Early posttraumatic seizures in pediatric traumatic brain injury: a multicenter analysis

Author(s):  
Shu-Ling Chong ◽  
Suyun Qian ◽  
Sarah Hui Wen Yao ◽  
John Carson Allen ◽  
Hongxing Dang ◽  
...  

OBJECTIVE Early posttraumatic seizures (EPTSs) in children after traumatic brain injury (TBI) increase metabolic stress on the injured brain. The authors sought to study the demographic and radiographic predictors for EPTS, and to investigate the association between EPTS and death, and between EPTS and poor functional outcomes among children with moderate to severe TBI in Asia. METHODS A secondary analysis of a retrospective TBI cohort among participating centers of the Pediatric Acute & Critical Care Medicine Asian Network was performed. Children < 16 years of age with a Glasgow Coma Scale (GCS) score ≤ 13 who were admitted to pediatric intensive care units between January 2014 and October 2017 were included. Logistic regression analysis was performed to study risk factors for EPTS and to investigate the association between EPTS and death, and between EPTS and poor functional outcomes. Poor functional outcomes were defined as moderate disability, severe disability, and coma as defined by the Pediatric Cerebral Performance Category scale. RESULTS Overall, 313 children were analyzed, with a median age of 4.3 years (IQR 1.8–8.9 years); 162 children (51.8%) had severe TBI (GCS score < 8), and 76 children (24.3%) had EPTS. After adjusting for age, sex, and the presence of nonaccidental trauma (NAT), only younger age was significantly associated with EPTS (adjusted odds ratio [aOR] 0.85, 95% CI 0.78–0.92; p < 0.001). Forty-nine children (15.6%) in the cohort died, and 87 (32.9%) of the 264 surviving patients had poor functional outcomes. EPTS did not increase the risk of death. After adjusting for age, sex, TBI due to NAT, multiple traumas, and a GCS score < 8, the presence of EPTS was associated with poor functional outcomes (aOR 2.08, 95% CI 1.05–4.10; p = 0.036). CONCLUSIONS EPTSs were common among children with moderate to severe TBI in Asia and were associated with poor functional outcomes among children who survived TBI.

2021 ◽  
Vol 11 (8) ◽  
pp. 1044
Author(s):  
Cristina Daia ◽  
Cristian Scheau ◽  
Aura Spinu ◽  
Ioana Andone ◽  
Cristina Popescu ◽  
...  

Background: We aimed to assess the effects of modulated neuroprotection with intermittent administration in patients with unresponsive wakefulness syndrome (UWS) after severe traumatic brain injury (TBI). Methods: Retrospective analysis of 60 patients divided into two groups, with and without neuroprotective treatment with Actovegin, Cerebrolysin, pyritinol, L-phosphothreonine, L-glutamine, hydroxocobalamin, alpha-lipoic acid, carotene, DL-α-tocopherol, ascorbic acid, thiamine, pyridoxine, cyanocobalamin, Q 10 coenzyme, and L-carnitine alongside standard treatment. Main outcome measures: Glasgow Coma Scale (GCS) after TBI, Extended Glasgow Coma Scale (GOS E), Disability Rankin Scale (DRS), Functional Independence Measurement (FIM), and Montreal Cognitive Assessment (MOCA), all assessed at 1, 3, 6, 12, and 24 months after TBI. Results: Patients receiving neuroprotective treatment recovered more rapidly from UWS than controls (p = 0.007) passing through a state of minimal consciousness and gradually progressing until the final evaluation (p = 0.000), towards a high cognitive level MOCA = 22 ± 6 points, upper moderate disability GOS-E = 6 ± 1, DRS = 6 ± 4, and an assisted gait, FIM =101 ± 25. The improvement in cognitive and physical functioning was strongly correlated with lower UWS duration (−0.8532) and higher GCS score (0.9803). Conclusion: Modulated long-term neuroprotection may be the therapeutic key for patients to overcome UWS after severe TBI.


2015 ◽  
Vol 122 (1) ◽  
pp. 211-218 ◽  
Author(s):  
Nils Petter Rundhaug ◽  
Kent Gøran Moen ◽  
Toril Skandsen ◽  
Kari Schirmer-Mikalsen ◽  
Stine B. Lund ◽  
...  

OBJECT The influence of alcohol is assumed to reduce consciousness in patients with traumatic brain injury (TBI), but research findings are divergent. The aim of this investigation was to study the effects of different levels of blood alcohol concentration (BAC) on the Glasgow Coma Scale (GCS) scores in patients with moderate and severe TBI and to relate the findings to brain injury severity based on the admission CT scan. METHODS In this cohort study, 265 patients (age range 16–70 years) who were admitted to St. Olavs University Hospital with moderate and severe TBI during a 7-year period were prospectively registered. Of these, 217 patients (82%) had measured BAC. Effects of 4 BAC groups on GCS score were examined with ordinal logistic regression analyses, and the GCS scores were inverted to give an OR > 1. The Rotterdam CT score based on admission CT scan was used to adjust for brain injury severity (best score 1 and worst score 6) by stratifying patients into 2 brain injury severity groups (Rotterdam CT scores of 1–3 and 4–6). RESULTS Of all patients with measured BAC, 91% had intracranial CT findings and 43% had BAC > 0 mg/dl. The median GCS score was lower in the alcohol-positive patients (6.5, interquartile range [IQR] 4–10) than in the alcohol-negative patients (9, IQR 6–13; p < 0.01). No significant differences were found between alcohol-positive and alcohol-negative patients regarding other injury severity variables. Increasing BAC was a significant predictor of lower GCS score in a dose-dependent manner in age-adjusted analyses, with OR 2.7 (range 1.4–5.0) and 3.2 (range 1.5–6.9) for the 2 highest BAC groups (p < 0.01). Subgroup analyses showed an increasing effect of BAC group on GCS scores in patients with Rotterdam CT scores of 1–3: OR 3.1 (range 1.4–6.6) and 6.7 (range 2.7–16.7) for the 2 highest BAC groups (p < 0.01). No such relationship was found in patients with Rotterdam CT scores of 4–6 (p = 0.14–0.75). CONCLUSIONS Influence of alcohol significantly reduced the GCS score in a dose-dependent manner in patients with moderate and severe TBI and with Rotterdam CT scores of 1–3. In patients with Rotterdam CT scores of 4–6, and therefore more CT findings indicating increased intracranial pressure, the brain injury itself seemed to overrun the depressing effect of the alcohol on the CNS. This finding is in agreement with the assumption of many clinicians in the emergency situation.


2021 ◽  
Vol 36 (6) ◽  
pp. 1151-1151
Author(s):  
Justin O'Rourke ◽  
Robert J Kanser ◽  
Marc A Silva

Abstract Objective Studies on Performance Validity Tests (PVTs) for tele-neuropsychology (TeleNP) are sparse. Verbal PVTs appear to better translate to TeleNP, so the primary objective of this study was to provide initial data on two well-established, verbal PVTs administered via TeleNP for research participants with traumatic brain injury (TBI). Methods This secondary analysis of the Veterans Affairs TBI Model Systems data included 53 participants enrolled in a PVT module study (3/01/2020–09/20/2020) with documented moderate-to-severe TBI per Glasgow Coma Score (M = 6.5, SD = 4.4), posttraumatic amnesia duration (M = 42.7 days, SD = 47.1), and/or time to follow commands (M = 10.5 days, SD = 16.3). Participants completed two PVTs—Reliable Digit Span (RDS) and the 21-Item Test (21-IT)—alongside telephone-based cognitive assessment 1–7 years after TBI. Descriptive analyses were performed to compare PVT performances to previously established cut scores. Chi square analyses were employed to examine 21-IT and RDS as dichotomous outcomes (pass/fail) at selected cutoffs. Results RDS ranged from 5 to 16 (M = 10.5, SD = 2.4). 21-IT ranged from 7 to 21 (M = 16.4, SD = 3.1). For RDS, 9.8% were invalid with a cutscore of ≤7 and 19.6% using a cutscore of ≤8. For the 21-IT, 7.8% were in invalid using a cutscore of ≤11, and 13.7% using a cutscore of ≤12. Conclusion(s) Using previously established cut scores, telephone-administered RDS and 21-IT resulted in relatively low rates of invalid performance among individuals with moderate-to-severe TBI. These findings provide preliminary support for the RDS and 21-IT in TeleNP.


2012 ◽  
Vol 117 (4) ◽  
pp. 729-734 ◽  
Author(s):  
Arash Farahvar ◽  
Linda M. Gerber ◽  
Ya-Lin Chiu ◽  
Nancy Carney ◽  
Roger Härtl ◽  
...  

Object Evidence-based guidelines recommend intracranial pressure (ICP) monitoring for patients with severe traumatic brain injury (TBI), but there is limited evidence that monitoring and treating intracranial hypertension reduces mortality. This study uses a large, prospectively collected database to examine the effect on 2-week mortality of ICP reduction therapies administered to patients with severe TBI treated either with or without an ICP monitor. Methods From a population of 2134 patients with severe TBI (Glasgow Coma Scale [GCS] Score <9), 1446 patients were treated with ICP-lowering therapies. Of those, 1202 had an ICP monitor inserted and 244 were treated without monitoring. Patients were admitted to one of 20 Level I and two Level II trauma centers, part of a New York State quality improvement program administered by the Brain Trauma Foundation between 2000 and 2009. This database also contains information on known independent early prognostic indicators of mortality, including age, admission GCS score, pupillary status, CT scanning findings, and hypotension. Results Age, initial GCS score, hypotension, and CT scan findings were associated with 2-week mortality. In addition, patients of all ages treated with an ICP monitor in place had lower mortality at 2 weeks (p = 0.02) than those treated without an ICP monitor, after adjusting for parameters that independently affect mortality. Conclusions In patients with severe TBI treated for intracranial hypertension, the use of an ICP monitor is associated with significantly lower mortality when compared with patients treated without an ICP monitor. Based on these findings, the authors conclude that ICP-directed therapy in patients with severe TBI should be guided by ICP monitoring.


2010 ◽  
Vol 113 (3) ◽  
pp. 539-546 ◽  
Author(s):  
Matthew A. Warner ◽  
Terence O'Keeffe ◽  
Premal Bhavsar ◽  
Rashmi Shringer ◽  
Carol Moore ◽  
...  

Object In this paper, the authors' goal was to examine the relationship between transfusion and long-term functional outcomes in moderately anemic patients (lowest hematocrit [HCT] level 21–30%) with traumatic brain injury (TBI). While evidence suggests that transfusions are associated with poor hospital outcomes, no study has examined transfusions and long-term functional outcomes in this population. The preferred transfusion threshold remains controversial. Methods The authors performed a retrospective review of patients who were admitted with TBI between September 2005 and November 2007, extracting data such as HCT level, status of red blood cell transfusion, admission Glasgow Coma Scale (GCS) score, serum glucose, and length of hospital stay. Outcome measures assessed at 6 months were Glasgow Outcome Scale-Extended score, Functional Status Examination score, and patient death. A multivariate generalized linear model controlling for confounding variables was used to assess the association between transfusion and outcome. Results During the study period, 292 patients were identified, and 139 (47.6%) met the criteria for moderate anemia. Roughly half (54.7%) underwent transfusions. Univariate analyses showed significant correlations between outcome score and patient age, admission GCS score, head Abbreviated Injury Scale score, number of days with an HCT level < 30%, highest glucose level, number of days with a glucose level > 200 mg/dl, length of hospital stay, number of patients receiving a transfusion, and transfusion volume. In multivariate analysis, admission GCS score, receiving a transfusion, and transfusion volume were the only variables associated with outcome (F = 2.458, p = 0.007; F = 11.694, p = 0.001; and F = 1.991, p = 0.020, respectively). There was no association between transfusion and death. Conclusions Transfusions may contribute to poor long-term functional outcomes in anemic patients with TBI. Transfusion strategies should be aimed at patients with symptomatic anemia or physiological compromise, and transfusion volume should be minimized.


2016 ◽  
Vol 124 (6) ◽  
pp. 1684-1692 ◽  
Author(s):  
Rahul Raj ◽  
Era D. Mikkonen ◽  
Jari Siironen ◽  
Juha Hernesniemi ◽  
Jaakko Lappalainen ◽  
...  

OBJECT Experimental studies have shown numerous neuroprotective properties of alcohol (“ethanol”) after TBI, but clinical studies have provided conflicting results. The authors aimed to assess the relationship between positive blood alcohol concentration (BAC) on hospital admission and mortality after moderate to severe traumatic brain injury (TBI). METHODS The authors searched 8 databases for observational studies reported between January 1, 1990, and October 7, 2013, and investigated the effect of BAC on mortality after moderate to severe TBI. Reviews of each study were conducted, and data were extracted according to the MOOSE and PRISMA guidelines. Study quality was assessed using the Newcastle-Ottawa scale. The Mantel-Haenszel fixed effect methodology was used to generate pooled estimates. Heterogeneity was dealt with by multiple sensitivity analyses. RESULTS Eleven studies with a total of 95,941 patients (42% BAC positive and 58% BAC negative) were identified for the primary analysis (overall mortality 12%). Primary analysis showed a significantly lower risk of death for BAC-positive patients compared with BAC-negative patients (crude mortality 11.0% vs 12.3%, pooled OR 0.84 [95% CI 0.81–0.88]), although flawed by heterogeneity (I2 = 68%). Multiple sensitivity analyses, including 55,949 and 51,772 patients, yielded similar results to the primary analysis (crude mortality 12.2% vs 14.0%, pooled OR 0.87 [95% CI 0.83–0.92] and crude mortality 8.7% vs 10.7%, pooled OR 0.78 [95% CI 0.74–0.83]) but with good study homogeneity (I2 = 36% and 14%). CONCLUSIONS Positive BAC was significantly associated with lower mortality rates in moderate to severe TBI. Whether this observation is due to selection bias or neuroprotective effects of alcohol remains unknown. Future prospective studies adjusting for TBI heterogeneity is advocated to establish the potential favorable effects of alcohol on outcome after TBI.


2020 ◽  
Vol 37 (3) ◽  
pp. 127-134 ◽  
Author(s):  
Amit Kochar ◽  
Meredith L Borland ◽  
Natalie Phillips ◽  
Sarah Dalton ◽  
John Alexander Cheek ◽  
...  

ObjectiveHead injury (HI) is a common presentation to emergency departments (EDs). The risk of clinically important traumatic brain injury (ciTBI) is low. We describe the relationship between Glasgow Coma Scale (GCS) scores at presentation and risk of ciTBI.MethodsPlanned secondary analysis of a prospective observational study of children<18 years who presented with HIs of any severity at 10 Australian/New Zealand centres. We reviewed all cases of ciTBI, with ORs (Odds Ratio) and their 95% CIs (Confidence Interval) calculated for risk of ciTBI based on GCS score. We used receiver operating characteristic (ROC) curves to determine the ability of total GCS score to discriminate ciTBI, mortality and need for neurosurgery.ResultsOf 20 137 evaluable patients with HI, 280 (1.3%) sustained a ciTBI. 82 (29.3%) patients underwent neurosurgery and 13 (4.6%) died. The odds of ciTBI increased steadily with falling GCS. Compared with GCS 15, odds of ciTBI was 17.5 (95% CI 12.4 to 24.6) times higher for GCS 14, and 484.5 (95% CI 289.8 to 809.7) times higher for GCS 3. The area under the ROC curve for the association between GCS and ciTBI was 0.79 (95% CI 0.77 to 0.82), for GCS and mortality 0.91 (95% CI 0.82 to 0.99) and for GCS and neurosurgery 0.88 (95% CI 0.83 to 0.92).ConclusionsOutside clinical decision rules, decreasing levels of GCS are an important indicator for increasing risk of ciTBI, neurosurgery and death. The level of GCS should drive clinician decision-making in terms of urgency of neurosurgical consultation and possible transfer to a higher level of care.


2002 ◽  
Vol 96 (1) ◽  
pp. 103-108 ◽  
Author(s):  
Michael N. Diringer ◽  
Tom O. Videen ◽  
Kent Yundt ◽  
Allyson R. Zazulia ◽  
Venkatesh Aiyagari ◽  
...  

Object. Recently, concern has been raised that hyperventilation following severe traumatic brain injury (TBI) could lead to cerebral ischemia. In acute ischemic stroke, in which the baseline metabolic rate is normal, reduction in cerebral blood flow (CBF) below a threshold of 18 to 20 ml/100 g/min is associated with energy failure. In severe TBI, however, the metabolic rate of cerebral oxygen (CMRO2) is low. The authors previously reported that moderate hyperventilation lowered global hemispheric CBF to 25 ml/100 g/min but did not alter CMRO2. In the present study they sought to determine if hyperventilation lowers CBF below the ischemic threshold of 18 to 20 ml/100 g/min in any brain region and if those reductions cause energy failure (defined as a fall in CMRO2). Methods. Two groups of patients were studied. The moderate hyperventilation group (nine patients) underwent hyperventilation to PaCO2 of 30 ± 2 mm Hg early after TBI, regardless of intracranial pressure (ICP). The severe hyperventilation group (four patients) underwent hyperventilation to PaCO2 of 25 ± 2 mm Hg 1 to 5 days postinjury while ICP was elevated (20–30 mm Hg). The ICP, mean arterial blood pressure, and jugular venous O2 content were monitored, and cerebral perfusion pressure was maintained at 70 mm Hg or higher by using vasopressors when needed. All data are given as the mean ± standard deviation unless specified otherwise. The moderate hyperventilation group was studied 11.2 ± 1.6 hours (range 8–14 hours) postinjury, the admission Glasgow Coma Scale (GCS) score was 5.6 ± 1.8, the mean age was 27 ± 9 years, and eight of the nine patients were men. In the severe hyperventilation group, the admission GCS score was 4.3 ± 1.5, the mean age was 31 ± 6 years, and all patients were men. Positron emission tomography measurements of regional CBF, cerebral blood volume, CMRO2, and oxygen extraction fraction (OEF) were obtained before and during hyperventilation. In all 13 patients an automated search routine was used to identify 2.1-cm spherical nonoverlapping regions with CBF values below thresholds of 20, 15, and 10 ml/100 g/min during hyperventilation, and the change in CMRO2 in those regions was determined. In the regions in which CBF was less than 20 ml/100 g/min during hyperventilation, it fell from 26 ± 6.2 to 13.7 ± 1 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.59 (p < 0.0001), and CMRO2 was unchanged (1.12 ± 0.29 compared with 1.14 ± 0.03 ml/100 g/min; p = 0.8). In the regions in which CBF was less than 15 ml/100 g/min during hyperventilation, it fell from 23.3 ± 6.6 to 11.1 ± 1.2 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.63 (p < 0.0001), and CMRO2 was unchanged (0.98 ± 0.19 compared with 0.97 ± 0.23 ml/100 g/min; p = 0.92). In the regions in which CBF was less than 10 ml/100 g/min during hyperventilation, it fell from 18.2 ± 4.5 to 8.1 ± 0 ml/100 g/min (p < 0.0001), OEF rose from 0.3 to 0.71 (p < 0.0001), and CMRO2 was unchanged (0.78 ± 0.26 compared with 0.84 ± 0.32 ml/100 g/min; p = 0.64). Conclusions. After severe TBI, brief hyperventilation produced large reductions in CBF but not energy failure, even in regions in which CBF fell below the threshold for energy failure defined in acute ischemia. Oxygen metabolism was preserved due to the low baseline metabolic rate and compensatory increases in OEF; thus, these reductions in CBF are unlikely to cause further brain injury.


2014 ◽  
Vol 8 (1) ◽  
pp. 53-59 ◽  
Author(s):  
Jiang-Biao Gong ◽  
Liang Wen ◽  
Ren-Ya Zhan ◽  
Heng-Jun Zhou ◽  
Fang Wang ◽  
...  

Abstract Background: Decompressing craniectomy (DC) is an important method for the management of severe traumatic brain injury (TBI). Objective: To analyze the effect of prophylactic DC within 24 hours after head trauma TBI. Methods: Seventy-two patients undergoing prophylactic DC for severe TBI were included in this retrospective study. Both of the early and late outcomes were studied and the prognostic factors were analyzed. Results: In this series, cumulative death in the first 30 days after DC was 26%, and 28 (53%) of 53 survivors in the first month had a good outcomes. The factors including Glasgow Coma Score (GCS) score at admission, whether the patient had an abnormal pupil response and whether the midline shift was greater than 5 mm were most important prognostic factors for the prediction of death in the first 30 days and the final outcome at 6 months after DC. Conclusion: Prophylactic DC plays an important role in the management of highly elevated ICP, especially when other methods of reduction of ICP are unavailable.


2008 ◽  
Vol 109 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Roger Härtl ◽  
Linda M. Gerber ◽  
Quanhong Ni ◽  
Jamshid Ghajar

Object Traumatic brain injury (TBI) remains a serious public health crisis requiring continuous improvement in pre-hospital and inhospital care. This condition results in a hypermetabolic state that increases systemic and cerebral energy requirements, but achieving adequate nutrition to meet this demand has not been a priority in reducing death due to TBI. The effect of timing and quantity of nutrition on death within the first 2 weeks of injury was analyzed in a large prospective database of adult patients with severe TBI in New York State. Methods The study is based on 797 patients with severe TBI (Glasgow Coma Scale [GCS] score < 9) treated at 22 trauma centers enrolled in a New York State quality improvement program between 2000 and 2006. The inhospital section of the prospectively collected database includes information on age, initial GCS score, weight and height, results of CT scanning, and daily parameters such as pupillary status, arterial hypotension, GCS score, and number of calories fed per day. Results Patients who were not fed within 5 and 7 days after TBI had a 2- and 4-fold increased likelihood of death, respectively. The amount of nutrition in the first 5 days was related to death; every 10-kcal/kg decrease in caloric intake was associated with a 30–40% increase in mortality rates. This held up even after controlling for factors known to affect mortality, including arterial hypotension, age, pupillary status, initial GCS score, and CT scan findings. Conclusions Nutrition is a significant predictor of death due to TBI. Together with prevention of arterial hypotension, hypoxia, and intracranial hypertension it is one of the few therapeutic interventions that can directly affect TBI outcome.


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