scholarly journals Does Complement-Mediated Hemostatic Disturbance Occur in Traumatic Brain Injury? A Literature Review and Observational Study Protocol

2020 ◽  
Vol 21 (5) ◽  
pp. 1596 ◽  
Author(s):  
Alexander Fletcher-Sandersjöö ◽  
Marc Maegele ◽  
Bo-Michael Bellander
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Complement System ◽  
Tertiary Care ◽  
Coagulation Cascade ◽  
Severe Tbi ◽  
Observational Cohort ◽  
Multiple Levels ◽  
The Complement System ◽  
Coagulation Pathway

Despite improvements in medical triage and tertiary care, traumatic brain injury (TBI) remains associated with significant morbidity and mortality. Almost two-thirds of patients with severe TBI develop some form of hemostatic disturbance, which contributes to poor outcome. In addition, the complement system, which is abundant in the healthy brain, undergoes significant intra- and extracranial amplification following TBI. Previously considered to be structurally similar but separate systems, evidence of an interaction between the complement and coagulation systems in non-TBI cohorts has accumulated, with the activation of one system amplifying the activation of the other, independent of their established pathways. However, it is not known whether this interaction exists in TBI. In this review we summarize the available literature on complement activation following TBI, and the crosstalk between the complement and coagulation systems. We demonstrate how the complement system interacts with the coagulation cascade by activating the intrinsic coagulation pathway and by bypassing the initial cascade and directly producing thrombin as well. This crosstalk also effects platelets, where evidence points to a relationship with the complement system on multiple levels, with complement anaphylatoxins being able to induce disproportionate platelet activation and adhesion. The complement system also stimulates thrombosis by inhibiting fibrinolysis and stimulating endothelial cells to release prothrombotic microparticles. These interactions see clinical relevance in several disorders where a deficiency in complement regulation seems to result in a prothrombotic clinical presentation. Finally, based on these observations, we present the outline of an observational cohort study that is currently under preparation and aimed at assessing how complement influences coagulation in patients with isolated TBI.

scholarly journals Chronic complement dysregulation drives neuroinflammation after traumatic brain injury: a transcriptomic study

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Amer Toutonji ◽  
Mamatha Mandava ◽  
Silvia Guglietta ◽  
Stephen Tomlinson
Keyword(s):  
Gene Expression ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Complement System ◽  
Classical Pathway ◽  
Post Injury ◽  
Complement Inhibition ◽  
Time Points ◽  
Complement Gene ◽  
The Complement System

AbstractActivation of the complement system propagates neuroinflammation and brain damage early and chronically after traumatic brain injury (TBI). The complement system is complex and comprises more than 50 components, many of which remain to be characterized in the normal and injured brain. Moreover, complement therapeutic studies have focused on a limited number of histopathological outcomes, which while informative, do not assess the effect of complement inhibition on neuroprotection and inflammation in a comprehensive manner. Using high throughput gene expression technology (NanoString), we simultaneously analyzed complement gene expression profiles with other neuroinflammatory pathway genes at different time points after TBI. We additionally assessed the effects of complement inhibition on neuropathological processes. Analyses of neuroinflammatory genes were performed at days 3, 7, and 28 post injury in male C57BL/6 mice following a controlled cortical impact injury. We also characterized the expression of 59 complement genes at similar time points, and also at 1- and 2-years post injury. Overall, TBI upregulated the expression of markers of astrogliosis, immune cell activation, and cellular stress, and downregulated the expression of neuronal and synaptic markers from day 3 through 28 post injury. Moreover, TBI upregulated gene expression across most complement activation and effector pathways, with an early emphasis on classical pathway genes and with continued upregulation of C2, C3 and C4 expression 2 years post injury. Treatment using the targeted complement inhibitor, CR2-Crry, significantly ameliorated TBI-induced transcriptomic changes at all time points. Nevertheless, some immune and synaptic genes remained dysregulated with CR2-Crry treatment, suggesting adjuvant anti-inflammatory and neurotropic therapy may confer additional neuroprotection. In addition to characterizing complement gene expression in the normal and aging brain, our results demonstrate broad and chronic dysregulation of the complement system after TBI, and strengthen the view that the complement system is an attractive target for TBI therapy.

The role of the complement system in traumatic brain injury

1998 ◽  
Vol 27 (3) ◽  
pp. 243-256 ◽  
Author(s):  
Philip F Stahel ◽  
Maria C Morganti-Kossmann ◽  
Thomas Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Complement System ◽  
The Complement System

Brain tissue oxygen–directed management and outcome in patients with severe traumatic brain injury

2010 ◽  
Vol 113 (3) ◽  
pp. 571-580 ◽  
Author(s):  
Alejandro M. Spiotta ◽  
Michael F. Stiefel ◽  
Vicente H. Gracias ◽  
Alicia M. Garuffe ◽  
W. Andrew Kofke ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Tertiary Care ◽  
Care Hospital ◽  
Tissue Oxygen ◽  
Brain Tissue Oxygen ◽  
Severe Tbi

Object The object of this study was to determine whether brain tissue oxygen (PbtO2)–based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)–based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI). Methods Seventy patients with severe TBI (postresuscitation GCS score ≤ 8), admitted to a neurosurgical intensive care unit at a university-based Level I trauma center and tertiary care hospital and managed with an ICP and PbtO2 monitor (mean age 40 ± 19 years [SD]) were compared with 53 historical controls who received only an ICP monitor (mean age 43 ± 18 years). Therapy for both patient groups was aimed to maintain ICP < 20 mm Hg and CPP > 60 mm Hg. Patients with PbtO2 monitors also had therapy to maintain PbtO2 > 20 mm Hg. Results Data were obtained from 12,148 hours of continuous ICP monitoring and 6,816 hours of continuous PbtO2 monitoring. The mean daily ICP and CPP and the frequency of elevated ICP (> 20 mm Hg) or suboptimal CPP (< 60 mm Hg) episodes were similar in each group. The mortality rate was significantly lower in patients who received PbtO2-directed care (25.7%) than in those who received conventional ICP and CPP–based therapy (45.3%, p < 0.05). Overall, 40% of patients receiving ICP/CPP–guided management and 64.3% of those receiving PbtO2–guided management had a favorable short-term outcome (p = 0.01). Among patients who received PbtO2-directed therapy, mortality was associated with lower mean daily PbtO2 (p < 0.05), longer durations of compromised brain oxygen (PbtO2 < 20 mm Hg, p = 0.013) and brain hypoxia (PbtO2 < 15 mm Hg, p = 0.001), more episodes and a longer cumulative duration of compromised PbtO2 (p < 0.001), and less successful treatment of compromised PbtO2 (p = 0.03). Conclusions These results suggest that PbtO2-based therapy, particularly when compromised PbtO2 can be corrected, may be associated with reduced patient mortality and improved patient outcome after severe TBI.

scholarly journals AN ANALYSIS OF TRAUMATIC BRAIN INJURY [TBI] IN TERMS OF 3-MONTH GLASGOW OUTCOME SCORE [GOS] AT A TERTIARY CARE CENTRE

2021 ◽  
pp. 13-15
Author(s):  
Shrikant Govindrao Palekar ◽  
Kailash K Mogal ◽  
Vedanti Rajesh Patil ◽  
I Vijay Sundar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Features ◽  
Tertiary Care ◽  
Glasgow Outcome Score ◽  
Tertiary Care Centre ◽  
Mild Tbi ◽  
Outcome Score ◽  
Severe Tbi

INTRODUCTION - Traumatic brain injury [TBI] most affects the working population and their earning capacity. The various sub categories of TBI in terms of clinical features,Glasgow coma scale [GCS] and radiology are well defined.We have attempted an analysis in terms of long term Glasgow outcome score [GOS] and tried to correlate with the various factors of TBI. MATERIALS AND METHODS – All patients of TBI over 12 years and below 60 years and those without other major trauma were included over a period of about two years. The clinical features, presentation GCS, treatment given, and outcomes were assessed.The three month GOS was scored for all patients and was used to analyse the the initial data in its light. RESULTS – A total of 200 patients were eligible for the study and were included. Of these 159 were males and 41 were females.The average age was 37.16 years.There was a relatively higher proportion of mild TBI and greater prevalence of fractures and EDH [extradural hematoma].On analyzing with three month GOS we found that 90.4 % of the patients with mild TBI had a three month GOS of 5 whereas only 31.9% of patients with moderate or severe TBI had a three month GOS of 5. CONCLUSION – The long term GOS is most representative of the extent to which the patient has been able to return to their pre TBI lives. In our study the three month GOS co related well with the initial GCS. Further prospective data can elaborate more on the effect of other clinical features and radiology on long term GOS

The CCL2/CCL7/CCL12/CCR2 pathway is substantially and persistently upregulated in mice after traumatic brain injury, and CCL2 modulates the complement system in microglia

2020 ◽  
Vol 54 ◽  
pp. 101671
Author(s):  
Katarzyna Popiolek-Barczyk ◽  
Agata Ciechanowska ◽  
Katarzyna Ciapała ◽  
Katarzyna Pawlik ◽  
Marco Oggioni ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Complement System ◽  
The Complement System

Clinical Significance of Vascular Occlusive Events following Moderate-to-Severe Traumatic Brain Injury: An Observational Cohort Study

2022 ◽  
Author(s):  
Alexander Fletcher-Sandersjöö ◽  
Charles Tatter ◽  
Jonathan Tjerkaski ◽  
Jiri Bartek Jr ◽  
Mikael Svensson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cohort Study ◽  
Brain Injury ◽  
Clinical Significance ◽  
Skull Fracture ◽  
Observational Cohort Study ◽  
Vein Thrombosis ◽  
Therapeutic Opportunity ◽  
Severe Tbi ◽  
Observational Cohort

AbstractPreventing hemorrhage progression is a potential therapeutic opportunity in traumatic brain injury (TBI) management, but its use has been limited by fear of provoking vascular occlusive events (VOEs). However, it is currently unclear whether VOE actually affects outcome in these patients. The aim of this study was to determine incidence, risk factors, and clinical significance of VOE in patients with moderate-to-severe TBI. A retrospective observational cohort study of adults (≥15 years) with moderate-to-severe TBI was performed. The presence of a VOE during hospitalization was noted from hospital charts and radiological reports. Functional outcome, using the Glasgow Outcome Scale (GOS), was assessed at 12 months posttrauma. Univariate and multivariate logistic regressions were used for endpoint assessment. In total, 848 patients were included, with a median admission Glasgow Coma Scale of 7. A VOE was detected in 54 (6.4%) patients, of which cerebral venous thrombosis was the most common (3.2%), followed by pulmonary embolism (1.7%) and deep vein thrombosis (1.3%). Length of ICU stay (p < 0.001), body weight (p = 0.002), and skull fracture (p = 0.004) were independent predictors of VOE. VOE development did not significantly impact 12-month GOS, even after adjusting for potential confounders using propensity score matching. In conclusion, VOE in moderate-to-severe TBI patients was relatively uncommon, and did not affect 12-month GOS. This suggests that the potential benefit of treating bleeding progression might outweigh the risks of VOE.

Severe Head Injury Management at a Tertiary Care Hospital in Dhaka City

2020 ◽  
Vol 6 (2) ◽  
pp. 124-128
Author(s):  
Md Monzurul Haque ◽  
Monsur Ahmed ◽  
Fazlul Haque ◽  
Md Shariful Islam ◽  
Rustom Ali Modhu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Severe Traumatic Brain Injury ◽  
Tertiary Care ◽  
Care Hospital ◽  
Good Recovery ◽  
Midline Shift ◽  
Severe Tbi ◽  
Group A ◽  
Group B

Background: Severe traumatic brain injury can be a serious condition. Objective: The purpose of the present study was to see the decompressive craniectomy (DC) of severe traumatic brain injury. Methodology: This clinical trial was conducted in the Department of Neurosurgery at Dhaka Medical College Hospital, Dhaka, Bangladesh from January 2012 to December 2013 for a period of two (02) years. Patients with the age of 18 years and above, GCS of the patients 8 to 4, severe traumatic brain injury (TBI) with multiple hemorrhagic contusions and midline shift, on CT scan and severe TBI with gradual neurological deterioration were included for this study. Total 60 patients were included. Result: A total of 60 patients were included in this study. Almost two third 18 (60.0%) patients had favorable outcome (GOS 4 and 5) in group A and exactly two third 20(66.7%) patients had Unfavorable outcome (GOS 1,2 and 3) in group B (p<0.05). In this study 8 patient died among which 5 had GCS 4 and 3 had GCS 5. One patient with GCS 5 became persistent vegetative. Eight patient with good recovery had GCS 8, 7 and 6. Death occurred at mean GCS 9±2.mm of midline shift followed by 8± mm in persistent vegetative, 5.67±2.08 mm in severe disability, 4.5±2.88 mm in moderate disability and 3.38±1.06 mm in good recovery. Conclusion: Group A had better clinical outcome than group B. So based on statistical analysis it can be concluded that DC is preferable to conservative management in case of severe TBI. Journal of National Institute of Neurosciences Bangladesh, 2020;6(2): 124-128

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