Abstract
Exposures to blast can cause injuries in the brain. Limited studies have been performed to investigate the blast levels needed to induce blast brain injuries. This study examines the effects from an exposure to blast using a gyrencephalic animal model. The ferret was selected as the preferred model for blast brain injury when compared with rodents and rabbits for its brain structure and compatibility to the human brain and its size, ease of animal care, and wide availability. In this study, sixty-seven ferrets were used as blast specimens and three were used as controls.
The blast waves were generated with a shock tube at varying ranges of overpressures and durations, simulating blasts at standoffs of 2.5 to 20 m and charge sizes to approximately 800 kg. To isolate the blast exposure to the head, the abdomen and thorax were protected to blast levels that were an order of magnitude below pulmonary injury threshold conditions.
Physiological parameters, such as heart rate and respiration rate, sensory evoked potentials, and histology were all used to assess the incidence of brain injury. Bradycardia and apnea were present after the blast exposure, but would return to normal physiological values, if the specimen survived. Bradycardia and apnea also appeared to be duration dependent, in that at longer durations, lower pressures were needed to cause them. For durations less than 6 ms, bradycardia occurred in all specimens exposed to overpressures greater than 700 kPa. For durations less than 8.5 ms, apnea occurred in all specimens exposed to overpressures greater than 625 kPa. Blast overpressure levels greater than 700 kPa also resulted in at least a moderate hemorrhagic injury. Injury, patterns seen during the tests suggested a mechanism of small displacement, but rapid iii compression of the skull. Signal loss of the sensory evoked potentials was also related to the blast input conditions. VEP signal loss did not occur at overpressures lower than 700 kPa, and BAEP signal loss did not occur at overpressures lower than 400 kPa. Using the histological data, a correlation of the blast input to the injured axonal area was made. Severe blast exposure conditions had significantly injured axonal areas two orders of magnitude greater than nonblasted specimens.
Most importantly, injury risk functions were developed for risk of mild and moderate to severe meningeal bleeding, initial apnea, and evoked potential signal loss from the application of a blast shock. In addition, a risk assessment was developed for fatality using data from the current study combined with previous rabbit data. The fatality injury risk for brain was found to be more than twice the fatality injury risk for lungs at low positive phase durations. The blast level for 50% risk of mild brain bleeding was found to occur at similar overpressure values as the 50% risk of unprotected pulmonary injury onset.
Note: Abstract extracted from PDF file via OCR.
