The most common mec… Clemens Pahl FRCA DICM Consultant Intensivist King’s College Hospital . Anosmia: Common; probably caused by the shearing of the olfactory nerves at the cribriform plate[3] 3. Traumatic injury to the immature brain: inflammation, oxidative injury, and iron-mediated damage as potential therapeutic targets. With an estimated global incidence of 106 per 100,000 people, TBI is a leading cause of death and disability worldwide [1–3]. By continuing you agree to the Use of Cookies. Cerebral ischaemia and intracranial hypertension refer to secondary insults and, in treatment terms, these types of injury are sensitive to therapeutic interventions. Published by Elsevier Inc. COVID-19 and the Anaesthetist: A Special Series, South African Society of Anaesthesiologists, Special Issue on Mass Casualty Medicine and Anaesthesia: Science and Clinical Practice (PDF), Special Issue on Memory and Awareness in Anesthesia (PDF), Clinical neuroscience: relevance to current practice, Biomechanical and neuropathological classification of injury, General pathophysiology of traumatic brain injury, Specific pathophysiology of traumatic brain injury, We use cookies to help provide and enhance our service and tailor content and ads. Traumatic brain injury (TBI) is physical injury to brain tissue that temporarily or permanently impairs brain function. The progression of tissue damage relates to direct release of neurotoxic mediators or indirectly to the release of nitric oxide and cytokines. Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options. The mechanisms by which vasospasm occurs include chronic depolarization of vascular smooth muscle due to reduced potassium channel activity,61 release of endothelin along with reduced availability of nitric oxide,75 cyclic GMP depletion of vascular smooth muscle,67 potentiation of prostaglandin-induced vasoconstriction,1 and free radical formation.16,45, Cerebral metabolism (as reflected by cerebral oxygen and glucose consumption) and cerebral energy state (as reflected by tissue concentrations of phosphocreatine and ATP or indirectly by the lactate/pyruvate ratio) are frequently reduced after TBI and present with considerable temporal and spatial heterogeneity.15,12,18,23 The degree of metabolic failure relates to the severity of the primary insult, and outcome is worse in patients with lower metabolic rates compared with those with minor or no metabolic dysfunction.72 The reduction in post-traumatic cerebral metabolism relates to the immediate (primary) insult leading to mitochondrial dysfunction with reduced respiratory rates and ATP-production, a reduced availability of the nicotinic co-enzyme pool, and intramitochondrial Ca2+-overload.66,70 However, the use of hyperoxia in an attempt to correct for metabolic failure produces inconsistent results.39,47 Interestingly, decreases in cerebral metabolic demand may15 or may not be associated with matching decreases in CBF.12,18 The latter reflects uncoupling of CBF and metabolism, probably due to increased adenosine availability.1254. The majority (75–80%) of all TBI cases are mild in nature and are accompanied by the rapid resolution of the immediate symptoms, including disorientation, dizziness, nausea, and balance problems (Table 1) [4]. The nature of apoptosis generally requires energy supply and imbalance between naturally occurring pro- and anti-apoptotic proteins. Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 229 patients. The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. Ca2+ activates lipid peroxidases, proteases, and phospholipases which in turn increase the intracellular concentration of free fatty acids and free radicals. Likewise, both patterns are the basis for the management of cerebral perfusion pressure (CPP) and ICP and impairment of these regulatory mechanisms reflect increased risk for secondary brain damage. These are called traumatic brain injuries (TBIs). superoxide dismutase, glutathione peroxidase, and catalase) induces peroxidation of cellular and vascular structures, protein oxidation, cleavage of DNA, and inhibition of the mitochondrial electron transport chain.3,11,60 Although these mechanisms are adequate to contribute to immediate cell death, inflammatory processes and early or late apoptotic programmes are induced by oxidative stress.11, Oedema formation frequently occurs after TBI. Anatomically, this pathology increases the volume of the extracellular space.16,68Cytotoxic brain oedema is characterized by intracellular water accumulation of neurons, astrocytes, and microglia irrespective of the integrity of the vascular endothelial wall. In the United States alone, 1.7 million traumatic events occur annually accounting for 50,000 deaths. Cortical spreading depression and peri-infarct depolarization in acutely injured human cerebral cortex. Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Traumatic brain injury (TBI) is one of the leading causes of disability in the United States, estimated at 13.5 million individuals . Transfusion of erythrocyte concentrates produces a variable increment on cerebral oxygenation in patients with severe traumatic brain injury. TBI can be classified based on severity (ranging from mild traumatic brain injury [mTBI/concussion] to severe traumatic brain injury), mechanism ( closed or penetrating head injury ), or other features (e.g., occurring in a specific location or over a widespread area). Evaluation of apoptosis in cerebrospinal fluid of patients with severe head injury. Hemodynamically significant cerebral vasospasm and outcome after head injury: a prospective study. Traumatic brain injury is a major source of death and disability worldwide. Understanding the multidimensional cascade of injury offers therapeutic options including the management of CPP, mechanical (hyper-) ventilation, kinetic therapy to improve oxygenation and to reduce ICP, and pharmacological intervention to reduce excitotoxicity and ICP. glutamate, aspartate), activation of, Studies in laboratory animals and humans have investigated the effects of TBI on CBF. Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biochemical mechanisms. Traumatic brain injury (TBI) occurs when a traumatic event causes the brain to move rapidly within the skull, leading to damage. Translocation of phosphatidylserine initiates discrete but progressive membrane disintegration along with lysis of nuclear membranes, chromatine condensation, and DNA-fragmentation. Posttraumatic vasospasm: the epidemiology, severity, and time course of an underestimated phenomenon: a prospective study performed in 229 patients, Traumatic injury to the immature brain: inflammation, oxidative injury, and iron-mediated damage as potential therapeutic targets, Increased adenosine in cerebrospinal fluid after severe traumatic brain injury in infants and children: association with severity of injury and excitotoxicity, Morphological features in human cortical brain microvessels after head injury: a three-dimensional and immunocytochemical study, Continuous monitoring of the microcirculation in neurocritical care: an update on brain tissue oxygenation. Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism. vessel distortion) as a result of mechanical displacement, hypotension in the presence of autoregulatory failure,46,55 inadequate availability of nitric oxide or cholinergic neurotransmitters,16,59 and potentiation of prostaglandin-induced vasoconstriction.1, Patients with TBI may develop cerebral hyperperfusion (CBF >55 ml 100 g−1 min−1) in the early stages of injury. Diagnosis is suspected clinically and confirmed by imaging (primarily CT). The upper limit of cerebral blood flow autoregulation in acute intracranial hypertension. It is important to note that diagnosing hypoperfusion or hyperperfusion is only valid after assessing measurements of CBF in relation to those of cerebral oxygen consumption. The first stages of cerebral injury after TBI are characterized by direct tissue damage and impaired regulation of CBF and metabolism. Although this mismatch is induced by several different vascular and haemodynamic mechanisms as indicated earlier, the final common endpoint is brain tissue hypoxia. In response to these inflammatory processes, injured and adjacent tissue (based on ‘spreading depressions’) will be eliminated and within hours, days, and weeks astrocytes produce microfilaments and neutropines ultimately to synthesize scar tissue.21 Proinflammatory enzymes such as tumour necrosis factor, interleukin-1-ß, and interleukin-6 are upregulated within hours from injury. Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain injury. These processes induce chemokines and adhesion molecules and in turn mobilize immune and glial cells in a parallel and synergistic fashion.38,53 For example, activated polymorphonuclear leucocytes adhere to defective but also intact endothelial cell layers as mediated through adhesion molecules. 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