Computed Tomography–Estimated Specific Gravity at Hospital Admission Predicts 6-Month Outcome in Mild-to-Moderate Traumatic Brain Injury Patients Admitted to the Intensive Care Unit

Degos, Vincent; Lescot, Thomas; Icke, Christian; Manach, Yannick Le; Fero, Katherine E.; Sánchez, Paola; Hadiji, Bassem; Zouaoui, Abederrezak; Boch, Anne‐Laure; Abdennour, Lamine; Apfel, Christian C.; Puybasset, Louis

doi:10.1213/ane.0b013e318249fe7a

Cited by 10 publications

(7 citation statements)

References 28 publications

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“…Brain imaging results have confirmed the frequent occurrence of BBB breakdown in patients with TBI and suggest that this pathology could be used as a biomarker in the clinic as well as in drug trials. Impairment of BBB after TBI has been associated with oedema formation [5–7]. Enhanced microvascular leakage was caused by disruption in vascular endothelial junction proteins (JPs) consisting of a complex of transmembrane (junctional adhesion molecule-1, occludin and claudins) and cytoplasmic (zonula occluden-1 (ZO-1), zonula occluden-2 (ZO-2), cingulin, AF-6 and 7H6) proteins, which are linked to the actin cytoskeleton [8].…”

Section: Traumatic Brain Injury and Vascular Dysfunctionmentioning

confidence: 99%

Role of fibrinogen in cerebrovascular dysfunction after traumatic brain injury

Muradashvili

Lominadze

2013

Brain Injury

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Traumatic brain injury (TBI) has been associated with various neurological disorders. However, the role of cerebrovascular dysfunction and its mechanisms associated with TBI are still not well understood. Inflammation is the main cause of vascular dysfunction. It affects properties of blood components and the vascular wall leading to changes in blood flow and in interaction of blood components and vascular endothelium exacerbating microcirculatory complications during inflammatory diseases. One of the markers of inflammation is a plasma adhesion protein, fibrinogen (Fg). At elevated levels, Fg can also cause inflammatory responses. One of the manifestations of inflammatory responses is an increase in microvascular permeability leading to accumulation of plasma proteins in the subendothelial matrix and causing vascular remodelling. This has a most devastating effect on cerebral circulation after TBI that is accompanied with an elevation of plasma level of Fg and with an increased cerebrovascular permeability in injury penumbra impairing the normal healing process. This study reviews cerebrovascular alterations after TBI, considers the consequences of increased blood–brain barrier permeability, defines the role of elevated level of Fg and discusses the potential mechanisms of its action leading to vascular dysfunction, which subsequently can cause impairment in neuronal function. Thus, possible mechanisms of vasculo-neuronal dysfunction after TBI are considered.

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Section: Traumatic Brain Injury and Vascular Dysfunctionmentioning

confidence: 99%

Role of fibrinogen in cerebrovascular dysfunction after traumatic brain injury

Muradashvili

Lominadze

2013

Brain Injury

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“…Confirmatory factor analysis was conducted using the Maximum Likelihood estimator. The measurement model included one latent variable, neurocognitive status, defined from the observed scores on the following scales: ( 1 ) MMSE; ( 2 ) PSI – 2 subscales; ( 3 ) Stroop Color-Word Test – 3 subscales; ( 4 ) GOS-E; ( 5 ) ERBI. The structural model included observed values of the serum biomarkers S100 and NSE at 4h and 72h as exogenous variables and latent cognitive status as an endogenous variable.…”

Section: Methodsmentioning

confidence: 99%

“…History of TBI has been associated with an increased risk of cognitive decline in older adults and an earlier age of dementia onset [ 3 , 4 ]. The risk factors for long-term cognitive impairment in patients with TBI include the severity of the injury [ 5 ], old age [ 6 ], length of hospital stay [ 7 ] and preinjury educational level [ 8 ]. Selecting the patients at risk of developing cognitive impairment after TBI is crucial for establishing a suitable treatment strategy, a personalized rehabilitation program, and communicating with the patients and their relatives.…”

Section: Introductionmentioning

confidence: 99%

Prediction of Neurocognitive Outcome after Moderate-Severe Traumatic Brain Injury Using Serum Neuron-Specific Enolase and S100 biomarkers

et al. 2020

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Seric biomarkers have been tested in a large number of studies on traumatic brain injuries (TBI) patients in order to predict severity, especially related to the short-term outcome. However, TBI patients have a high risk of developing long-term complications such as physical disability, cognitive impairment, psychiatric pathology, epilepsy, and others. The aim of this study was to assess the correlation between protein biomarkers S100 and neuron-specific enolase (NSE) and neurocognitive status at 10- and 90-days post-injury. Both biomarkers were tested in the first 4h and after 72h post-injury in 62 patients with moderate-severe TBI. The patients were evaluated by a series of neurocognitive tests: Early Rehabilitation Barthel Index (ERBI), Glasgow Outcome Scale-Extended (GOSE), The Mini-Mental State Examination (MMSE), Processing Speed Index (PSI), and Stroop Test, at 10 and 90 days post-injury and supplementary by the Hospital Anxiety and Depression Scale at 90 days. For evaluating the whole neurocognitive status instead of every scale separately, we used Structural Equation Modeling (SEM), while for anxiety and depressive symptoms, we used multiple regression analyses. SEM showed that NSE values at 4 hours were significant predictors of the cognitive status at 10 (p=0.034) and 90 days (p= 0.023). Also, there were found significant correlations between NSE at 4h and the anxiety level. This study demonstrated a significant correlation between NSE at 4h and short and medium-term neuropsychological outcomes, which recommends using this biomarker for selecting patients with a higher risk of cognitive dysfunction.

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“…This mechanism is of short duration and occurs in about 1/4 of the patients with severe TBI, independently of lesions at magnetic resonance images (MRI), thus remaining sequelae for about 2 weeks. It can also worsen the prognosis ( 138 ) through cerebral herniation ( 139 , 140 ) MRI with apparent diffusion coefficient is used to distinguish between vasogenic and cytotoxic edema in TBI patients. While freely diffusible water at MRI is marker of vasogenic edema, restrict water movement represents cytotoxic edema ( 139 ).…”

Section: Research Agendamentioning

confidence: 99%

Escalate and De-Escalate Therapies for Intracranial Pressure Control in Traumatic Brain Injury

et al. 2020

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Severe traumatic brain injury (TBI) is frequently associated with an elevation of intracranial pressure (ICP), followed by cerebral perfusion pressure (CPP) reduction. Invasive monitoring of ICP is recommended to guide a step-by-step “staircase approach” which aims to normalize ICP values and reduce the risks of secondary damage. However, if such monitoring is not available clinical examination and radiological criteria should be used. A major concern is how to taper the therapies employed for ICP control. The aim of this manuscript is to review the criteria for escalating and withdrawing therapies in TBI patients. Each step of the staircase approach carries a risk of adverse effects related to the duration of treatment. Tapering of barbiturates should start once ICP control has been achieved for at least 24 h, although a period of 2–12 days is often required. Administration of hyperosmolar fluids should be avoided if ICP is normal. Sedation should be reduced after at least 24 h of controlled ICP to allow neurological examination. Removal of invasive ICP monitoring is suggested after 72 h of normal ICP. For patients who have undergone surgical decompression, cranioplasty represents the final step, and an earlier cranioplasty (15–90 days after decompression) seems to reduce the rate of infection, seizures, and hydrocephalus.

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Computed Tomography–Estimated Specific Gravity at Hospital Admission Predicts 6-Month Outcome in Mild-to-Moderate Traumatic Brain Injury Patients Admitted to the Intensive Care Unit

Abstract: In this MM-TBI cohort admitted to the ICU, eSG of routine CT scans was correlated with mortality, ICU severity, and predicted 6-month poor outcome. An external validation with studies that include the spectrum of TBI severities is warranted to confirm our results.

Cited by 10 publications

References 28 publications

Role of fibrinogen in cerebrovascular dysfunction after traumatic brain injury

Role of fibrinogen in cerebrovascular dysfunction after traumatic brain injury

Prediction of Neurocognitive Outcome after Moderate-Severe Traumatic Brain Injury Using Serum Neuron-Specific Enolase and S100 biomarkers

Escalate and De-Escalate Therapies for Intracranial Pressure Control in Traumatic Brain Injury

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