Purpose: Primary blast injury (PBI) mostly affects air-filled organs, although it is sporadically reported in fluid-filled organs, including the eye. The purpose of the present paper is to explain orbit blast injury mechanisms through finite element modeling (FEM).
Methods: FEM meshes of the eye, orbit, and skull were generated. Pressure, strain, and strain rates were calculated at the cornea, vitreous base, equator, macula, and orbit apex for pressures known to cause tympanic rupture, lung damage, and 50% chance of mortality.
Results: Pressures within the orbit ranged between +0.25 and -1.4 MegaPascal (MPa) for tympanic rupture, +3 and -1 MPa for lung damage, and +20 and -6 MPa for 50% mortality. Higher trinitrotoluene (TNT) quantity and closer explosion caused significantly higher pressures, and the impact angle significantly influenced pressure at all locations. Pressure waves reflected and amplified to create steady waves resonating within the orbit. Strain reached 20% along multiple axes, and strain rates exceeded 30,000 s(-1) at all locations even for the smallest amount of TNT.
Conclusions: The orbit's pyramidlike shape with bony walls and the mechanical impedance mismatch between fluidlike content and anterior air-tissue interface determine pressure wave reflection and amplification. The resulting steady wave resonates within the orbit and can explain both macular holes and optic nerve damage after ocular PBI.