• Michael C Dewan, Vijay M Ravindra, Stephen Gannon, Colin T Prather, George L Yang, Lori C Jordan, David Limbrick, Andrew Jea, Jay Riva-Cambrin, and Robert P Naftel.
• *Department of Neurosurgery, Vanderbilt University, Division of Pediatric Neurosurgery, Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee; ‡Department of Neurosurgery, University of Utah School of Medicine, Division of Pediatric Neurosurgery, Primary Children's Hospital, Salt Lake City, Utah; §Department of Pediatrics, Division of Pediatric Neurology, Vanderbilt University, Nashville, Tennessee; ¶Department of Neurosurgery, Washington University in St. Louis, Division of Pediatric Neurosurgery, St. Louis Children's Hospital, St. Louis, Missouri; ‖Department of Neurosurgery, Baylor College of Medicine, Division of Pediatric Neurosurgery, Texas Children's Hospital, Houston, Texas.
• Neurosurgery. 2016 Dec 1; 79 (6): 872-878.

BackgroundPediatric blunt cerebrovascular injury (BCVI) lacks accepted treatment algorithms, and postinjury outcomes are ill defined.ObjectiveTo compare treatment practices among pediatric trauma centers and to describe outcomes for available treatment modalities.MethodsClinical and radiographic data were collected from a patient cohort with BCVI between 2003 and 2013 at 4 academic pediatric trauma centers.ResultsAmong 645 pediatric patients evaluated with computed tomography angiography for BCVI, 57 vascular injuries (82% carotid artery, 18% vertebral artery) were diagnosed in 52 patients. Grade I (58%) and II (23%) injuries accounted for most lesions. Severe intracranial or intra-abdominal hemorrhage precluded antithrombotic therapy in 10 patients. Among the remaining patients, primary therapy was an antiplatelet agent in 14 (33%), anticoagulation in 8 (19%), endovascular intervention in 3 (7%), open surgery in 1 (2%), and no treatment in 16 (38%). Among 27 eligible grade I injuries, 16 (59%) were not treated, and the choice to not treat varied significantly among centers (P < .001). There were no complications from medical management. Glasgow Coma Scale (GCS) score <8 and increasing injury grade were predictors of injury progression (P = .001 and .004, respectively). Poor GCS score (P = .02), increasing injury grade (P = .03), and concomitant intracranial injury (P = .02) correlated with increased risk of mortality. Treatment modality did not correlate with progression of vascular injury or mortality.ConclusionTreatment of BCVI with antiplatelet or anticoagulant therapy is safe and may confer modest benefit. Nonmodifiable factors, including presenting GCS score, vascular injury grade, and additional intracranial injury, remain the most important predictors of poor outcome.AbbreviationsATT, antithrombotic therapyBCVI, blunt cerebrovascular injuryCTA, computed tomography angiographyGCS, Glasgow Coma Scale.

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