Shengwen Liu1, Xueyan Wan1, Sheng Wang2, Lulu Huang1, Mingxin Zhu1, Suojun Zhang1, Xing Liu1, Qungen Xiao1, Chao Gan1, Chaoxi Li1, Kai Shu1, Ting Lei1. 1. Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan, Hubei Province, 430030, People's Republic of China. 2. Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan, Hubei Province, 430030, People's Republic of China. wangsheng@tjh.tjmu.edu.cn.
Abstract
BACKGROUND: Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of traumatic brain injury (TBI). This study aimed to evaluate the characteristics and risk factors of PTCI after severe TBI (sTBI) and explore possible mechanism. METHODS: This retrospective study included a cohort of 339 patients with sTBI; they were divided into the PTCI and non-PTCI groups. Clinical data and follow-up charts were reviewed for comparison. The logistic regression model was used for multivariate analysis to detect the risk factors of PTCI. The Glasgow Outcome Scale (GOS) and Barthel index (BI) for activities of daily living (ADL) were applied to evaluate their outcome. RESULTS: PTCI led to an increased mortality (43.5 % vs. 10.7 %, P < 0.001) and days of intensive care unit stay (14.3 days vs. 7.1 days, P < 0.001), decreased GOS (3.1 vs. 4.1, P < 0.001) and BI (25.0 vs. 77.9, P < 0.001). Increased infarction volume led to poor outcome assessed by GOS (r = -0.46, P < 0.0001) and BI for ADL (r = -0.36, P = 0.026) for surviving patients. Compared with non-PTCI patients, PTCI patients had a high incidence of midline shift (36.2 % vs. 20.7 %, P = 0.011) and posttraumatic vasospasm (PTV) (42.0 % vs. 27.4 %, P = 0.027). Daily prevalence of PTCI occurred in two peaks: one (73.9 %) was in the first 24 h after injury, while the other (18.8 %) was in the span of 43 to 60 h postinjury. In multivariate analysis, hyperthermia [adjusted odds ratio (OR), 3.11; P = 0.001] in the first 24 h, thrombocytopenia (OR, 27.08; P < 0.001), abnormal prothrombin time (OR, 7.66; P < 0.001) and traumatic subarachnoid hemorrhage (OR, 2.33; P = 0.022) were independent predictors for PTCI. CONCLUSIONS: PTCI deteriorates the outcome of sTBI patients. Mechanical compression and hemocoagulative disturbance serve as potential mechanisms mediating this pathophysiological process. PTV may also contribute to PTCI, but its association with PTCI is weak and needs further exploration. Early recognition and intervention of these factors might be beneficial for preventing PTCI.
BACKGROUND:Posttraumatic cerebral infarction (PTCI) is a severe secondary insult of traumatic brain injury (TBI). This study aimed to evaluate the characteristics and risk factors of PTCI after severe TBI (sTBI) and explore possible mechanism. METHODS: This retrospective study included a cohort of 339 patients with sTBI; they were divided into the PTCI and non-PTCI groups. Clinical data and follow-up charts were reviewed for comparison. The logistic regression model was used for multivariate analysis to detect the risk factors of PTCI. The Glasgow Outcome Scale (GOS) and Barthel index (BI) for activities of daily living (ADL) were applied to evaluate their outcome. RESULTS:PTCI led to an increased mortality (43.5 % vs. 10.7 %, P < 0.001) and days of intensive care unit stay (14.3 days vs. 7.1 days, P < 0.001), decreased GOS (3.1 vs. 4.1, P < 0.001) and BI (25.0 vs. 77.9, P < 0.001). Increased infarction volume led to poor outcome assessed by GOS (r = -0.46, P < 0.0001) and BI for ADL (r = -0.36, P = 0.026) for surviving patients. Compared with non-PTCIpatients, PTCIpatients had a high incidence of midline shift (36.2 % vs. 20.7 %, P = 0.011) and posttraumatic vasospasm (PTV) (42.0 % vs. 27.4 %, P = 0.027). Daily prevalence of PTCI occurred in two peaks: one (73.9 %) was in the first 24 h after injury, while the other (18.8 %) was in the span of 43 to 60 h postinjury. In multivariate analysis, hyperthermia [adjusted odds ratio (OR), 3.11; P = 0.001] in the first 24 h, thrombocytopenia (OR, 27.08; P < 0.001), abnormal prothrombin time (OR, 7.66; P < 0.001) and traumatic subarachnoid hemorrhage (OR, 2.33; P = 0.022) were independent predictors for PTCI. CONCLUSIONS:PTCI deteriorates the outcome of sTBI patients. Mechanical compression and hemocoagulative disturbance serve as potential mechanisms mediating this pathophysiological process. PTV may also contribute to PTCI, but its association with PTCI is weak and needs further exploration. Early recognition and intervention of these factors might be beneficial for preventing PTCI.
Authors: Nicola Latronico; Simone Piva; Nazzareno Fagoni; Lorenzo Pinelli; Michele Frigerio; Davide Tintori; Maurizio Berardino; Andrea Bottazzi; Livio Carnevale; Tiziana Casalicchio; Carlo Alberto Castioni; Simona Cavallo; Davide Cerasti; Giuseppe Citerio; Marco Fontanella; Serena Galiberti; Alan Girardini; Paolo Gritti; Ornella Manara; Paolo Maremmani; Roberta Mazzani; Giuseppe Natalini; Mirko Patassini; Maria Elena Perna; Ilaria Pesaresi; Danila Katia Radolovich; Maurizio Saini; Roberto Stefini; Cosetta Minelli; Roberto Gasparotti; Francesco A Rasulo Journal: Crit Care Date: 2020-02-03 Impact factor: 9.097