Dewan Michael C, Ravindra Vijay M, Gannon Stephen, Prather Colin T, Yang George L, Jordan Lori C, Limbrick David, Jea Andrew, Riva-Cambrin Jay, Naftel Robert P
*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;79(6):872-878. doi: 10.1227/NEU.0000000000001352.
Pediatric blunt cerebrovascular injury (BCVI) lacks accepted treatment algorithms, and postinjury outcomes are ill defined.
To compare treatment practices among pediatric trauma centers and to describe outcomes for available treatment modalities.
Clinical and radiographic data were collected from a patient cohort with BCVI between 2003 and 2013 at 4 academic pediatric trauma centers.
Among 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.
Treatment 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.
ATT, antithrombotic therapyBCVI, blunt cerebrovascular injuryCTA, computed tomography angiographyGCS, Glasgow Coma Scale.
小儿钝性脑血管损伤(BCVI)缺乏公认的治疗方案,损伤后的结局也不明确。
比较小儿创伤中心的治疗方法,并描述现有治疗方式的结局。
收集了2003年至2013年间4家学术性小儿创伤中心的BCVI患者队列的临床和影像学数据。
在645例接受计算机断层血管造影评估BCVI的小儿患者中,52例患者诊断出57处血管损伤(82%为颈动脉,18%为椎动脉)。Ⅰ级(58%)和Ⅱ级(23%)损伤占大多数病变。10例患者因严重颅内或腹腔内出血而无法进行抗栓治疗。在其余患者中,初始治疗为抗血小板药物的有14例(33%),抗凝治疗的有8例(19%),血管内介入治疗的有3例(7%),开放手术的有1例(2%),未治疗的有16例(38%)。在27例符合条件的Ⅰ级损伤中,16例(59%)未接受治疗,各中心不治疗的选择差异显著(P <.001)。药物治疗无并发症。格拉斯哥昏迷量表(GCS)评分<8分和损伤分级增加是损伤进展的预测因素(分别为P =.001和.004)。GCS评分低(P =.02)、损伤分级增加(P =.03)和合并颅内损伤(P =.02)与死亡风险增加相关。治疗方式与血管损伤进展或死亡率无关。
用抗血小板或抗凝治疗BCVI是安全的,可能有一定益处。不可改变的因素,包括就诊时的GCS评分、血管损伤分级和额外的颅内损伤,仍然是预后不良的最重要预测因素。
ATT,抗栓治疗;BCVI,钝性脑血管损伤;CTA,计算机断层血管造影;GCS,格拉斯哥昏迷量表