Background and Purpose-While the evolution of mass effect after cerebral infarction is well characterized, similar data regarding intracerebral hemorrhage (ICH) are scant. Our goal was to determine the time course and cause for progression of mass effect after ICH. Methods-Patients with spontaneous supratentorial ICH who underwent Ն2 CT scans were identified in our prospectively collected database. CT lesion size and midline shift of the pineal and septum pellucidum were retrospectively measured and correlated with clinical and CT characteristics. Causes for increased midline shift were determined by 2 independent observers. Results-Seventy-six patients underwent 235 scans (3.1Ϯ1.3 per patient). Initial CT was obtained within 24 hours of ICH in 66. Twenty-five scans were repeated on day 1, 80 on days 2 through 7, 31 on days 8 through 14, and 24 Ͼ14 days after ICH. Midline shift was present on 88% of the initial scans. There were 17 instances of midline shift progression: 10 occurred early (0.2 to 1.7 days) and were associated with hematoma enlargement, and 7 occurred late (9 to 21 days) and were associated with edema progression. Progression of mass effect due to edema occurred with larger hemorrhages (PϽ0.05). Of 65 scans repeated for clinical deterioration, only 10 were associated with increased mass effect. Conclusions-Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks, associated with increase in edema. The clinical significance of later-developing edema is unclear.

Background and Purpose-Although several factors have been identified that predict outcome after intracerebral hemorrhage (ICH), no previous study has investigated the impact of hydrocephalus. The purpose of this study was to determine whether the presence of hydrocephalus after ICH would predict mortality and functional outcome. Methods-Patients with spontaneous supratentorial ICH were identified in our prospectively collected database to determine the following: age, sex, race, past medical history; Glasgow Coma Scale (GCS) score and blood pressure on admission; use of mechanical ventilation, mannitol, and ventriculostomy; and medical complications. CT scans performed within 24 hours of hemorrhage were retrospectively analyzed to determine lesion size and location, pineal shift, cisternal effacement, intraventricular hemorrhage (IVH), and hydrocephalus. Outcome was determined with use of hospital disposition (dead, nursing home, rehabilitation, home) and functional outcome (Functional Independence Measure [FIM]) at 3 months. Patients with and without hydrocephalus were compared and univariate and multivariate analyses performed to determine whether hydrocephalus was an independent predictor of mortality. Data are presented as meanϮSD. Results-Of the 81 patients studied, 40 had hydrocephalus. Those with hydrocephalus were younger (57Ϯ15 versus 67Ϯ15 years), had lower GCS scores (8.2Ϯ4.2 versus 11Ϯ2.9), were more likely to have ganglionic or thalamic hemorrhages, and were intubated more frequently (70% versus 27%). Hospital mortality was higher in patients with hydrocephalus (51% versus 2%), and fewer patients went home (21% versus 35%). Those who died had higher hydrocephalus scores (9.67Ϯ7.1 versus 5.75Ϯ4.5). Outcome was no different if a ventriculostomy was placed. The final logistic regression model included hydrocephalus score, gender, GCS, and pineal shift, and it correctly predicted 85% of patients as dead or alive. Multivariate analyses indicated that hydrocephalus is an independent predictor of mortality. Conclusions-We conclude that hydrocephalus is an independent predictor of mortality after ICH. (Stroke.1998;29:1352-1357.)

A zone of hypoperfusion surrounding acute intracerebral hemorrhage (ICH) has been interpreted as regional ischemia. To determine if ischemia is present in the periclot area, the authors measured cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) with positron emission tomography (PET) in 19 patients 5 to 22 hours after hemorrhage onset. Periclot CBF, CMRO2, and OEF were determined in a 1-cm-wide area around the clot. In the 16 patients without midline shift, periclot data were compared with mirror contralateral regions. All PET images were masked to exclude noncerebral structures, and all PET measurements were corrected for partial volume effect due to clot and ventricles. Both periclot CBF and CMRO2 were significantly reduced compared with contralateral values (CBF: 20.9 +/- 7.6 vs. 37.0 +/- 13.9 mL 100 g(-1) min(-1), P = 0.0004; CMRO2: 1.4 +/- 0.5 vs. 2.9 +/- 0.9 mL 100 g(-1) min(-1), P = 0.00001). Periclot OEF was less than both hemispheric OEF (0.42 +/- 0.15 vs. 0.47 +/- 0.13, P = 0.05; n = 19) and contralateral regional OEF (0.44 +/- 0.16 vs. 0.51 +/- 0.13, P = 0.05; n = 16). In conclusion, CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia. Thus, the authors found no evidence for ischemia in the periclot zone of hypoperfusion in acute ICH patients studied 5 to 22 hours after hemorrhage onset.

SummaryBackgroundIntracerebral haemorrhage growth is associated with poor clinical outcome and is a therapeutic target for improving outcome. We aimed to determine the absolute risk and predictors of intracerebral haemorrhage growth, develop and validate prediction models, and evaluate the added value of CT angiography.MethodsIn a systematic review of OVID MEDLINE—with additional hand-searching of relevant studies' bibliographies— from Jan 1, 1970, to Dec 31, 2015, we identified observational cohorts and randomised trials with repeat scanning protocols that included at least ten patients with acute intracerebral haemorrhage. We sought individual patient-level data from corresponding authors for patients aged 18 years or older with data available from brain imaging initially done 0·5–24 h and repeated fewer than 6 days after symptom onset, who had baseline intracerebral haemorrhage volume of less than 150 mL, and did not undergo acute treatment that might reduce intracerebral haemorrhage volume. We estimated the absolute risk and predictors of the primary outcome of intracerebral haemorrhage growth (defined as >6 mL increase in intracerebral haemorrhage volume on repeat imaging) using multivariable logistic regression models in development and validation cohorts in four subgroups of patients, using a hierarchical approach: patients not taking anticoagulant therapy at intracerebral haemorrhage onset (who constituted the largest subgroup), patients taking anticoagulant therapy at intracerebral haemorrhage onset, patients from cohorts that included at least some patients taking anticoagulant therapy at intracerebral haemorrhage onset, and patients for whom both information about anticoagulant therapy at intracerebral haemorrhage onset and spot sign on acute CT angiography were known.FindingsOf 4191 studies identified, 77 were eligible for inclusion. Overall, 36 (47%) cohorts provided data on 5435 eligible patients. 5076 of these patients were not taking anticoagulant therapy at symptom onset (median age 67 years, IQR 56–76), of whom 1009 (20%) had intracerebral haemorrhage growth. Multivariable models of patients with data on antiplatelet therapy use, data on anticoagulant therapy use, and assessment of CT angiography spot sign at symptom onset showed that time from symptom onset to baseline imaging (odds ratio 0·50, 95% CI 0·36–0·70; p<0·0001), intracerebral haemorrhage volume on baseline imaging (7·18, 4·46–11·60; p<0·0001), antiplatelet use (1·68, 1·06–2·66; p=0·026), and anticoagulant use (3·48, 1·96–6·16; p<0·0001) were independent predictors of intracerebral haemorrhage growth (C-index 0·78, 95% CI 0·75–0·82). Addition of CT angiography spot sign (odds ratio 4·46, 95% CI 2·95–6·75; p<0·0001) to the model increased the C-index by 0·05 (95% CI 0·03–0·07).InterpretationIn this large patient-level meta-analysis, models using four or five predictors had acceptable to good discrimination. These models could inform the location and frequency of observations on patients in clinical practice, explain treatment effects i...

Non–vitamin K oral anticoagulants (NOACs) are now widely used as alternatives to warfarin for stroke prevention in atrial fibrillation and management of venous thromboembolism. In clinical practice, there is still widespread uncertainty on how to manage patients on NOACs who bleed or who are at risk for bleeding. Clinical trial data related to NOAC reversal for bleeding and perioperative management are sparse, and recommendations are largely derived from expert opinion. Knowledge of time of last ingestion of the NOAC and renal function is critical to managing these patients given that laboratory measurement is challenging because of the lack of commercially available assays in the United States. Idarucizumab is available as an antidote to rapidly reverse the effects of dabigatran. At present, there is no specific antidote available in the United States for the oral factor Xa inhibitors. Prothrombin concentrate may be considered in life-threatening bleeding. Healthcare institutions should adopt a NOAC reversal and perioperative management protocol developed with multidisciplinary input.