Posttraumatic Cerebral Infarction Research Articles

Post-Traumatic Cerebral Infarction: A Narrative Review of Pathophysiology, Diagnosis, and Treatment.

Traumatic brain injury (TBI) is a common diagnosis requiring acute hospitalization. Long-term, TBI is a significant source of health and socioeconomic impact in the United States and globally. The goal of clinicians who manage TBI is to prevent secondary brain injury. In this population, post-traumatic cerebral infarction (PTCI) acutely after TBI is an important but under-recognized complication that is associated with negative functional outcomes. In this comprehensive review, we describe the incidence and pathophysiology of PTCI. We then discuss the diagnostic and treatment approaches for the most common etiologies of isolated PTCI, including brain herniation syndromes, cervical artery dissection, venous thrombosis, and post-traumatic vasospasm. In addition to these mechanisms, hypercoagulability and microcirculatory failure can also exacerbate ischemia. We aim to highlight the importance of this condition and future clinical research needs with the goal of improving patient outcomes after TBI.

Post-traumatic Cerebral Infarction: A Severe form of Secondary Brain Injury in Traumatic Brain Injury Patients with a Critical Neutrophil-to-lymphocyte Ratio

Post-traumatic cerebral infarction (PTCI) is one of the most severe forms of secondary brain injury (SBI) post-traumatic brain injury (TBI). The PTCI incidence is not very often and is associated with a high mortality rate even after appropriate medical and surgical interventions. SBI is still challenging to prevent even though several laboratory tests such as neutrophil-to-lymphocyte ratio (NLR) were available for early detection and monitoring the severity of SBI progression. This study aimed to report the case of PTCI post-TBI which was correlated with an extremely high NLR result. This case report shows that early recognition and close monitoring is necessary to prevent the occurrence of PTCI in TBI patients. NLR is very beneficial to be used to monitor and detect the early progression of SBI post-TBI.

Post-traumatic Early Cerebral Infarct: MRI-based Analysis of Incidence and Radiological Distribution

Introduction: Traumatic Brain Injury (TBI) is an alteration in brain function brought on by external trauma. Computed Tomography (CT) scanning is the mainstay diagnostic modality for evaluating the primary injury, as well as secondary events such as oedema, mass effect, herniation, infarction, etc., which are often catastrophic and responsible for morbidity and mortality. Early cerebral infarction, unless large and in a defined vascular territory, is quite likely to be missed on CT scans and can even be confused with cerebral oedema. In the diagnosis of early infarctions, especially the lacunar types, the detection rate of lesions with Magnetic Resonance Imaging (MRI) is significantly higher than that of CT. Aim: To observe the incidence, distribution, and pattern of Post-traumatic Cerebral Infarction (PTCI) and its association with neurological deterioration. Materials and Methods: In this cross-sectional study, 55 patients with head injuries admitted to the Department of Neurosurgery were evaluated between 72 to 96 hours posttrauma using Magnetic Resonance Imaging (MRI) of the brain (1.5 Tesla Siemens). Observations were made regarding the presence and pattern of any infarction, as well as its impact on the patients. Results: Post-traumatic early cerebral infarction was detected in 19 out of 55 (34.5%) patients. Infarct distribution was observed in nearly all defined vascular territories, with the most common occurrence in the Middle Cerebral Artery (MCA) territory. Neurological deficit was observed in four out of 19 infarcted cases during the hospitalisation period. Conclusion: Post-traumatic early cerebral infarction is common in head injuries and can lead to neurological deterioration. MRI is sensitive in detecting infarcts, especially the lacunar ones.

Predictive role of shock index in the early formation of cerebral infarction in patients with TBI and cerebral herniation.

Background and purposeTraumatic brain injury (TBI) with brain herniation predisposes to posttraumatic cerebral infarction (PTCI), which in turn seriously affects the prognosis of patients. At present, there is a lack of effective indicators that can accurately predict the occurrence of PTCI. We aimed to find possible risk factors for the development of PTCI by comparing the preoperative and postoperative clinical data of TBI patients with brain herniation.MethodsThe clinical data of 120 patients with craniocerebral trauma and brain herniation were retrospectively analyzed. Among them, 54 patients had cerebral infarction within 3–7 days after injury. The two groups of patients were compared through univariate and multivariate logistic regression analysis, and a classification tree model and a nomogram model were constructed. Finally, receiver operating characteristic curve analysis and decision curve analysis were conducted to analyze the clinical utility of the prediction model.ResultsLogistic regression analysis showed that factors like the Glasgow Coma Scale (GCS) score (P = 0.002), subarachnoid hemorrhage (SAH) (P = 0.005), aspiration pneumonia (P < 0.001), decompressive craniectomy (P < 0.05), intracranial pressure (ICP) monitoring (P = 0.006), the shock index (SI) (P < 0.001), the mean arterial pressure (MAP) (P = 0.005), and blood glucose (GLU) (P < 0.011) appeared to show a significant statistical correlation with the occurrence of infarction (P < 0.05), while age, sex, body temperature (T), D-dimer levels, and coagulation tests were not significantly correlated with PTCI after cerebral herniation. Combined with the above factors, Classification and Regression Tree was established, and the recognition accuracy rate reached 76.67%.ConclusionsGCS score at admission, no decompressive craniectomy, no ICP monitoring, combined SAH, combined aspiration pneumonia, SI, MAP, and high GLU were risk factors for infarction, of which SI was the primary predictor of PTCI in TBI with an area under the curve of 0.775 (95% CI = 0.689–0.861). Further large-scale studies are needed to confirm these results.

Post-traumatic cerebral infarction (PTCI), an institutional experience

Post-traumatic cerebral infarction (PTCI), an institutional experience

Serum CXC chemokine ligand-12 as a potential predictor for in-hospital major adverse events after severe traumatic brain injury

BackgroundCXC chemokine ligand-12 (CXCL12) is associated with brain inflammation. We attempted to discern whether serum CXCL12 is a promising predictor for in-hospital major adverse events (IMAEs) after traumatic brain injury (TBI), including death, acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction. MethodsIn this prospective, observational study, serum CXCL12 levels were quantified among 117 severe TBI patients. We investigated the relation of CXCL12 levels to IMAEs using a multivariate analysis. ResultsMedian value of serum CXCL12 concentrations was substantially higher in patients with IMAEs than in other remainders (21.1 vs. 11.6 ng/ml). With an increasing number of IMAEs, serum CXCL12 concentrations were significantly increased (r = 0.702). Serum CXCL12 independently predicted IMAEs (odds ratio, 1.253; 95% CI, 1.100–1.428). Serum CXCL12 concentrations discriminated risk of IMAEs with area under receiver operating characteristic curve of 0.759 (95% CI, 0.672–0.834), its concentrations >16.0 ng/ml distinguished IMAEs with 83.9% sensitivity and 67.2% specificity and its combination with Glasgow coma scale scores produced the best predictive ability compared with each one alone (p = 0.0116 or 0.0004). ConclusionSerum CXCL12 concentrations are independently associated with IMAEs following TBI, substantializing serum CXCL12 as a useful prognostic biomarker for head trauma patients.

The Effect of Controlled Decompression for Severe Traumatic Brain Injury: A Randomized, Controlled Trial.

Background: Experimental evidence has indicated the benefits of intraoperative controlled decompression for the treatment of severe traumatic brain injury (sTBI). Intraoperative rapid decompression (conventional decompression) for the treatment of sTBI may result in intra- and post-operative complications. Controlled decompression may reduce these complications. Previous clinical trials in China have not yielded conclusive results regarding controlled decompression for sTBI. Therefore, we explored whether controlled decompression treatment decreases the rates of complications and improves the outcomes of patients with sTBI.Methods: We performed this randomized, controlled trial at our hospital. Patients with sTBI aged 18–75 years old were randomly (1:1) divided into controlled decompression surgery (n = 124) or rapid decompression surgery groups (n = 124). The primary outcome measures were the Extended Glasgow Outcome Scale (GOS-E) score at 6 months and 30-days all-cause mortality. The secondary outcomes were the incidences of intraoperative brain swelling, post-traumatic cerebral infarction, and delayed hematoma.Results: Compared with the rapid decompression group, the controlled decompression group had reduced 30-days all-cause mortality (18.6 vs. 30.8%, P = 0.035) and improved the 6-months GOS-E scores, and the difference was significant. In addition, the patients in the controlled decompression group had a lower intraoperative brain swelling rate (13.3 vs. 24.3%, P = 0.036), a lower delayed hematoma rate (17.7 vs. 29.0%, P = 0.048) and a relatively lower post-traumatic cerebral infarction rate (15.0 vs. 22.4%, P = 0.127) than those in the rapid decompression group.Conclusions: Our data suggest that controlled decompression surgery significantly improves sTBI outcomes and decreases the rates of sTBI-related complications. However, this was a single-hospital study, and well-designed multicenter randomized controlled trials are needed to evaluate the effects of controlled decompression surgery for the management of patients with sTBI.Clinical Trial Registration: Chinese Clinical Trial Registry; Date: 14/Dec/2013; Number: ChiCTR-TCC-13004002.

Impact of a posttraumatic cerebral infarction on outcome in patients with TBI: the Italian multicenter cohort INCEPT study

BackgroundPost-traumatic cerebral infarction (PTCI) is common after traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors.MethodsThis was a prospective multicenter cohort study of moderate and severe TBI patients. The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models.ResultsWe enrolled 143 patients, of whom 47 (32.9%) developed a PTCI. In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC = 0.73, 95% C.I. 0.66–0.82; increased to AUC = 0.79, 95% CI 0.71–0.83, p = 0.0007) and extended model (AUC = 0.74, 95% C.I. 0.65–0.81 increased to AUC = 0.80, 95% C.I. 0.69–0.85; p = 0.00008). Patients with PTCI showed higher ICU mortality and 6-month mortality, whereas hospital mortality did not differ between the two groups.ConclusionsPTCI is a common complication in patients suffering from a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS.Trial registrationThe present study was registered in ClinicalTrial.gov with the ID number NCT02430324.

The Utility of Thromboelastography for Predicting the Risk of Post-Traumatic Cerebral Infarction in Traumatic Brain Injury

Abstract INTRODUCTION Post-traumatic cerebral infarction (PTCI) is a severe secondary insult of head injury and often leads to a poor prognosis. Hemocoagulation disorder is recognized to have important effects on hemorrhagic or ischemic damages. We sought to assess if post-traumatic coagulopathy determined using thrombelastography was associated with cerebral infarction after head trauma. METHODS We prospectively reviewed 316 patients with head trauma to evaluate the effects of demographics, admission Glasgow Coma Scale (GCS) score, and TEG data on the development of PTCI. Multivariate logistic regression analysis was used to identify independent risk factors. RESULTS Patients with PTCI had a shorter R, greater a-Angle, and shorter K, indicating faster clotting. Additionally, TEG results were independently associated with an increased risk of PTCI. CONCLUSION TEG demonstrates that many PTCI patients are hypercoaguable and the risk of developing PTCI may be higher in patients with a shorter R, greater a-Angle, and shorter K.

Usefulness of serum interleukin-33 as a prognostic marker of severe traumatic brain injury

BackgroundInterleukin-33 is recently identified as a brain injury biomarker. We determined whether serum interlerukin-33 concentrations are associated with inflammation, severity and prognosis after traumatic brain injury (TBI). MethodsWe detected serum interlerukin-33 concentrations of 102 healthy controls and 102 severe TBI patients, as well as serum concentrations of 3 inflammatory biomarkers (interleukin-6, tumor necrosis factor-alpha and C-reactive protein) and 7 cell-specific proteins (myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1) in 102 severe TBI patients. The recorded poor prognosis variables included acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury, posttraumatic cerebral infarction and six-month mortality and poor outcome (Glasgow score of 1–3). ResultsMedian interlerukin-33 concentration of patients (692 pg/mL) was substantially raised, as compared to controls. Interlerukin-33 concentrations were significantly correlated with Glasgow coma scale (GCS) score and the preceding biomarkers concentrations. Interlerukin-33 concentration > 692 pg/mL emerged as an independent prognostic predictor and its discriminatory capability exceeded those of the above-mentioned inflammatory biomarkers concentrations and was in the range of GCS scores and the aforementioned cell-specific proteins concentrations. ConclusionAscending serum interlerukin-33 concentrations could reflect inflammation, severity and worse prognosis following TBI.

Acute and Subacute Outcome Predictors in Moderate and Severe Traumatic Brain Injury: A Retrospective Monocentric Study

Prognostic factors affecting outcome of traumatic brain injury (TBI), despite their importance, are still under discussion. The purpose of this study was to describe risk factors of in-hospital mortality and outcome at 1 year in a homogeneously treated population of patients with moderate/severe TBI. A total of 193 consecutive patients with moderate or severe TBI (Glasgow Coma Scale [GCS] score 13-3, including patients with initial GCS score of 13 at high risk for subsequent neurologic deterioration), admitted to the intensive care unit, were retrospectively analyzed. In-hospital mortality and unfavorable outcome at 1 year, based on a Glasgow Outcome Scale-Extended score ≤4, were considered as primary and secondary outcomes. At 1 year, unfavorable outcome occurred in 47.2%, including an in-hospital mortality of 19.7%. Increasing age, GCS motor score <3, coagulation disorders, and intracranial hypertension were acute risk factors of in-hospital mortality. In the 155 remaining survivors, Oxford Handicap Scale (OHS), posttraumatic cerebral infarction, cerebrospinal fluid disturbances, and length of intensive care unit stay were associated with unfavorable outcome at 1 year, in univariate analysis. A cutoff OHS score ≥3 discriminated the probability of an unfavorable outcome (area under the curve, 0.87; P < 0.001; specificity, 74%; sensitivity, 84%). Combining the effect of acute and subacute variables in a multivariate analysis, increasing age and OHS score were independent predictors of outcome. The results of this retrospective study confirmed age as the main acute risk factor and identified OHS as new potential subacute predictor of unfavorable outcome in moderate and severe TBI.

Management of subdural effusion and hydrocephalus following decompressive craniectomy for posttraumatic cerebral infarction in a patient with traumatic brain injury: a case report

BackgroundSubdural effusion with hydrocephalus (SDEH) is a rare complication of traumatic brain injury, especially following decompressive craniectomy (DC) for posttraumatic cerebral infarction. The diagnosis and treatment are still difficult and controversial for neurosurgeons.Case presentationA 45-year-old man developed traumatic cerebral infarction after traumatic brain injury and underwent DC because of the mass effect of cerebral infarction. Unfortunately, the complications of traumatic subdural effusion (SDE) and hydrocephalus occurred in succession following DC. Burr-hole drainage and subdural peritoneal shunt were performed in sequence because of the mass effect of SDE, which only temporarily improved the symptoms of the patient. Cranioplasty and ventriculoperitoneal shunt were performed ultimately, after which SDE disappeared completely. However, the patient remains severely disabled, with a Glasgow Outcome Scale of 3.ConclusionsIt is important for neurosurgeons to consider the presence of accompanying hydrocephalus when treating patients with SDE. Once the diagnosis of SDEH is established and the SDE has no mass effect, timely ventriculoperitoneal shunt may be needed to avoid multiple surgical procedures, which is a safe and effective surgical method to treat SDEH.

Impact of a Posttraumatic Cerebral Infarction on the Long-Term Outcome of Patients with Moderate and Severe Traumatic Brain Injuries: The Italian Multicenter Cohort INCEPT Study

Background: Post-traumatic cerebral infarction (PTCI) is common in patients dying after a traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors. Methods: This was a prospective multicenter cohort study of moderate and severe TBI patients admitted to nine Italian intensive care units (ICUs). The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models. Findings: We enrolled 143 patients; 47 (32·9%) developed a PTCI for a total of 94. The mean (SD) onset time of a PTCI was 6·2 (11·4). In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC=0·73, 95% C.I. 0·66-0·82; increased to AUC=0·79, 95% CI 0·71-0·83, p=0·0007) and extended model (AUC=0·74, 95% C.I.: 0·65-0·81 increased to AUC=0·80, 95% C.I. 0·69-0·85; p=0·00008). Patients with a PTCI showed higher ICU mortality (10 patients [21·3%] vs one patient [1·0%], p<0·0001) and 6-month mortality (13 patients [27·7%] vs seven patients [7·3%], p<0·0001); whereas, hospital mortality did not differ between the two groups. Interpretation: A PTCI is a common complication in patients suffering a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS. Trial Registration Number: This study was registered with ClinicalTrials.gov (number NCT02430324). Funding Statement: The present study was self-funded. The authors declare none to funding. Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The study was conducted in accordance with the Declaration of Helsinki and was approved by the local Ethics Committees of each participating center. Patients’ informed consent was waived due to the lack of definition of a legal representative of temporarily incapacitated adult patients in the Italian legislation.11 The informed consent was obtained from the surviving patients as soon as they regained their mental competency. Family members received detailed information on the study scope and protocol. We followed the STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) guidelines for reporting cohort studies.

Risk factors of post traumatic cerebral infarction after craniotomy for severe traumatic brain injury

Objective To investigate the risk factors associated with post traumatic cerebral infarction (PTCI) after craniotomy hematoma evacuation for severe traumatic brain injury (sTBI) so as to provide clinical reference for the early prevention of postoperative PTCI. Methods A retrospective case control study was conducted to analyze the clinical data of 558 sTBI patients who received craniotomy hematoma evacuation admitted to Changsha Hospital of Traditional Chinese Medicine from October 2006 to June 2016. There were 340 males and 218 females, aged 15-71 years, with an average of 47.8 years. Among them, 75 patients were at the age of less than 30 years, 315 were at 30-50 years, and 168 were above 50 years. According to the Glasgow coma score (GCS), there were 127 patients with 3-4 points, 124 with 5-6 points, and 307 with 7-8 points. The patients were divided into PTCI group (51 patients) and non-PTCI group (507 patients). The related indicators of the two groups of patients after admission were collected, including gender, age, injury cause, GCS, skull base fracture, traumatic subarachnoid hemorrhage (tSAH), cerebral hernia, hypotension, the time from injury to craniotomy, and whether decompressive craniectomy was performed. Univariate analysis was first performed for these factors, followed by multivariate logistic regression analysis. Results There were no significant differences in gender, age, injury cause, skull base fracture, and decompressive craniectomy between PTCI group and control group (P>0.05). In the PTCI group, there were 29 patients with GCS of 3-4 points, 17 with 5-6 points, and five with 7-8 points; there were 48 patients with tSAH, 37 patients with cerebral hernia, and 18 patients with hypotension. In terms of the time from injury to craniotomy, it took 12 hours in four. In the non-PTCI group, there were 98 patients with GCS of 3-4 points, 107 with 5-6 points, and 302 with 7-8 points. There were 34 patients with tSAH, 117 with cerebral hernia, and 35 with hypotension. In terms of the time from injury to craniotomy, it took 12 hours in 15. The differences between the two groups were statistically significant (P<0.05). Multivariate logistic regression analysis indicated that GCS of 3-6 points, tSAH, cerebral hernia, time from injury to craniotomy, and hypotension were significantly associated with PTCI after operation for sTBI (P<0.01). Conclusions GCS of 3-6 points, tSAH, cerebral hernia, duration from injury to craniotomy, and hypotension time >3 hours are the high risk factors of PTCI in sTBI patients after craniotomy. For patients with these high risk factors, craniotomy should be performed in time, and the perioperative blood pressure and intracranial pressure stability should be maintained so as to relieve vasospasm. Key words: Brain injuries; Decompressive craniectomy; Cerebral infarction; Hypotension

Prognostic significance of serum translocator protein in patients with traumatic brain injury

BackgroundTranslocator protein (TP) is related to inflammation and is involved in brain injury. The objective of this study was to ascertain whether serum TP concentrations are associated with the severity and prognosis of traumatic brain injury (TBI). MethodsWe quantified the serum concentrations of TP in 106 healthy controls and 106 patients with severe TBI. Recorded prognostic variables included acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury, posttraumatic cerebral infarction, 6-month mortality and 6-month poor outcome (Glasgow Outcome Scale score of 1–3). Trauma severity was assessed by Glasgow coma scale (GCS) score. Extent of inflammatory response was indicated by serum interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a) and C-reactive protein (CRP) concentrations. ResultsPatients had significantly higher serum TP concentrations than controls. Among patients, serum TP concentrations strongly and independently correlated with GCS score and serum IL-6, TNF-a and CRP concentrations. Serum TP was identified as an independent predictor for the preceding prognostic variables, its prognostic predictive ability was similar to that of GCS score and it also significantly improved prognostic predictive ability of GCS score. ConclusionSerum TP may be intimately linked with in inflammation, disease progression and poor prognosis in TBI patients.

Serum ST2 as a potential prognostic biomarker for traumatic brain injury

BackgroundST2, a receptor of interleukin-33, is involved in inflammation. We discerned the relationship between serum soluble ST2 (sST2) concentrations, inflammation, severity and prognosis following traumatic brain injury (TBI). MethodsWe measured serum sST2, interleukin-6, tumor necrosis factor-alpha, C-reactive protein, myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1 concentrations in 106 healthy controls and 106 severe TBI patients. We recorded long-term prognosis (i.e., 6-month mortality and functional outcome) and in-hospital major adverse events, including in-hospital mortality, acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction. ResultssST2 concentrations were significantly higher in patients than in controls and were significantly correlated with Glasgow coma scale (GCS) score and the preceding biomarkers concentrations. Serum sST2 was an independent prognostic predictor and its predictive ability significantly exceeded those of serum interleukin-6, tumor necrosis factor-alpha and C-reactive protein concentrations and was similar to those of GCS scores and serum concentrations of other remaining biomarkers. Moreover, sST2 concentrations significantly improved predictive ability of GCS score. ConclusionIncreased serum sST2 concentrations are significantly related to inflammation, severity and prognosis, substantialized ST2 as a potential prognostic biomarker for TBI.

Predictors Associated With Post-Traumatic Hydrocephalus in Patients With Head Injury Undergoing Unilateral Decompressive Craniectomy.

Post-traumatic hydrocephalus (PTH) makes recovery from head trauma after decompression more complicated and is associated with high risks of clinical deterioration and poor outcomes. The aim of this study was to verify the predictors associated with the development of PTH in patients with head injury undergoing unilateral decompressive craniectomy (DC). Among traumatic brain injury (TBI) patients who underwent unilateral DC between January 2013 and December 2016, the clinical medical records, radiological information, and changes of patients' conditions in the 3-month after injury were reviewed retrospectively. 183 TBI patients after unilateral DC were analyzed, and 50 (27.32%) of them suffered PTH based on head CT scans. Univariate and multivariable analyses revealed that older age (p = 0.002), the Glasgow Coma Scale (GCS) score at admission (p < 0.001), intraventricular hemorrhage (IVH; p = 0.008), post-traumatic cerebral infarction (PCI; p = 0.007), and postoperative meningitis (p = 0.016) were independent predictors for the hydrocephalus after DC. Receiver operating characteristic curves were created and the area under the curve (AUC) were calculated to further assess the accuracy of the variables for predicting PTH. The AUC was 0.836 for the combined all five independent factors (95% confidence interval: 0.775-0.887). TBI patients who undergo unilateral DC with advanced age, lower GCS score at admission, coexisting IVH, PCI, and/or postoperative meningitis should be closely monitored at follow-up assessments for earlier prediction of PTH.

Serum S100A12 as a prognostic biomarker of severe traumatic brain injury

BackgroundS100A12 is related to acute brain injury and inflammation. We investigated the clinical prognostic value of serum S100A12 in patients with severe traumatic brain injury (sTBI). MethodsSerum S100A12, S100B, C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) concentrations were measured in 102 healthy controls and 102 sTBI patients. We recorded 30-day mortality and in-hospital major adverse events (IMAEs) including acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction. Trauma severity was assessed by admission Glasgow Coma Scale scores. ResultsWhen compared to the controls, serum S100A12, S100B, CRP, IL-6 and TNF-α concentrations were significantly increased in the patients. Serum concentrations of S100A12 significantly correlated with admission Glasgow Coma Scale scores and serum concentrations of S100B, CRP, IL-6 and TNF-α. Patients with any IMAEs or non-survivors within 30 days had obviously higher serum concentrations of S100A12, S100B, CRP, IL-6 and TNF-α than other remaining ones. Serum S100A2 was independently associated with IMAEs and 30-day mortality and overall survival. Receiver operating characteristic curve analysis showed that S100A12 concentrations had significant discriminatory ability for patients at risk of any IMAEs and death within 30 days. ConclusionS100A12 might be associated with brain inflammation and evaluation of serum concentrations of S100A12 could be helpful in the early prognostic prediction in sTBI patients.

Serum macrophage migration inhibitory factor concentrations correlate with prognosis of traumatic brain injury

BackgroundMacrophage migration inhibitory factor (MIF) is a well-known pro-inflammatory cytokine. Serum MIF concentrations are associated with the severity and prognosis of ischemic stroke. MethodsIn this prospective, observational study, white blood cell (WBC) count and serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and MIF among 108 severe traumatic brain injury (TBI) patients and 108 controls were measured. We determined whether serum MIF concentrations are associated with inflammation, severity, in-hospital major adverse events (IMAEs) (i.e., in-hospital mortality, acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction) and long-term clinical outcome (i.e., 6-month functional outcome) after TBI. ResultsAs compared to the controls, serum CRP, IL-6, TNF-α and MIF concentrations were significantly increased. MIF concentrations correlated with WBC count, CRP, IL-6 and TNF-α concentrations and Glasgow coma scale (GCS) scores. MIF in serum was independently associated with IMAEs and long-term clinical outcome. Area under receiver operating characteristic curve of MIF concentrations was similar to GCS scores'. Moreover, MIF concentrations markedly improved the predictive value of GCS scores for 6-month unfavorable outcome. ConclusionIncreased serum MIF concentrations have close relation to inflammation, trauma severity and clinical outcomes, substantializing MIF as a good prognostic biomarker after TBI.

Serum thioredoxin and in-hospital major adverse events after traumatic brain injury

BackgroundIn-hospital major adverse events (IMAEs), mainly including acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction, are associated with poor prognosis after traumatic brain injury (TBI). Thioredoxin, a potent anti-oxidant, has been identified as an oxidative stress marker. This study was designed to explore the association of serum thioredoxin concentrations with IMAEs of patients with severe TBI. MethodsThis prospective, observational study recruited a total of 108 healthy controls and 108 patients with severe TBI. We investigated the possible relation of serum thioredoxin concentrations to IMAEs and trauma severity (reflected by Glasgow coma scale scores) following TBI using a multivariate analysis. ResultsSerum thioredoxin concentrations were higher in the patients than in the controls. Serum concentrations of thioredoxin significantly correlated with admission Glasgow coma scale scores. Thioredoxin in serum independently predicted any IMAEs. As compared to admission Glasgow coma scale scores, thioredoxin concentrations had similar areas under receiver operating characteristic curve for any IMAEs. ConclusionIncreased serum thioredoxin concentrations are highly associated with trauma severity and IMAEs, indicating thioredoxin might be a potential prognostic biomarker after TBI.