June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Primary Blast-Induced Ocular Trauma Modulated by Peak Pressure
Author Affiliations & Notes
  • Daniel Sherwood
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
  • Brian Lund
    Institute of Surgical Research, San Antonio, TX
  • Randolph Glickman
    University of Texas Health Science Center at San Antonio, San Antonio, TX
  • Walter Gray
    Geological Sciences, University of Texas at San Antonio, San Antonio, TX
  • Richard Watson
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
  • Kimberly Thoe
    WESMDPA, San Antonio, TX
  • William Sponsel
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
    WESMDPA, San Antonio, TX
  • Matthew Reilly
    Biomedical Engineering, University of Texas at San Antonio, San Antonio, TX
  • Footnotes
    Commercial Relationships Daniel Sherwood, None; Brian Lund, None; Randolph Glickman, None; Walter Gray, None; Richard Watson, None; Kimberly Thoe, None; William Sponsel, New World Medical (P); Matthew Reilly, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 3043. doi:
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      Daniel Sherwood, Brian Lund, Randolph Glickman, Walter Gray, Richard Watson, Kimberly Thoe, William Sponsel, Matthew Reilly, Australian Research Council Centre of Excellence in Vision Science (ACEVS); Primary Blast-Induced Ocular Trauma Modulated by Peak Pressure. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3043.

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      © ARVO (1962-2015); The Authors (2016-present)

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In proportion to surface area, battlefield ocular trauma is 20 to 50 times more likely than other exposed areas (Sobaci et al., Am J Ophthalmol 2000). Although the ability of secondary-blast effects (fragments, shrapnel) to cause ocular trauma is well known, it is not yet known whether ocular trauma may be induced by primary blast effects (i.e., those due solely to the shock-wave). We hypothesized that primary, sub-lethal blast alone is sufficient to induce ocular trauma with the corollary that the level of trauma is correlated with the peak overpressure. We tested this hypothesis using a shock-tube capable of replicating physically accurate shock-waves within a controlled environment.


Porcine eyes were enucleated and set in a rigid mimic of the orbit filled with gelatin (Sponsel et al., IOVS 2011). The porcine eyes were imaged via UBM and B-scan ultrasound along 12 vectors both before and after blast. Each eye was re-pressurized via intracameral injection using a 30 gauge needle with balanced salt solution and placed in a shock-tube (Fig. 1). The eyes were then exposed to blasts of 2 ms duration with peak pressures ranging from 7-22 psi. After post-blast imaging, eyes were fixed in formalin for later dissection or histopathology.


We observed corneal abrasion and fissuring, angle recession, circumferential iris plication into the zonule, uveal pigment forced between the axonal fasciculi of the optic nerve (Fig. 2a). Mid peripheral chorioretinal detachments, radial peripapillary retinal detachments (Fig 2b), and intrinsic internal scleral delamination (Fig 2c) were also observed. In an extreme case, an incident pressure of 22 psi caused axial-posterior displacement of 8 mm within 67 ms and eventual evulsion of the eye from its orbit mimic on rebound.


Primary blast in the absence of particle insult was sufficient to cause a range of significant ocular trauma. The magnitude of the incident peak-pressure was correlated with the probability of trauma occurrence and severity of damage. The ability of primary blast overpressure to produce severe eye damage underscores the necessity of developing protective eyewear specifically designed to shield the eye and orbital structures from this source of trauma.

Keywords: 742 trauma  

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