Browsing by Subject "Blast"

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 high-explosive 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.

Blast related injuries have become a common occurrence among soldiers and civilians serving in Iraq and Afghanistan, and minor traumatic brain injuries associated with such incidents have increased correspondingly. Advances in protection and treatment have allowed many individuals to survive what would have previously been deadly blasts but there is a concern that there are additional negative side effects associated with such exposure. This study hypothesizes that human T leukocytes and promyelocytes respond to blasts by initiating cell death processes and releasing microparticles that could lead to further systemic inflammation. It was found that there was a significant (p<0.05) increase in lactase dehydrogenase activity and microparticle release in HL-60 cells blasted using a shock tube (with an incident blast overpressure of either 1000 or 1300 kPA and a duration of 2 ms) compared to control populations after 24 hours. There were no corresponding increases in Jurkat cells exposed to similar conditions.

Explosions are associated with more than 80% of the casualties in the Iraq and Afghanistan wars. Given the widespread use of thoracic protective armor, the most prevalent injury for combat personnel is blast-related traumatic brain injury (TBI). Almost 20% of veterans returning from duty had one or more clinically confirmed cases of TBI. In the decades of research prior to 2000, neurotrauma was under-recognized as a blast injury and the etiology and pathology of these injuries remains unclear.

This dissertation used the finite element (FE) method to address many of the biomechanics-based questions related to blast brain injuries. FE modeling is a powerful tool for studying the biomechanical response of a human or animal body to blast loading, particularly because of the many challenges related to experimental work in this field. In this dissertation, novel FE models of the human and ferret head were developed for blast and blunt impact simulation, and the ensuing response of the brain was investigated. The blast conditions simulated in this research were representative of peak overpressures and durations of real-world explosives. In general, intracranial pressures were dependent on the peak pressure of the impinging blast wave, but deviatoric responses in the brain were dependent on both peak pressure and duration. The biomechanical response of the ferret brain model was correlated with in vivo injury data from shock tube experiments. This accomplishment was the first of its kind in the blast neurotrauma field.

This dissertation made major contributions to the field of blast brain injury and to the understanding of blast neurotrauma. This research determined that blast brain injuries were brain size-dependent. For example, mouse-sized brains were predicted to have approximately 7 times larger brain tissue strains than the human-sized brains for the same blast exposure. This finding has important implications for in vivo injury model design, and a scaling model was developed to relate animal experimental models to humans via scaling blast duration by the fourth-root of the ratio of brain masses.

This research also determined that blast neurotrauma is correlated to deviatoric metrics of the brain tissue rather than dilatational metrics. In addition, strains in the blasted brain were an order-of-magnitude lower than expected to produce injury with traditional closed-head TBI, but an order-of-magnitude higher in strain rate. The 50th percentile peak principle strain metric of values of 0.6%, 1.8%, and 1.6% corresponded to the 50% risk of mild brain bleeding, moderate brain bleeding, and apnea respectively. These findings imply that the mechanical thresholds for brain tissue are strain-based for primary blast injury, and different from the thresholds associated with blunt impact or concussive brain injury because of strain rate effects.

The conclusions in this dissertation provide an important guide to the biomechanics community for studying neurotrauma using in vivo, in vitro, and in silico models. Additionally, the injury risk curves developed in this dissertation provide an injury risk metric for improving the effectiveness of personal protective equipment or evaluating neurotrauma from blast.