Quantitative analysis of computed tomography images and early detection of cerebral edema for pediatric traumatic brain injury patients: retrospective study

Kim, Hakseung; Kim, Gwang-dong; Yoon, Byung Chul; Kim, Keewon; Kim, Byung Jo; Choi, Young Hoon; Czosnyka, Marek; Oh, Byung-Mo; Kim, Dong-Joo

doi:10.1186/preaccept-1735769794135509

Cited by 7 publications

(14 citation statements)

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“…The analysis was conducted using an in-house software program implemented in JAVA (Oracle Inc.). 11 The software allows the exclusion of minor intracranial entities (cranium, calcifications, etc.) from the analysis and accurately derives the density distribution of major intracranial entities (i.e., CSF, blood, and parenchyma), which have an HU range of 0-79.…”

Section: Quantitative Densitometric Analysismentioning

confidence: 99%

“…18 A more recent approach for a quantitative CT analysis of patients with an acquired brain injury is densitometric analysis. 11,12 Instead of relying on specific, localized ROIs to investigate pathological changes in the density of brain tissues, this approach measures changes in the overall density of the entire brain in a completely automated manner. 11,12 Of particular interest, the densitometric analysis enables a quantitative examination of the parenchymal density distribution, thereby enabling subsequent measurements of the proportions of GM and WM showing a normal density.…”

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confidence: 99%

“…11,12 Instead of relying on specific, localized ROIs to investigate pathological changes in the density of brain tissues, this approach measures changes in the overall density of the entire brain in a completely automated manner. 11,12 Of particular interest, the densitometric analysis enables a quantitative examination of the parenchymal density distribution, thereby enabling subsequent measurements of the proportions of GM and WM showing a normal density. 11,35 If both the deep GM and WM densities decrease in response to ischemic-edematous insults after TBI, then the quantification of the material density of these structures could significantly enhance the prognostic capacity of noncontrast CT images in patients with acute TBI.…”

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confidence: 99%

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Changes in the gray and white matter of patients with ischemic-edematous insults after traumatic brain injury

Kim

Song

et al. 2019

Journal of Neurosurgery

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OBJECTIVEGray matter (GM) and white matter (WM) are vulnerable to ischemic-edematous insults after traumatic brain injury (TBI). The extent of secondary insult after brain injury is quantifiable using quantitative CT analysis. One conventional quantitative CT measure, the gray-white matter ratio (GWR), and a more recently proposed densitometric analysis are used to assess the extent of these insults. However, the prognostic capacity of the GWR in patients with TBI has not yet been validated. This study aims to test the prognostic value of the GWR and evaluate the alternative parameters derived from the densitometric analysis acquired during the acute phase of TBI. In addition, the prognostic ability of the conventional TBI prognostic models (i.e., IMPACT [International Mission for Prognosis and Analysis of Clinical Trials in TBI] and CRASH [Corticosteroid Randomisation After Significant Head Injury] models) were compared to that of the quantitative CT measures.METHODSThree hundred patients with TBI of varying ages (92 pediatric, 94 adult, and 114 geriatric patients) and admitted between 2008 and 2013 were included in this retrospective cohort study. The normality of the density of the deep GM and whole WM was evaluated as the proportion of CT pixels with Hounsfield unit values of 31–35 for GM and 26–30 for WM on CT images of the entire supratentorial brain. The outcome was evaluated using the Glasgow Outcome Scale (GOS) at discharge (GOS score ≤ 3, n = 100).RESULTSLower proportions of normal densities in the deep GM and whole WM indicated worse outcomes. The proportion of normal WM exhibited a significant prognostic capacity (area under the curve [AUC] = 0.844). The association between the outcome and the normality of the WM density was significant in adult (AUC = 0.792), pediatric (AUC = 0.814), and geriatric (AUC = 0.885) patients. In pediatric patients, the normality of the overall density and the density of the GM were indicative of the outcome (AUC = 0.751). The average GWR was not associated with the outcome (AUC = 0.511). IMPACT and CRASH models showed adequate and reliable performance in the pediatric and geriatric groups but not in the adult group. The highest overall predictive performance was achieved by the densitometry-augmented IMPACT model (AUC = 0.881).CONCLUSIONSBoth deep GM and WM are susceptible to ischemic-edematous insults during the early phase of TBI. The extent of the secondary injury was better evaluated by analyzing the normality of the deep GM and WM rather than by calculating the GWR.

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Section: Quantitative Densitometric Analysismentioning

confidence: 99%

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Changes in the gray and white matter of patients with ischemic-edematous insults after traumatic brain injury

Kim

Song

et al. 2019

Journal of Neurosurgery

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“…The pressure increase is more common in children experiencing TBI than adults (48) Hounsfield unit values from brain CT mapped across an intracranial area can be used to accurately predict brain edema following TBI in children (82). A new imaging modality, shear wave elastography, has also been tested in rodents and gives an accurate representation of edema (184).…”

Section: Vasospasms Subarachnoid Hemorrhage Edema and Ischemic Hypoxiamentioning

confidence: 99%

Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

Logsdon

Lucke‐Wold

Turner

et al. 2015

Comprehensive Physiology

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Traumatic brain injury (TBI) is acquired from an external force, which can inflict devastating effects to the brain vasculature and neighboring neuronal cells. Disruption of vasculature is a primary effect that can lead to a host of secondary injury cascades. The primary effects of TBI are rapidly occurring while secondary effects can be activated at later time points and may be more amenable to targeting. Primary effects of TBI include diffuse axonal shearing, changes in blood brain barrier (BBB) permeability, and brain contusions. These mechanical events, especially changes to the BBB, can induce calcium perturbations within brain cells producing secondary effects, which include cellular stress, inflammation, and apoptosis. These secondary effects can be potentially targeted to preserve the tissue surviving the initial impact of TBI. In the past, TBI research had focused on neurons without any regard for glial cells and the cerebrovasculature. Now a greater emphasis is being placed on the vasculature and the neurovascular unit following TBI. A paradigm shift in the importance of the vascular response to injury has opened new avenues of drug treatment strategies for TBI. However, a connection between the vascular response to TBI and the development of chronic disease has yet to be elucidated. Long-term cognitive deficits are common amongst those sustaining severe or multiple mild TBIs. Understanding the mechanisms of cellular responses following TBI is important to prevent the development of neuropsychiatric symptoms. With appropriate intervention following TBI, the vascular network can perhaps be maintained and the cellular repair process possibly improved to aid in the recovery of cellular homeostasis.

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“…Brain edema following TBI can cause serious complications by limiting brain oxygen delivery and increasing intracranial pressure (Nirula et al, 2014). The pressure increase is more common in children experiencing TBI than adults (Ewing-Cobbs et al, 2000) Hounsfield unit values from brain CT mapped across an intracranial area can be used to accurately predict brain edema following TBI in children (Kim et al, 2014). A new imaging modality, shear wave elastography, has also been tested in rodents and gives an accurate representation of edema (Xu et al, 2014b).Ulinastatin, a serine protease inhibitor, is currently being investigated for reduction of edema in rodents following TBI (Cui and Zhu, 2014).…”

Section: Vasospasms Subarachnoid Hemorrhage Edema and Ischemic Hypoxiamentioning

confidence: 99%

Elucidating Mechanisms of Neurobehavioral Dysfunction in a Rodent Model of Traumatic Brain Injury

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Quantitative analysis of computed tomography images and early detection of cerebral edema for pediatric traumatic brain injury patients: retrospective study

Cited by 7 publications

References 50 publications

Changes in the gray and white matter of patients with ischemic-edematous insults after traumatic brain injury

Changes in the gray and white matter of patients with ischemic-edematous insults after traumatic brain injury

Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

Elucidating Mechanisms of Neurobehavioral Dysfunction in a Rodent Model of Traumatic Brain Injury

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