Blast exposure is a growing cause of injury for military personnel, and is the leading cause of ocular injuries in service members. In three recent military conflicts, Operation Enduring Freedom (Afghanistan), Operation Iraqi Freedom (Iraq), and Operation New Dawn (Iraq), 13% of all casualties had visual system injury. In some cases, ocular damage does not present immediately after blast, but is diagnosed weeks or months after the exposure(s). The mechanisms and outcomes of ocular blast exposure have not been well investigated, with only a few studies performing computational, in vivo, or in vitro experiments in the field. This project aimed to fill a gap in literature by studying the closed globe injury progression from primary blast exposure. Specifically, the goal of this research was to understand long-term closed globe ocular sequelae subsequent to primary blast exposure, and to identify potential physical injury mechanisms involved in blast exposure.

To achieve this goal, a shock tube capable of reproducing ocular blast trauma in a rat was created. Computational and experimental studies characterized the shock tube to replicate an open-field Friedlander waveform. The shock tube was used to expose rats to a realistic primary blast insult with peak overpressure 228.49 ± 28.49 kPa and duration 7.06 ± 0.64 ms. Contrast sensitivity testing revealed deficits in visual function that began one day after blast and did not resolve over eight subsequent weeks. Optical coherence tomography imaging of the cornea and retina revealed corneal inflammation that presented as delayed swelling (between two to six weeks after blast) and eventual scarring. Retinal thickness changes were not detected. Intraocular pressure (IOP) was measured at high speed in a subset of the blast-exposed animals to translate external forces to intraocular load conditions, and was found to correlate strongly with the external tube pressure. A parametric finite element model of the rodent eye was developed to simulate the experimental ocular blast exposure and validated against experimentally measured IOP. The intraocular pressure was most significantly linked to the blast overpressure, globe size, and lens size. A scaling equation was developed to predict IOP as a function of these variables, and to allow equivalent comparison between the various experimental models and human blast exposure levels.

The benefits of this work are two-fold. Identification of the injuries and injury mechanisms from blast will improve the design and effectiveness of wartime ocular protective devices. The unique two-week time delay of corneal swelling suggests a possible treatment window to mitigate corneal swelling and scarring after blast exposure, and potentially improve long-term visual outcomes.