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contributor authorTong, Junfei
contributor authorKedar, Sachin
contributor authorGhate, Deepta
contributor authorGu, Linxia
date accessioned2019-09-18T09:01:22Z
date available2019-09-18T09:01:22Z
date copyright7/29/2019 12:00:00 AM
date issued2019
identifier issn0148-0731
identifier otherbio_141_10_101011
identifier urihttp://yetl.yabesh.ir/yetl1/handle/yetl/4257971
description abstractCurrent knowledge of traumatic ocular injury is still limited as most studies have focused on the ocular injuries that happened at the anterior part of the eye, whereas the damage to the optic nerve known as traumatic optic neuropathy (TON) is poorly understood. The goal of this study is to understand the mechanism of the TON following the primary blast through a fluid–structure interaction model. An axisymmetric three-dimensional (3D) eye model with detailed orbital components was developed to capture the dynamics of the eye under the blast wave. Our numerical results demonstrated a transient pressure elevation in both vitreous and cerebrospinal fluid (CSF). A high strain rate over 100 s−1 was observed throughout the optic nerve during the blast with the most vulnerable part located at the intracanalicular region. The optic nerve deforming at such a high strain rate may account for the axonal damage and vision loss in patients subjected to the primary blast. The results from this work would enhance the understanding of indirect TON and provide guidance in the design of protective eyewear against such injury.
publisherAmerican Society of Mechanical Engineers (ASME)
titleIndirect Traumatic Optic Neuropathy Induced by Primary Blast: A Fluid–Structure Interaction Study
typeJournal Paper
journal volume141
journal issue10
journal titleJournal of Biomechanical Engineering
identifier doi10.1115/1.4043668
journal fristpage101011
journal lastpage101011-7
treeJournal of Biomechanical Engineering:;2019:;volume( 141 ):;issue: 010
contenttypeFulltext


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