CTA spot sign predicts hematoma expansion in patients with delayed presentation after intracerebral hemorrhage.

BACKGROUND: Hematoma expansion after acute intracerebral hemorrhage occurs most frequently in patients presenting within 3 h of symptom onset. However, the majority of patients present outside this window or with an unknown onset time. We investigated the prevalence of hematoma expansion in these patients and assessed the accuracy of the CT angiography (CTA) spot sign for identifying risk of hematoma expansion. METHODS: We analyzed 391 consecutive patients undergoing CTA and a followup CT. CTA spot sign readings were performed by two experienced readers and hematoma expansion was assessed by means of semi-automated software. RESULTS: Hematoma expansion occurred in 18 % of patients. When stratified by time from symptom onset to initial CT, hematoma expansion rates were: 39 % within 3 h; 11 % between 3 and 6 h, 11 % beyond 6 h (but with known onset), and 20 % in patients with unknown symptom onset. Of patients who developed hematoma expansion, only 38 % presented within 3 h. The accuracy of the spot sign in predicting hematoma expansion was 0.67 for patients presenting within 3 h, 0.83 between 3 and 6 h, 0.88 after 6 h, and 0.76 for patients presenting with an unknown onset time. CONCLUSIONS: A substantial number of patients destined to suffer from hematoma expansion present either late or with an unknown symptom onset time. The CTA spot sign accurately identifies patients destined to expand regardless of time from symptom onset, and may therefore open a path to offer clinical trials and novel therapies to the many patients who do not present acutely.

A comparison of acute hemorrhagic stroke outcomes in 2 populations: the Crete-Boston study.

BACKGROUND AND PURPOSE: Although corticosteroid use in acute hemorrhagic stroke is not widely adopted, management with intravenous dexamethasone has been standard of care at the University Hospital of Heraklion, Crete with observed outcomes superior to those reported in the literature. To explore this further, we conducted a retrospective, multivariable-adjusted 2-center study. METHODS: We studied 391 acute hemorrhagic stroke cases admitted to the University Hospital of Heraklion, Crete between January 1997 and July 2010 and compared them with 510 acute hemorrhagic stroke cases admitted to Massachusetts General Hospital, Boston, from January 2003 to September 2009. Of the Cretan cases, 340 received a tapering scheme of intravenous dexamethasone, starting with 16 to 32 mg/day, whereas the Boston patients were managed without steroids. RESULTS: The 2 cohorts had comparable demographics and stroke severity on admission, although anticoagulation was more frequent in Boston. The in-hospital mortality was significantly lower on Crete (23.8%, n=340) than in Boston (38.0%, n=510; P<0.001) as was the 30-day mortality (Crete: 25.4%, n=307; Boston: 39.4%, n=510; P<0.001). Exclusion of patients on anticoagulants showed even greater differences (30-day mortality: Crete 20.8%; n=259; Boston 37.0%; n=359; P<0.001). The improved survival on Crete was observed 3 days after initiation of intravenous dexamethasone and was pronounced for deep-seated hemorrhages. After adjusting for acute hemorrhagic stroke volume/location, Glasgow Coma Scale, hypertension, diabetes mellitus, smoking, coronary artery disease and statin, antiplatelet, and anticoagulant use, intravenous dexamethasone treatment was associated with better functional outcomes and significantly lower risk of death at 30 days (OR, 0.357; 95% CI, 0.174-0.732). CONCLUSIONS: This study suggests that intravenous dexamethasone improves outcome in acute hemorrhagic stroke and supports a randomized clinical trial using this approach.

Management of thrombolysis-associated symptomatic intracerebral hemorrhage.

BACKGROUND: Symptomatic intracerebral hemorrhage (sICH) is the most devastating complication of thrombolytic therapy for acute stroke. It is not clear whether patients with sICH continue to bleed after diagnosis, nor has the most appropriate treatment been determined. METHODS: We performed a retrospective analysis of our prospectively collected Get With the Guidelines-Stroke database between April 1, 2003, and December 31, 2007. Radiologic images and all procoagulant agents used were reviewed. Multivariable logistic regression was performed to identify factors associated with in-hospital mortality. RESULTS: Of 2362 patients with acute ischemic stroke during the study period, sICH occurred in 19 of the 311 patients (6.1%) who received intravenous tissue plasminogen activator and 2 of the 72 (2.8%) who received intra-arterial thrombolysis. In-hospital mortality was significantly higher in patients with sICH than in those without (15 of 20 [75.0]% vs 56 of 332 [16.9%], P < .001). Eleven of 20 patients (55.0%) received therapy for coagulopathy: 7 received fresh frozen plasma; 5, cryoprecipitate; 4, phytonadione (vitamin K(1)); 3, platelets; and 1, aminocaproic acid. Independent predictors of in-hospital mortality included sICH (odds ratio, 32.6; 95% confidence interval, 8.8-120.2), increasing National Institutes of Health Stroke Scale score (1.2; 1.1-1.2), older age (1.3; 1.0-1.7), and intra-arterial thrombolysis (2.9; 1.4-6.0). Treatment for coagulopathy was not associated with outcome. Continued bleeding (>33% increase in intracerebral hemorrhage volume) occurred in 4 of 10 patients with follow-up scans available (40.0%). CONCLUSIONS: In many patients with sICH after thrombolysis, coagulopathy goes untreated. Our finding of continued bleeding after diagnosis in 40.0% of patients suggests a powerful opportunity for intervention. A multicenter registry to analyze management of thrombolysis-associated intracerebral hemorrhage and outcomes is warranted.

The spot sign score in primary intracerebral hemorrhage identifies patients at highest risk of in-hospital mortality and poor outcome among survivors.

BACKGROUND AND PURPOSE: The spot sign score is a potent predictor of hematoma expansion in patients with primary intracerebral hemorrhage (ICH). We aim to determine the accuracy of this scoring system for the prediction of in-hospital mortality and poor outcome among survivors in patients with primary ICH. METHODS: Three neuroradiologists retrospectively reviewed CT angiograms (CTAs) performed in 573 consecutive patients who presented to our Emergency Department with primary ICH over a 9-year period to determine the presence and scoring of spot signs according to strict criteria. Baseline ICH and intraventricular hemorrhage volumes were independently determined by computer-assisted volumetric analysis. Medical records were independently reviewed for baseline clinical characteristics and modified Rankin Scale (mRS) at hospital discharge and 3-month follow-up. Poor outcome among survivors was defined as a mRS > or =4 at 3-month follow-up. RESULTS: We identified spot signs in 133 of 573 CTAs (23.2%), 11 of which were delayed spot signs (8.3%). The presence of any spot sign increased the risk of in-hospital mortality (55.6%, OR 4.0, 95% CI 2.6 to 5.9, P<0.0001) and poor outcome among survivors at 3-month follow-up (50.8%, OR 2.5, 95% CI 1.4 to 4.3, P<0.0014). The spot sign score successfully predicted an escalating risk of both outcome measures. In multivariate analysis, the spot sign score was an independent predictor of in-hospital mortality (OR 1.5, 95% CI 1.2 to 1.9, P<0.0002) and poor outcome among survivors at 3-month follow-up (OR 1.6, 95% CI 1.1 to 2.1, P<0.0065). CONCLUSIONS: The spot sign score is an independent predictor of in-hospital mortality and poor outcome among survivors in primary ICH.

Systematic characterization of the computed tomography angiography spot sign in primary intracerebral hemorrhage identifies patients at highest risk for hematoma expansion: the spot sign score.

BACKGROUND AND PURPOSE: The presence of active contrast extravasation (the spot sign) on computed tomography (CT) angiography has been recognized as a predictor of hematoma expansion in patients with intracerebral hemorrhage. We aim to systematically characterize the spot sign to identify features that are most predictive of hematoma expansion and construct a spot sign scoring system. METHODS: We retrospectively reviewed CT angiograms performed in all patients who presented to our emergency department over a 9-year period with primary intracerebral hemorrhage and had a follow-up noncontrast head CT within 48 hours of the baseline CT angiogram. Three neuroradiologists reviewed the CT angiograms and determined the presence and characteristics of spot signs according to strict radiological criteria. Baseline and follow-up intracerebral hemorrhage volumes were determined by computer-assisted volumetric analysis. RESULTS: We identified spot signs in 71 of 367 CT angiograms (19%), 6 of which were delayed spot signs (8%). The presence of any spot sign increased the risk of significant hematoma expansion (69%, OR=92, P<0.0001). Among the spot sign characteristics examined, the presence of > or =3 spot signs, a maximum axial dimension > or =5 mm, and maximum attenuation > or =180 Hounsfield units were independent predictors of significant hematoma expansion, and these were subsequently used to construct the spot sign score. In multivariate analysis, the spot sign score was the strongest predictor of significant hematoma expansion, independent of time from ictus to CT angiogram evaluation. CONCLUSIONS: The spot sign score predicts significant hematoma expansion in primary intracerebral hemorrhage. If validated in other data sets, it could be used to select patients for early hemostatic therapy.

CT angiography for intracerebral hemorrhage does not increase risk of acute nephropathy.

BACKGROUND AND PURPOSE: CT angiography (CTA) is receiving increased attention in intracerebral hemorrhage (ICH) for its role in ruling out vascular abnormalities and potentially predicting ongoing bleeding. Its use is limited by the concern for contrast induced nephropathy (CIN); however, the magnitude of this risk is not known. METHODS: We performed a retrospective analysis of a prospectively collected cohort of consecutive patients with ICH presenting to a single tertiary care hospital from 2002 to 2007. Demographic, clinical, and radiographic data were prospectively collected for all patients. Laboratory data and clinical course over the first 48 hours were retrospectively reviewed. Acute nephropathy was defined as any rise in creatinine of >25% or >0.5 mg/dL, such that the highest creatinine value was above 1.5 mg/dL. RESULTS: 539 patients presented during the study period and had at least 2 creatinine measurements. 348 (65%) received a CTA. Acute nephropathy developed in 6% of patients who received a CTA and in 10% of those who did not (P=0.1). Risk of nephropathy was 14% in those receiving no contrast (130 patients), 5% in those receiving 1 contrast study (124 patients), and 6% in those receiving >1 contrast study (244 patients). Neither CTA nor any use of contrast predicted nephropathy in univariate or multivariate analysis. CONCLUSIONS: The risk of acute nephropathy after ICH was not increased by use of CTA. Studies of CIN that do not include a control group may overestimate the influence of contrast. Patients with ICH appear to have an 8% risk of developing "Hospital-Acquired Nephropathy."