عنوان

Blast-Induced Neurotrauma and the Cavitation Mechanism of Injury

Number

TL50775

.Language of Text, Soundtrack etc

انگلیسی

Title Proper

Blast-Induced Neurotrauma and the Cavitation Mechanism of Injury

General Material Designation

[Thesis]

First Statement of Responsibility

Yu, Allen Wei

Subsequent Statement of Responsibility

Bass, Cameron R.

Name of Publisher, Distributor, etc.

Duke University

Date of Publication, Distribution, etc.

2019

Text of Note

319 p.

Dissertation or thesis details and type of degree

Ph.D.

Body granting the degree

Duke University

Text preceding or following the note

2019

Text of Note

Traumatic brain injuries (TBIs) are a major public health concern and socioeconomic burden worldwide. In recent years, brain injuries in US service personnel have focused attention on TBI affecting the military population (Bass et al., 2012). Blast injuries have become the most common cause of mortality and morbidity in soldiers returning from Iraq and Afghanistan (Owens et al., 2008, Warden, 2006). The frequency of blast-related sequelae found in allied forces has led some to call it the 'signature wound' of the wars abroad. The growing incidence of TBI has spurred an increase in research efforts within the neurotrauma community to define TBI etiology. Identification of the critical injury mechanisms underlying TBI is an area of greatest need. Our understanding of TBI etiology, physical damaging mechanisms, and pathophysiology remains inadequate. The ability to design specific countermeasures and targeted prevention strategies is restricted by an incomplete understanding of the underlying damaging mechanisms. Cavitation, the formation of vapor filled cavities in a liquid medium, has been proposed as a damaging mechanism of TBI in both blunt impacts (Ward et al., 1948, Gross, 1958) and blast-induced neurotrauma (Moore et al., 2008, Panzer et al., 2012c). The cavitation hypothesis of TBI centers on observation that high energy events such as highexplosive blast impingement onto the head generate large pressure transients in and around the brain. Localized areas of low pressure may surpass the tensile limits of the cerebrospinal fluid vaporizing the fluid and forming cavitation bubbles. These voids grow, potentially displacing surrounding tissue. When the bubbles collapse, perhaps violently, jets of liquid with potentially large localized pressures and temperatures may be created, damaging surrounding tissue. The main objective of this dissertation was to develop an experimental foundation and provide empirical evidence for cavitation as a damaging mechanism of blast-induced TBI. This dissertation uses biofidelic surrogate head models of blast and in vivo animal models of blast injury to address the unanswered questions surrounding cavitation and blast neurotrauma. Foremost, cavitation response was observed in the surrogate head form exposed to blast conditions associated with injury. The 50% risk of cavitation occurs at a blast level of 262 kPa incident overpressure and 1.96 ms duration. This blast dosage represents a 62% chance of mild intracranial bleeding from scaled ferret experiments (Rafaels et al., 2012). Cavitation onsert, growth, and collapse were confirmed through high-speed imaging of the fluid layers of the contrecoup, while strong acoustic emission signatures associated with cavity collapse were captured and time matched with the video. Near-harmonic frequencies at 64 kHz, 126 kHz, and 267 kHz were associated with the energetic collapse of the bubbles. Our results provide compelling evidence that primary blast alone may induce cavitation that leads to TBI. Evidence of cavitation was recorded in live porcine specimen exposed to blast. Acoustic sensors mounted to the skull of each specimen recorded acoustic emissions during blast exposure. Scaled spectral analysis revealed acoustic energy in higher frequencies bands with peaks at 64 kHz, 139 kHz, and 251 kHz, closely matching the spectral peaks associated with void collapse in surrogate experiments. To our knowledge, this study is the first to present evidence of blast-induced cavitation in a live animal model in the field of cavitation TBI research. The results presented in this dissertation also greatly improve our understanding of how mechanical loads are imparted onto the head during a blast exposure and how this loading leads to cavitation onset. Strain analysis of the surrogate head indicates wall compliance from skull deformation and shear wave propagation through the skull as significant physical factors driving the tensile fluid responses in the head. Future design considerations for preventative measures should account for these physical mechanisms. This dissertation also makes important contributions to blast injury research by presenting a clinically relevant murine model of blast TBI. Murine blast lethality risk and functional behavior outcomes before and after blast injury are presented. We provide guidelines for small animal blast testing, along with methodological recommendations for benchtop shock tube design and specimen placement in relation to the shock tube. The contributions of this dissertation further serve as an important methodological guide to the neurotrauma and biomechanics community studying blast-related TBI and cavitation as a damaging mechanism. The developed surrogate head system and cavitation detection techniques provide a research template and are a springboard to future research efforts elucidating the damaging effects of cavitation during TBI.

Subject Term

Bioengineering

Subject Term

Biomechanics

Subject Term

Biomedical engineering

Yu, Allen Wei

Bass, Cameron R.

Duke University

Electronic name

p

[Thesis]

276903

a

Y