Background: Improvised explosive devices have resulted in a unique polytrauma injury pattern termed dismounted complex blast injury (DCBI), which is frequent in the modern military theater. Dismounted complex blast injury is characterized by extremity amputations, junctional vascular injury, and blast traumatic brain injury (bTBI). We developed a combat casualty relevant DCBI swine model, which combines hemorrhagic shock (HS) and tissue injury (TI) with a bTBI, to study interventions in this unique and devastating military injury pattern.
Methods: A 50-kg male Yorkshire swine were randomized to the DCBI or SHAM group (instrumentation only). Those in the DCBI group were subjected to HS, TI, and bTBI. The blast injury was applied using a 55-psi shock tube wave. Tissue injury was created with bilateral open femur fractures. Hemorrhagic shock was induced by bleeding from femoral arteries to target pressure. A resuscitation protocol modified from the Tactical Combat Casualty Care guidelines simulated battlefield resuscitation for 240 minutes.
Results: Eight swine underwent the DCBI model and five were allocated to the SHAM group. In the DCBI model the mean base excess achieved at the end of the HS shock was -8.57 ± 5.13 mmol·L -1 . A significant coagulopathy was detected in the DCBI model as measured by prothrombin time (15.8 seconds DCBI vs. 12.86 seconds SHAM; p = 0.02) and thromboelastography maximum amplitude (68.5 mm DCBI vs. 78.3 mm in SHAM; p = 0.0003). For the DCBI models, intracranial pressure (ICP) increased by a mean of 13 mm Hg, reaching a final ICP of 24 ± 7.7 mm Hg.
Conclusion: We created a reproducible large animal model to study the combined effects of severe HS, TI, and bTBI on coagulation and ICP in the setting of DCBI, with significant translational applications for the care of military warfighters. Within the 4-hour observational period, the swine developed a consistent coagulopathy with a concurrent brain injury evidenced by increasing ICP.
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http://dx.doi.org/10.1097/TA.0000000000003674 | DOI Listing |
Alzheimers Dement
December 2024
University of Texas Medical Branch, Galveston, TX, USA.
Background: The misfolding and aggregation of the tau protein into neurofibrillary tangles constitute a central feature of tauopathies. Traumatic brain injury (TBI) has emerged as a potential risk factor, triggering the onset and progression of tauopathies. Our previous research revealed distinct polymorphisms in soluble tau oligomers originating from single versus repetitive mild TBIs.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Miami, Miami, FL, USA.
Background: Exposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age-related cognitive impairment. While the role of noise-induced hearing loss in long-term health consequences, such as progression or development of Alzheimer's Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss, and the progression of AD pathology, and determine the underlying mechanisms.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Missouri, Columbia, MO, USA.
Background: This study was to elucidate the impact of blast-induced neurotrauma (BINT) on phosphoproteome networks and cognition in a genetically heterogeneous population of mice (rTg4510) with the human tau P301L mutation linked to Alzheimer's disease-related dementia (ADRD) including frontotemporal dementia.
Method: Mild traumatic brain injury was induced in rTg4510 mice exposed to a single low-density blast (LIB) at an upright position. After assessment of cognitive function by the automated-Home Cage Monitoring (aHCM) system, frontal cortex tissue was collected at 40 days post-injury.
Alzheimers Dement
December 2024
Louis Stokes Cleveland VA Medical Center, Cleveland, OH, USA.
Background: TBI is the 3rd greatest risk factor for developing AD, behind genetics and aging. TBI is associated with a 3-4 year earlier onset of cognitive impairment, and increased cortical thinning and amyloid plaques in people with AD. The underlying mechanisms of this relationship are not understood, and as a result there are no treatments that protect patients from accelerated AD after TBI.
View Article and Find Full Text PDFNeurotrauma Rep
December 2024
Department of Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
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