secondary outcomes were hemorrhagic volume change, thromboembolic complications, and functional outcomes. Overall, six trials with 2800 patients were included in this meta-analysis. Tranexamic acid was associated with a reduced risk of hematoma expansion (relative risk 0.87, 95% confidence interval [CI] 0.77-0.99, p=0.03, I2=0%, six trials with 2800 participants) and a lessening of hematoma volume change (mean difference -1.28, 95% CI -2.44 to -0.12; p=0.03; I2=0%, four trials with 2626 participants), without a corresponding higher rate of major thromboembolic complications (relative risk 1.20, 95% CI 0.85-1.69; p=0.80; I2=0%, five trials with 2759 participants). The present analysis also demonstrated that tranexamic acid had no effect on reducing 90-day mortality (relative risk 1.02, 95% CI 0.88-1.19; p=0.80; I2=0%, five trials with 2770 participants). In adults with spontaneous intracerebral hemorrhage, tranexamic acid reduced the risk of intracerebral hemorrhage growth compared with the control. The effects on 90-day mortality remained inconclusive. Further studies should report death within 24h and death due to bleeding whenever possible.

Hematoma Expansion and Clinical Outcomes in Patients With Factor-Xa Inhibitor-Related Atraumatic Intracerebral Hemorrhage Treated Within the ANNEXA-4 Trial Versus Real-World Usual Care.

It is unestablished whether andexanet alfa, compared with guideline-based usual care including prothrombin complex concentrates, is associated with reduced hematoma expansion (HE) and mortality in patients with factor-Xa inhibitor-related intracerebral hemorrhage (ICH). We compared the occurrence of HE and clinical outcomes in patients treated either with andexanet alfa or with usual care during the acute phase of factor-Xa inhibitor-related ICH. Data were extracted from the multicenter, prospective, single-arm ANNEXA-4 trial (Andexanet Alfa, a Novel Antidote to the Anticoagulation Effects of Factor Xa Inhibitors) and a multicenter observational cohort study, RETRACE-II (German-Wide Multicenter Analysis of Oral Anticoagulant-Associated Intracerebral Hemorrhage - Part Two). HE was based on computed tomography scans performed within 36 hours from baseline imaging. Inverse probability of treatment weighting was performed to adjust for baseline comorbidities and ICH severity. Patients presenting with atraumatic ICH while receiving apixaban or rivaroxaban within 18 hours of admission were included. Patients with secondary ICH or not fulfilling the inclusion criteria for the ANNEXA-4 trial were excluded. We compared ANNEXA-4 patients, who received andexanet alfa for hemostatic treatment, with RETRACE-II patients who were treated with usual care, primarily administration of prothrombin complex concentrates. Primary outcome was rate of HE defined as relative increase of ≥35%. Secondary outcomes comprised mean absolute change in hematoma volume, as well as in-hospital mortality and functional outcome. Overall, 182 patients with factor-Xa inhibitor-related ICH (85 receiving andexanet alfa versus 97 receiving usual care) were selected for analysis. There were no relevant differences regarding demographic or clinical characteristics between both groups. HE occurred in 11 of 80 (14%) andexanet alfa patients compared with 21 of 67 (36%) usual care patients (adjusted relative risk, 0.40 [95% CI, 0.20-0.78]; P=0.005), with a reduction in mean overall hematoma volume change of 7 mL. There were no statistically significant differences among in-hospital mortality or functional outcomes. Sensitivity analysis including only usual care patients receiving prothrombin complex concentrates demonstrated consistent results. As compared with usual care, andexanet alfa was associated with a lower rate of HE in atraumatic factor-Xa inhibitor-related ICH, however, without translating into significantly improved clinical outcomes. A comparative trial is needed to confirm the benefit on limiting HE and to explore clinical outcomes across patient subgroups and by time to treatment. Registration: URL: https://clinicaltrials.gov; Unique identifier: NCT02329327 and NCT03093233.

Hematoma Expansion Shift Analysis to Assess Acute Intracerebral Hemorrhage Treatments.

Hematoma expansion (HE) is commonly analyzed as a dichotomous outcome in intracerebral hemorrhage (ICH) trials. In this proof-of-concept study, we propose an HE shift analysis model as a method to improve the evaluation of candidate ICH therapies. Using data from the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-2) trial, we performed HE shift analysis in response to intensive blood pressure lowering by generating polychotomous strata based on previously established HE definitions, percentile/absolute quartiles of hematoma volume change, and quartiles of 24-hour follow-up hematoma volumes. The relationship between blood pressure treatment and HE shift was explored with proportional odds models. The primary analysis population included 863 patients. In both treatment groups, approximately one-third of patients exhibited no HE. With the use of a trichotomous HE stratification, the highest strata of ≥33% revealed a 5.8% reduction in hematoma growth for those randomized to intensive therapy (adjusted odds ratio [aOR] 0.77, 95% confidence interval [CI] 0.60-0.99). Using percentile quartiles of hematoma volume change, we observed a favorable shift to reduce growth in patients treated with intensive therapy (aOR 0.73, 95% CI 0.57-0.93). Similarly, in a tetrachotomous analysis of 24-hour follow-up hematoma volumes, shifts in the highest stratum (>21.9 mL) were most notable. Our findings suggest that intensive blood pressure reduction may preferentially mitigate growth in patients at risk of high volume HE. A shift analysis model of HE provides additional insights into the biological effects of a given therapy and may be an additional way to assess hemostatic agents in future studies. ClinicalTrials.gov Identifier:NCT01176565.

A novel rat model of chronic subdural hematoma: Induction of inflammation and angiogenesis in the subdural space mimicking human-like features of progressively expanding hematoma

Pathophysiological mechanisms of chronic subdural hematoma (CSDH) involve localized inflammation, angiogenesis, and dysregulated coagulation and fibrinolysis. The scarcity of reproducible and clinically relevant animal models of CSDH hinders further understanding the underlying pathophysiology and improving new treatment strategies. Here, we developed a novel rat model of CSDH using extracellular matrices (Matrigel) and brain microvascular endothelial cell line (bEnd.3 cells). One hundred-microliter of Matrigel-bEnd.3 cell (106 cells per milliliter) mixtures were injected into the virtual subdural space of elderly male Sprague-Dawley rats. This approach for the first time led to a spontaneous and expanding subdural hematoma, encapsulated by internal and external neomembranes, formed as early as 3 d, reached its peak at 7 d, and lasted for more than 14 d, mimicking the progressive hemorrhage observed in patients with CSDH. The external neomembrane and hematoma fluid involved numerous inflammatory cells, fibroblasts, and highly fragile neovessels. Furthermore, a localized pathophysiological process was validated as evidenced by the increased expressions of inflammatory and angiogenic mediators in external neomembrane and hematoma fluid rather than in peripheral blood. Notably, the specific expression profiles of these mediators were closely associated with the dynamic changes in hematoma volume and neurological outcome. In summary, the CSDH model described here replicated the characteristics of human CSDH, and might serve as an ideal translational platform for preclinical studies. Meanwhile, the crucial roles of angiogenesis and inflammation in CSDH formation were reaffirmed.

Tranexamic Acid Inhibits Hematoma Expansion in Intracerebral Hemorrhage and Traumatic Brain Injury. Does Blood Pressure Play a Potential Role? A Meta-Analysis from Randmized Controlled Trials

BackgroundTranexamic acid (TXA) is an antifibrinolytic agent, which has shown an effect on reducing blood loss in many diseases. Many studies focus on the effect of TXA on cerebral hemorrhage, however, whether TXA can inhibit hematoma expansion is still controversial. Our meta-analysis performed a quantitative analysis to evaluate the efficacy of TXA for the hematoma expansion in spontaneous and traumatic intracranial hematoma. MethodPubmed (MEDLINE), Embase, and Cochrane Library were searched from January 2001 to May 2020 for randomized controlled trials (RCTs). ResultWe pooled 3102 patients from 7 RCTs to evaluate the efficacy of TXA for hematoma expansion. Hematoma expansion (HE) rate and hematoma volume (HV) change from baseline were used to analyze. We found that TXA led to a significant reduction in HE rate (P = 0.002) and HV change (P = 0.03) compared with the placebo. Patients with moderate or serious hypertension benefit more from TXA. (HE rate: P = 0.02, HV change: P = 0.04) TXA tends to have a better efficacy on HV change in intracerebral hemorrhage (ICH). (P = 0.06) ConclusionsTXA showed good efficacy for hematoma expansion in spontaneous and traumatic intracranial hemorrhage. Patients with moderate/severe hypertension and ICH may be more suitable for TXA administration in inhibiting hematoma expansion .

Mouse nerve growth factor promotes neurological recovery in patients with acute intracerebral hemorrhage: A proof-of-concept study

Backgroundew drugs were confirmed to be effective in the treatments of neurological dysfunction caused by acute intracerebral hemorrhage (ICH). The present prospective clinical trial aims to evaluate the effect of mouse nerve growth factor (mNGF) on neurological function in patients with acute ICH. Methods60 patients with acute spontaneous ICH were randomized to receive mNGF (mNGF group) and citicoline (control group) for 4 weeks within 24–72 h after onset, respectively. The primary outcome was difference in the neurological functional outcome at 3 months by the modified Rankin Scale score (mRS). The secondary outcomes were the changes in hematoma volume at 4 weeks and 3 months. ResultsThere were 55 patients receiving treatment (29 patients in the mNGF group, 26 patients in the control group). Among the patients, 46 patients finished the trial at 3 months; the odds of a shift towards death or dependence (mRS > 3) at 3 months in the mNGF group were lower than that in the control group with adjustment for age, sex, NIHSS at admission, and hematoma volume at admission (adjusted OR, 0.185; 95%CI, 0.059–0.582; P = 0.0039). The hematoma was gradually reduced in all 46 patients and absorbed after non-surgical treatment at 3 months. There was no significant difference in hematoma volume between the two groups. No serious adverse event was found. ConclusionsThe administration of mNGF and citicoline was well-tolerated in patients with acute ICH. mNGF was associated with improved neurological function and less disability in patients with ICH. Therefore, the quality of life of patients with ICH may be improved by mNGF. Trial registrationThe trial is registered with the Chinese Clinical Trial Registry, number ChiCTR1800020258.

The dynamics of hematoma surface regularity and hematoma expansion in acute intracerebral hemorrhage

The clarification of factors that contribute to hematoma expansion in the setting of intracerebral hemorrhage (ICH) and the relevant physical dynamics are implemental for development of management strategies. Herein, we assessed the interplay between hematoma expansion and surface regularity of intracerebral bleeds. To do so, hematoma contours were outlined on admission and follow-up computed tomography (CT) studies using semi-automated thresholding algorithms in 133 ICH patients. Hematoma volume, surface area and surface regularity [SR=6√πvolumesurfacearea3, ranging from 0 (very irregular surface) to 1 (perfectly regular surface suggestive of 3D spherical structure)] were determined by 3D Slicer software (www.slicer.org). Hematoma growth was defined as ≥33% relative growth, or ≥ 6 mL absolute growth. Our results are as follows: The median (IQR) hematoma volume was 14.2 (6.0–34.9) mL on admission CT obtained 2.4 (1.5–4.4) hours after symptom onset; the mean ± SD SR value was calculated as 0.62 ± 0.14. Patients who underwent imaging at earlier time points were more likely to have higher SR (r = 0.18; p = 0.035). The median hematoma volume at follow-up, 35 (21–47) hours after the initial scan, was 19.7 (6.9–44.4) mL. The regularity index decreased significantly at this time point to 0.58 ± 0.13 (p < 0.001) and corresponding increase of surface irregularity was independent of change in hematoma volume. Baseline hematoma volume, INR, and time to initial imaging were significant predictors of hematoma expansion. In conclusion, our findings suggest that hematomas evolve into more irregular 3D shapes during follow-up. These observations are consistent with the ‘domino’ hypothesis put forward for ICH expansion.

Effects of Andexanet Alfa on Thrombin Generation in Bleeding Associated with Factor Xa Inhibitors

Effects of Andexanet Alfa on Thrombin Generation in Bleeding Associated with Factor Xa Inhibitors

Therapeutic effect of early intensive antihypertensive treatment on rebleeding and perihematomal edema in acute intracerebral hemorrhage.

To observe the effect of early intensive blood pressure (BP)-lowering treatment on rebleeding and perihematomal edema (PE) in patients with acute intracerebral hemorrhage (ICH). A total of 121 patients with ICH were randomly assigned to an early intensive antihypertensive treatment group (IG) (n=62) or control group (CG) (n=59). For both groups, 25mg of urapidil injection was slowly administered intravenously in 6hours of the onset. For the IG, 100mg of urapidil and 30mL of 0.9% sodium chloride were then slowly administered. Repeat computed tomography imaging was performed at 24hours, 72hours, day 7, and day 14 to detect any rebleeding via changes in hematoma volume and the changes in PE. Finally, NIHSS scores and Barthel Index (BI) were calculated at 24hours, 72hours, day 7, day 14, day 30, and day 90. The average hematoma volume in IG patients was significantly smaller than that of CG patients after 24hours (P<.05). The volume of PE in the CG increased more than in the IG within 24hours of onset, but was not statistically significant (P>.05); however, this trend was statistically significant after 72hours (P<.05). On day 30 and day 90, the average NIHSS score of IG patients was lower than that of CG patients, and the BI was higher (P<.05) than that of CG patients. There was no significant difference in mortality between the two groups. Early intensive antihypertensive treatment in ICH patients reduces rebleeding and PE, improving short-term quality of life.

Abstract TP426: Description of Early Hematoma Expansion Trajectory and Rate of Expansion in Patients With Intracranial Hemorrhage

Introduction: Expansion of intracerebral hemorrhage (ICH) is associated with increased disability and mortality. The trajectory and rate of hematoma expansion (HE) have not been well described. We evaluated ultra-early baseline and follow up CT and MRI scans to describe the direction and rate of expansion. Methods: We analyzed consecutive ICH patients enrolled in the multicenter, NIH Field Administration of Stroke Therapy-Magnesium (FAST-MAG) clinical trial with baseline and follow up imaging between 6 to 48 hours. HE was defined as growth more than 33% or more than 6mL. Topographic locations were determined using x-, y-, and z- coordinates on OsiriX software. Direction of HE was described by a change in coordinates and correlated with anatomic location. Hematoma growth (HG) rate was described as hematoma volume divided by symptoms onset to scan time in hours. HE rate was described as change in hematoma volume between initial and follow up imaging divided by the time lapse in hours. Results: There were 387 patients with intracerebral hemorrhage enrolled in the FAST-MAG clinical trial. 260 patients had initial and follow up imaging without undergoing hematoma evacuation. The median age was 64, 176 (66.7%) were male. 97 patients were on antiplatelets and 25 were on anticoagulation. Median SBP on admission was 178 and median DBP was 95. 80 (30.7%) patients demonstrated hematoma expansion. The most common location observed was the basal ganglia (69.6%). These hemorrhages tend to expand in all x-, y- and z- coordinates with the greatest change in z- expanding cortically through the corona radiata. There is a high rate of intraventricular hemorrhage (51.5%). Average HG rate was 18.09mL/hr (17.9) and the average HE rate was 1.37mL/hr (1.86). Interestingly, basal ganglia and thalamic hemorrhages had higher rates of expansion. Both HG rate and HE rate were influenced by changes in blood pressure and use of antiplatelets or anticoagulantion. Conclusion: Hematoma expansion location can be predicted based on the location of the initial hemorrhage location. Hematoma trajectory and HE rate can help predict poor outcomes in ICH.

Safety and Efficacy of Atorvastatin for Chronic Subdural Hematoma in Chinese Patients

Chronic subdural hematoma (CSDH) is a trauma-associated condition commonly found in elderly patients. Surgery is currently the treatment of choice, but it carries a significant risk of recurrence and death. Nonsurgical treatments remain limited and ineffective. Our recent studies suggest that atorvastatin reduces hematomas and improves the clinical outcomes of patients with CSDH. To investigate the safety and therapeutic efficacy of atorvastatin to nonsurgically treat patients with CSDH. The Effect of Atorvastatin on Chronic Subdural Hematoma (ATOCH) randomized, placebo-controlled, double-blind phase II clinical trial was conducted in multiple centers in China from February 2014 to November 2015. For this trial, we approached 254 patients with CSDH who received a diagnosis via a computed tomography scan; of these, 200 (78.7%) were enrolled because 23 patients (9.1%) refused to participate and 31 (12.2%) were disqualified. Patients were randomly assigned to receive either 20 mg of atorvastatin or placebo daily for 8 weeks and were followed up for an additional 16 weeks. The primary outcome was change in hematoma volume (HV) by computed tomography after 8 weeks of treatment. The secondary outcomes included HV measured at the 4th, 12th, and 24th weeks and neurological function that was evaluated using the Markwalder grading scale/Glasgow Coma Scale and the Barthel Index at the 8th week. One hundred ninety-six patients received treatment (169 men [86.2%]; median [SD] age, 63.6 [14.2] years). The baseline HV and clinical presentations were similar between patients who were taking atorvastatin (98 [50%]) and the placebo (98 [50%]). After 8 weeks, the HV reduction in patients who were taking atorvastatin was 12.55 mL more than those taking the placebo (95% CI, 0.9-23.9 mL; P = .003). Forty-five patients (45.9%) who were taking atorvastatin significantly improved their neurological function, but only 28 (28.6%) who were taking the placebo did, resulting in an adjusted odds ratio of 1.957 for clinical improvements (95% CI, 1.07-3.58; P = .03). Eleven patients (11.2%) who were taking atorvastatin and 23 (23.5%) who were taking the placebo underwent surgery during the trial for an enlarging hematoma and/or a deteriorating clinical condition (hazard ratio, 0.47; 95% CI, 0.24-0.92; P = .03). No significant adverse events were reported. Atorvastatin may be a safe and efficacious nonsurgical alternative for treating patients with CSDH. ClinicalTrials.gov Identifier: NCT02024373.

Reader response: Magnesium, hemostasis, and outcomes in patients with intracerebral hemorrhage.

We read with interest the article by Liotta et al.,1 in which lower admission serum magnesium (ASM) was associated with worse outcomes in spontaneous intracerebral hemorrhage (SICH). We reevaluated the prognostic role of ASM in 395 SICH patients in the West China Hospital during 2011 and 2016: 269 male (68.1%), mean age of 57.63 (13.06) years, hematoma volume of 25.599 (25.452) mL, Glasgow Coma Scale (GCS) of 12, and ASM of 2.030 (0.368) mg/dL. With t tests, 91 patients with favorable outcomes had higher ASM levels (2.111 [0.438] vs 2.006 [0.341] mg/dL, p = 0.016); lower ASM levels were found in 97 patients who died within 30 days (2.062 [0.387] vs 1.931 [0.279] mg/dL, p = 0.002). After adjusting for the factors seen in Liotta et al., the GCS (odds ratio [OR] 0.711, 95% confidence interval [CI] 0.652–0.777, p < 0.001), hematoma volume (OR 1.012, 95% CI 1.000–1.025, p = 0.049), hematoma volume change (OR 2.102, 95% CI, 1.637–2.699, p < 0.001), and ASM (OR 0.673, 95% CI, 0.490–0.924, p = 0.015) were associated with 30-day mortality. Moreover, the GCS (OR 0.642, 95% CI 0.554–0.744, p < 0.001) and hematoma volume (OR 1.034, 95% CI 1.013–1.056, p = 0.001) were associated with 3-month outcomes, which kept with previous studies.1–3 However, ASM was not a predictor for 3-month outcomes (OR 0.519, 95% CI 0.099–2.713, p = 0.437). Therefore, our findings add new and important data (i.e., ASM is associated with 30-day mortality) to the literature. However, the association of ASM and 3-month outcomes needs further study.

Abstract WP342: Description of Pericavity Edema in Patients With Intracerebral Hemorrhage Who Have Undergone Endoscopic Minimally Invasive Evacuation

Introduction: Perihematomal edema (PHE) impacts outcome in spontaneous intracerebral hemorrhage (ICH) and has been well defined. As minimally invasive evacuation methods are formally evaluated, the degree of edema following evacuation may differ from PHE in measurement and time course characteristics. Here we define pericavity edema (PCE) as a new entity and formally evaluate its measurement with a semi-automated threshold-guided technique. Methods: Patients (n=46) with a primary supratentorial ICH who underwent endoscopic evacuation were included in this study. AnalyzePro software was used to perform semi-automated threshold-guided volume assessment on pre and post evacuation noncontrast head CTs of the hematoma, PHE, the cavity, PCE, and pneumocephalus if present. Two raters analyzed each subject, the first twice, and intraclass correlation coefficient (ICC) values were determined to assess the inter-rater reliability. Statistical analysis was performed on the mean results to determine the change in hematoma volume, edema, cavity size, and degree of pneumocephalus. Results: ICC values for all variables were greater than 0.75, indicating good to excellent reliability. The median preoperative PHE was 18.21 cm3, while the postoperative edema was 16.2cm3. There was a mean 78.9% decrease in hematoma and a mean 76.4% increase in edema. In patients with a cavity present, the median size was 10.4cm3. Conclusions: In conclusion, PCE was successfully measured using AnalyzePro based on ICC. A mean increase in edema was shown following endoscopic evacuation, similar previous research revealing an increase in edema volume growth immediately following ICH. Further research will aim to define the time course of edema volume change following endoscopic evacuation.

Effects of Atorvastatin on Conservative and Surgical Treatments of Chronic Subdural Hematoma in Patients

To investigate effects of atorvastatin on conservative and surgical treatment of patients with chronic subdural hematoma. A retrospective analysis was performed of 109 patients (including 3 outpatients) with chronic subdural hematoma at Northern Jiangsu People's Hospital from April 2014 to October 2015. Patients' gender, age, Glasgow Coma Scale score, symptoms, history of antiplatelet or anticoagulant use, hematoma location, volume of hematoma, operation methods, and application of atorvastatin and its duration were recorded. Prognostic indicators including changes in hematoma volume and neurologic status were extracted. Statistical methods were conducted to evaluate drug efficacy. Seven conservative patients received atorvastatin for 1-6 months (range, 3.57 ± 1.72 months). The volume of hematomas was ± 4.49 mL to 11.40 ± 4.46 mL (P > 0.05) after 1 month's atorvastatin treatment. Hematomas disappeared after 6 months in all 7 patients. In surgical patients, gender (P= 0.797), age (P= 0.063), Glasgow Coma Scale score (P= 0.216), history of antiplatelet or anticoagulant (P= 0.350), volume of hematoma after admission (P= 0.896), location (P= 0.282), and operation methods (P= 0.832) were nonsignificantly associated with follow-up groups, but atorvastatin was significantly associated with follow-up results (P= 0.045). Atorvastatin has preliminarily been proved to be safe and effective for chronic subdural hematomas in both conservative and surgical patients and can provide a drug treatment strategy for neurosurgeons.