scholarly journals Endothelial glycocalyx in traumatic brain injury associated coagulopathy: potential mechanisms and impact

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Zhimin Zou ◽  
Li Li ◽  
Nadine Schäfer ◽  
Qiaobing Huang ◽  
Marc Maegele ◽  
...  

AbstractTraumatic brain injury (TBI) remains one of the leading causes of death and disability worldwide; more than 10 million people are hospitalized for TBI every year around the globe. While the primary injury remains unavoidable and not accessible to treatment, the secondary injury which includes oxidative stress, inflammation, excitotoxicity, but also complicating coagulation abnormalities, is potentially avoidable and profoundly affects the therapeutic process and prognosis of TBI patients. The endothelial glycocalyx, the first line of defense against endothelial injury, plays a vital role in maintaining the delicate balance between blood coagulation and anticoagulation. However, this component is highly vulnerable to damage and also difficult to examine. Recent advances in analytical techniques have enabled biochemical, visual, and computational investigation of this vascular component. In this review, we summarize the current knowledge on (i) structure and function of the endothelial glycocalyx, (ii) its potential role in the development of TBI associated coagulopathy, and (iii) the options available at present for detecting and protecting the endothelial glycocalyx.

2018 ◽  
Vol 17 (9) ◽  
pp. 689-695 ◽  
Author(s):  
Nidhi Khatri ◽  
Manisha Thakur ◽  
Vikas Pareek ◽  
Sandeep Kumar ◽  
Sunil Sharma ◽  
...  

Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.


2014 ◽  
Vol 100 (3) ◽  
pp. 293-300
Author(s):  
IA Edgar ◽  
G Hadjipavlou ◽  
JE Smith

AbstractSevere Traumatic Brain Injury (sTBI) is a devastating cause of morbidity and mortality, especially among those aged less than 45 years. Advances in clinical practice continue to focus on preventing primary injury through developing ballistic head and eye protection, and through minimising secondary brain injury (secondary prevention).Managing sTBI is challenging in well-developed, well-resourced healthcare systems. Achieving management aims in the military maritime environment poses even greater challenges.Strategies for the management of sTBI in the maritime environment should be in keeping with current best evidence. Provision of specialist interventions for sTBI in military maritime environments may require alternative approaches matched to the skills of the staff and environmental restrictions.


2013 ◽  
Vol 14 (3) ◽  
pp. 415-424 ◽  
Author(s):  
Hinemoa Elder

Background: Application of salient cultural knowledge held by families following child and adolescent traumatic brain injury (TBI) has yet to be documented in the literature. While the importance of the family is a well-established determinant of enhanced outcomes in child and adolescent TBI, the emphasis to date has been on the leading role of professional knowledge. The role of whānau (extended family) is recognised as an essential aspect of hauora (wellbeing) for Māori, who are overrepresented in TBI populations. However, whānau knowledge systems as a potent resource for enhancing recovery outcomes have not previously been explored. This paper describes the development of an indigenous intervention, Te Waka Oranga.Method: Rangahau Kaupapa Māori (Māori determined research methods) theory building was used to develop a TBI intervention for working with Māori. The intervention emerged from the findings and analysis of data from 18 wānanga (culturally determined fora) held on rural, remote and urban marae (traditional meeting houses).Results: The intervention framework, called Te Waka Oranga, describes a process akin to teams of paddlers working together to move a waka (canoe, vessel) in a desired direction of recovery. This activity occurs within a Māori defined space, enabling both world views, that of the whānau and the clinical world, to work together. Whānau knowledge therefore has a vital role alongside clinical knowledge in maximising outcomes in mokopuna (infants, children, adolescents and young adults) with TBI.Conclusion: Te Waka Oranga provides for the equal participation of two knowledge systems, that of whānau and of clinical staff in their work in the context of mokopuna TBI. This framework challenges the existing paradigm of the role of families in child and adolescent TBI rehabilitation by highlighting the essential role of cultural knowledge and practices held within culturally determined groups. Further research is needed to test the intervention.


Brain Injury ◽  
2018 ◽  
Vol 33 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Philippe Allain ◽  
Leanne Togher ◽  
Philippe Azouvi

2019 ◽  
Vol 24 (9) ◽  
pp. 480-487 ◽  
Author(s):  
Neus Elias ◽  
Ana-Maria Rotariu ◽  
Tobias Grave

Traumatic brain injury is common in companion animals and can occur from many different types of trauma such as road traffic accidents or bites. Following the primary injury, which is beyond control of the clinician, secondary injury occurs minutes to days following the trauma. The secondary injury will lead to neuronal death, and is the focus of treatment strategies for the emergency veterinary surgeon. Treatment of traumatic brain injury includes nursing strategies, intravenous fluid therapy, hyperosmolar therapy and diuretics, pain management, maintenance of oxygenation and ventilation, temperature regulation, anticonvulsant therapy and glycaemic control. All of these are discussed in this clinical review.


2012 ◽  
Vol 15 (3) ◽  
pp. 253-263 ◽  
Author(s):  
Karen M. O’Connell ◽  
Marguerite T. Littleton-Kearney

Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.


2017 ◽  
Vol 312 (2) ◽  
pp. F259-F265 ◽  
Author(s):  
Sandeep K. Mallipattu ◽  
Chelsea C. Estrada ◽  
John C. He

Krüppel-like factors (KLFs) are a family of zinc-finger transcription factors critical to mammalian embryonic development, regeneration, and human disease. There is emerging evidence that KLFs play a vital role in key physiological processes in the kidney, ranging from maintenance of glomerular filtration barrier to tubulointerstitial inflammation to progression of kidney fibrosis. Seventeen members of the KLF family have been identified, and several have been well characterized in the kidney. Although they may share some overlap in their downstream targets, their structure and function remain distinct. This review highlights our current knowledge of KLFs in the kidney, which includes their pattern of expression and their function in regulating key biological processes. We will also critically examine the currently available literature on KLFs in the kidney and offer some key areas in need of further investigation.


2013 ◽  
Vol 217 (3) ◽  
pp. S32 ◽  
Author(s):  
Cecilie H. Jepsen ◽  
Pär I. Johansson ◽  
Anders Perner ◽  
Martin H. Sillesen ◽  
Hasan B. Alam ◽  
...  

2014 ◽  
Vol 77 (2) ◽  
pp. 292-297 ◽  
Author(s):  
Cecilie Heerdegen Jepsen ◽  
Marc A. deMoya ◽  
Anders Perner ◽  
Martin Sillesen ◽  
Sisse R. Ostrowski ◽  
...  

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