H Bart Brouwers1, Thomas W K Battey2, Hayley H Musial2, Viesha A Ciura2, Guido J Falcone2, Alison M Ayres2, Anastasia Vashkevich2, Kristin Schwab2, Anand Viswanathan2, Christopher D Anderson2, Steven M Greenberg2, Stuart R Pomerantz2, Claudia J Ortiz2, Joshua N Goldstein2, R Gilberto Gonzalez2, Jonathan Rosand2, Javier M Romero2. 1. From the Department of Neurosurgery, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands (H.B.B.); Center for Human Genetic Research (H.B.B., T.W.K.B., H.H.M., G.J.F., C.D.A., J.R.), Division of Neurocritical Care and Emergency Neurology, Department of Neurology (H.B.B., G.J.F., A. Viswanathan, C.D.A., J.N.G., J.R.), Hemorrhagic Stroke Research Group (H.B.B., T.W.K.B., H.H.M., G.J.F., A.M.A., A. Vashkevich, K.S., A. Viswanathan, C.D.A., S.M.G., J.N.G., J.R.), J. Philip Kistler Stroke Research Center (H.B.B., T.W.K.B., H.H.M., G.J.F., A.M.A., A. Vashkevich, K.S., A. Viswanathan, C.D.A., S.M.G., J.N.G., J.R.), Neuroradiology Service, Department of Radiology (V.A.C., S.R.P., C.J.O., R.G.G., J.M.R.), and Department of Emergency Medicine (J.N.G.), Massachusetts General Hospital, Harvard Medical School, Boston. H.B.Brouwers-4@umcutrecht.nl. 2. From the Department of Neurosurgery, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands (H.B.B.); Center for Human Genetic Research (H.B.B., T.W.K.B., H.H.M., G.J.F., C.D.A., J.R.), Division of Neurocritical Care and Emergency Neurology, Department of Neurology (H.B.B., G.J.F., A. Viswanathan, C.D.A., J.N.G., J.R.), Hemorrhagic Stroke Research Group (H.B.B., T.W.K.B., H.H.M., G.J.F., A.M.A., A. Vashkevich, K.S., A. Viswanathan, C.D.A., S.M.G., J.N.G., J.R.), J. Philip Kistler Stroke Research Center (H.B.B., T.W.K.B., H.H.M., G.J.F., A.M.A., A. Vashkevich, K.S., A. Viswanathan, C.D.A., S.M.G., J.N.G., J.R.), Neuroradiology Service, Department of Radiology (V.A.C., S.R.P., C.J.O., R.G.G., J.M.R.), and Department of Emergency Medicine (J.N.G.), Massachusetts General Hospital, Harvard Medical School, Boston.
Abstract
BACKGROUND AND PURPOSE: In primary intracerebral hemorrhage, the presence of contrast extravasation after computed tomographic angiography (CTA), termed the spot sign, predicts hematoma expansion and mortality. Because the biological underpinnings of the spot sign are not fully understood, we investigated whether the rate of contrast extravasation, which may reflect the rate of bleeding, predicts expansion and mortality beyond the simple presence of the spot sign. METHODS: Consecutive intracerebral hemorrhage patients with first-pass CTA followed by a 90-second delayed postcontrast CT (delayed CTA) were included. CTAs were reviewed for spot sign presence by 2 blinded readers. Spot sign volumes on first-pass and delayed CTA and intracerebral hemorrhage volumes were measured using semiautomated software. Extravasation rates were calculated and tested for association with hematoma expansion and mortality using uni- and multivariable logistic regressions. RESULTS: One hundred and sixty-two patients were included, 48 (30%) of whom had ≥1 spot sign. Median spot sign volume was 0.04 mL on first-pass CTA and 0.4 mL on delayed CTA. Median extravasation rate was 0.23 mL/min overall and 0.30 mL/min among expanders versus 0.07 mL/min in nonexpanders. Extravasation rates were also significantly higher in patients who died in hospital: 0.27 mL/min versus 0.04 mL/min. In multivariable analysis, the extravasation rate was independently associated with in-hospital mortality (odds ratio, 1.09 [95% confidence interval, 1.04-1.18], P=0.004), 90-day mortality (odds ratio, 1.15 [95% confidence interval, 1.08-1.27]; P=0.0004), and hematoma expansion (odds ratio, 1.03 [95% confidence interval, 1.01-1.08]; P=0.047). CONCLUSIONS: Contrast extravasation rate, or spot sign growth, further refines the ability to predict hematoma expansion and mortality. Our results support the hypothesis that the spot sign directly measures active bleeding in acute intracerebral hemorrhage.
BACKGROUND AND PURPOSE: In primary intracerebral hemorrhage, the presence of contrast extravasation after computed tomographic angiography (CTA), termed the spot sign, predicts hematoma expansion and mortality. Because the biological underpinnings of the spot sign are not fully understood, we investigated whether the rate of contrast extravasation, which may reflect the rate of bleeding, predicts expansion and mortality beyond the simple presence of the spot sign. METHODS: Consecutive intracerebral hemorrhagepatients with first-pass CTA followed by a 90-second delayed postcontrast CT (delayed CTA) were included. CTAs were reviewed for spot sign presence by 2 blinded readers. Spot sign volumes on first-pass and delayed CTA and intracerebral hemorrhage volumes were measured using semiautomated software. Extravasation rates were calculated and tested for association with hematoma expansion and mortality using uni- and multivariable logistic regressions. RESULTS: One hundred and sixty-two patients were included, 48 (30%) of whom had ≥1 spot sign. Median spot sign volume was 0.04 mL on first-pass CTA and 0.4 mL on delayed CTA. Median extravasation rate was 0.23 mL/min overall and 0.30 mL/min among expanders versus 0.07 mL/min in nonexpanders. Extravasation rates were also significantly higher in patients who died in hospital: 0.27 mL/min versus 0.04 mL/min. In multivariable analysis, the extravasation rate was independently associated with in-hospital mortality (odds ratio, 1.09 [95% confidence interval, 1.04-1.18], P=0.004), 90-day mortality (odds ratio, 1.15 [95% confidence interval, 1.08-1.27]; P=0.0004), and hematoma expansion (odds ratio, 1.03 [95% confidence interval, 1.01-1.08]; P=0.047). CONCLUSIONS: Contrast extravasation rate, or spot sign growth, further refines the ability to predict hematoma expansion and mortality. Our results support the hypothesis that the spot sign directly measures active bleeding in acute intracerebral hemorrhage.
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