A comparison of CT lung voxel density analysis in a blast and non blast injured casualty.

2018 ◽  
Vol 165 (3) ◽  
pp. 166-168
Author(s):  
Sebastian Bourn ◽  
T E Scott ◽  
E J Hulse

IntroductionPrimary blast lung injury (PBLI) is a prominent feature in casualties following exposure to blast. PBLI carries high morbidity and mortality, but remains difficult to diagnose and quantify. Radiographic diagnosis of PBLI was historically made with the aid of plain radiographs; more recently, qualitative review of CT images has assisted diagnosis.MethodsWe report a novel way of measuring post-traumatic acute lung injury using CT lung density analysis in two casualties. One casualty presented following blast exposure with confirmed blast lung injury and the other presented following extremity injury without blast exposure. Three-dimensional lung maps of each casualty were produced from their original trauma CT scan. Analysis of the lung maps allowed quantitative radiological comparison exposing areas of reduced aeration of the patient’s lungs.Results45% of the blast-exposed lungs were non-aerated compared with 10% in the non-blast-exposed lungs.DiscussionIn these example cases quantitative CT lung density analysis allowed blast-injured lungs to be distinguished from non-blast-exposed lungs.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Chang Yang ◽  
Zhang Dong-hai ◽  
Liu Ling-ying ◽  
Yu Yong-hui ◽  
Wu Yang ◽  
...  

Abstract Blast lung injury (BLI) caused by both military and civilian explosions has become the main cause of death for blast injury patients. By building three-dimensional (3D) models of rat explosion regions, we simulated the surface pressure of the skin and lung. The pressure distributions were performed at 5 distances from the detonation center to the center of the rat. When the distances were 40 cm, 50 cm, 60 cm, 70 cm and 80 cm, the maximum pressure of the body surface were 634.77kPa, 362.46kPa, 248.11kPa, 182.13kPa and 109.29kPa and the surfaces lung pressure ranges were 928–2916 Pa, 733–2254 Pa, 488–1236 Pa, 357–1189 Pa and 314–992 Pa. After setting 6 virtual points placed on the surface of each lung lobe model, simulated pressure measurement and corresponding pathological autopsies were then conducted to validate the accuracy of the modeling. For the both sides of the lung, when the distance were 40 cm, 50 cm and 60 cm, the Pearson’s values showed strong correlations. When the distances were 70 cm and 80 cm, the Pearson’s values showed weak linear correlations. This computational simulation provided dynamic anatomy as well as functional and biomechanical information.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Chang Yang ◽  
Zhang Dong-hai ◽  
Liu Ling-ying ◽  
Yu Yong-hui ◽  
Wu Yang ◽  
...  

An amendment to this paper has been published and can be accessed via a link at the top of the paper.


Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P<0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mian Wang ◽  
Hua Zhong ◽  
Xian Zhang ◽  
Xin Huang ◽  
Jing Wang ◽  
...  

AbstractAcute lung injury (ALI), which could be induced by multiple factors such as lipopolysaccharide (LPS), refer to clinical symptoms of acute respiratory failure, commonly with high morbidity and mortality. Reportedly, active ingredients from green tea have anti-inflammatory and anticancer properties, including epigallocatechin-3-gallate (EGCG). In the present study, protein kinase C alpha (PRKCA) is involved in EGCG protection against LPS-induced inflammation and ALI. EGCG treatment attenuated LPS-stimulated ALI in mice as manifested as improved lung injury scores, decreased total cell amounts, neutrophil amounts and macrophage amounts, inhibited the activity of MPO, decreased wet-to-dry weight ratio of lung tissues, and inhibited release of inflammatory cytokines TNF-α, IL-1β, and IL-6. PRKCA mRNA and protein expression showed to be dramatically decreased by LPS treatment while reversed by EGCG treatment. Within LPS-stimulated ALI mice, PRKCA silencing further aggravated, while PRKCA overexpression attenuated LPS-stimulated inflammation and ALI through MAPK signaling pathway. PRKCA silencing attenuated EGCG protection. Within LPS-induced RAW 264.7 macrophages, EGCG could induce PRKCA expression. Single EGCG treatment or Lv-PRKCA infection attenuated LPS-induced increases in inflammatory factors; PRKCA silencing could reverse the suppressive effects of EGCG upon LPS-stimulated inflammatory factor release. In conclusion, EGCG pretreatment inhibits LPS-induced ALI in mice. The protective mechanism might be associated with the inhibitory effects of PRKCA on proinflammatory cytokine release via macrophages and MAPK signaling pathway.


Author(s):  
John N. Cronin ◽  
João Batista Borges ◽  
Douglas C. Crockett ◽  
Andrew D. Farmery ◽  
Göran Hedenstierna ◽  
...  

Abstract Background Dynamic single-slice CT (dCT) is increasingly used to examine the intra-tidal, physiological variation in aeration and lung density in experimental lung injury. The ability of dCT to predict whole-lung values is unclear, especially for dual-energy CT (DECT) variables. Additionally, the effect of inspiration-related lung movement on CT variables has not yet been quantified. Methods Eight domestic pigs were studied under general anaesthesia, including four following saline-lavage surfactant depletion (lung injury model). DECT, dCT and whole-lung images were collected at 12 ventilatory settings. Whole-lung single energy scans images were collected during expiratory and inspiratory apnoeas at positive end-expiratory pressures from 0 to 20 cmH2O. Means and distributions of CT variables were calculated for both dCT and whole-lung images. The cranio-caudal displacement of the anatomical slice was measured from whole-lung images. Results Mean CT density and volume fractions of soft tissue, gas, iodinated blood, atelectasis, poor aeration, normal aeration and overdistension correlated between dCT and the whole lung (r2 0.75–0.94) with agreement between CT density distributions (r 0.89–0.97). Inspiration increased the matching between dCT and whole-lung values and was associated with a movement of 32% (SD 15%) of the imaged slice out of the scanner field-of-view. This effect introduced an artefactual increase in dCT mean CT density during inspiration, opposite to that caused by the underlying physiology. Conclusions Overall, dCT closely approximates whole-lung aeration and density. This approximation is improved by inspiration where a decrease in CT density and atelectasis can be interpreted as physiological rather than artefactual.


2018 ◽  
Vol 165 (1) ◽  
pp. 51-56
Author(s):  
Jason E Smith ◽  
S Watts ◽  
A M Spear ◽  
C Wilson ◽  
E Kirkman

IntroductionPrimary blast lung injury causes intrapulmonary haemorrhage. A number of case reports have suggested the efficacy of recombinant activated factor VII (rFVIIa) in the treatment of diffuse alveolar haemorrhage from a range of medical causes, but its efficacy in blast lung is unknown. The aim of this study was to investigate whether nebulised rFVIIa attenuates the haemorrhagic effects of blast lung injury in an animal model.MethodsTerminally anaesthetised rabbits subjected to blast lung injury were randomised to receive either rFVIIa or placebo via a nebuliser. The primary outcome was the level of blood iron–transferrin complex, a marker of the extent of blast lung injury, analysed using low temperature electron paramagnetic resonance spectroscopy.ResultsBlast exposure led to a significant fall in iron-bound transferrin in both groups of animals (p<0.001), which remained depressed during the study. There were no significant differences in iron–transferrin between the rFVIIa and placebo treatment groups over the duration of the study (p=0.081), and there was no trend towards elevated iron–transferrin in the rFVIIa-treated group once drug treatment had started. There was suggestive evidence of systemic absorption of rFVIIa given via the inhaled route.ConclusionA single dose of nebulised rFVIIa did not attenuate pulmonary haemorrhage in a rabbit model of blast lung injury. As there was some evidence of systemic absorption, the inhaled route does not avoid the concern about potential thromboembolic complications from administration of rFVIIa.


2012 ◽  
Vol 73 (5) ◽  
pp. 1121-1129 ◽  
Author(s):  
Lisa N. MacFadden ◽  
Philemon C. Chan ◽  
Kevin H.-H. Ho ◽  
James H. Stuhmiller

Author(s):  
Vikas P. Chaubey ◽  
Kevin B. Laupland ◽  
Christopher B. Colwell ◽  
Gina Soriya ◽  
Shelden Magder ◽  
...  

2015 ◽  
pp. 209-210
Author(s):  
Sara J. Aberle

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