Eric Peter Thelin1,2, Bo-Michael Bellander3,1, Alexander Fletcher-Sandersjöö4,5, Charles Tatter3,1, Jonathan Tjerkaski1, Jiri Bartek3,1,6, Marc Maegele7,8, David W Nelson9,10, Mikael Svensson3,1. 1. Department of Clinical Neuroscience, Karolinska Institutet, Bioclinicum J5:20, 171 64 , Solna, Stockholm, Sweden. 2. Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. 3. Department of Neurosurgery, Karolinska University Hospital, Stockholm, Sweden. 4. Department of Neurosurgery, Karolinska University Hospital, Stockholm, Sweden. alexander.fletcher-sandersjoo@ki.se. 5. Department of Clinical Neuroscience, Karolinska Institutet, Bioclinicum J5:20, 171 64 , Solna, Stockholm, Sweden. alexander.fletcher-sandersjoo@ki.se. 6. Department of Neurosurgery, Rigshospitalet, Copenhagen, Denmark. 7. Department for Trauma and Orthopedic Surgery, Cologne-Merheim Medical Center, Witten/Herdecke University, Cologne, Germany. 8. Institute for Research in Operative Medicine, Witten/Herdecke University, Cologne, Germany. 9. Department of Physiology and Pharmacology, Section of Perioperative Medicine and Intensive Care, Karolinska Institutet, Stockholm, Sweden. 10. Function Perioperative Care and Medicine, Karolinska University Hospital, Stockholm, Sweden.
Abstract
BACKGROUND: Preventing 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. METHODS: Single-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). RESULTS: In 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. CONCLUSIONS: Hematoma 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.
BACKGROUND: Preventing 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. METHODS: Single-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). RESULTS: In 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. CONCLUSIONS: Hematoma 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.