June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Intraocular pressure change from ocular compression: a study of aqueous outflow facility
Author Affiliations & Notes
  • Andrew KC Lam
    School of Optometry, The Hong Kong Polytechnic University, Hong Kong, China
  • Fang Yu Xu
    School of Optometry, The Hong Kong Polytechnic University, Hong Kong, China
  • Footnotes
    Commercial Relationships   Andrew Lam, None; Fang Yu Xu, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 4627. doi:
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      Andrew KC Lam, Fang Yu Xu; Intraocular pressure change from ocular compression: a study of aqueous outflow facility. Invest. Ophthalmol. Vis. Sci. 2020;61(7):4627.

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

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Abstract

Purpose : High myopia is a risk factor of glaucoma. Its etiology may be related to poor aqueous outflow in high myopes. Currently there is no non-invasive in vivo measurement of aqueous outflow. Intraocular pressure (IOP) can be easily elevated from ocular compression. We hypothesize that change in IOP through ocular compression may be dependent on severity of myopia which may indirectly indicate aqueous outflow facility.

Methods : A Proview™ eye pressure monitor was modified and calibrated. Twenty-six young healthy adult myopes were recruited and ocular compression was performed (Fig 1). Baseline rebound tonometry was performed 3 times within 1 minute (baseline, 30-second, and 60-second). IOP was elevated by ocular compression using the modified Proview™ for 1 minute, then force was released. Rebound tonometry was performed during ocular compression (immediately, 30-second, and 60-second) and after ocular compression for 5 minutes (immediately, then at 30-second intervals).

Results : A force between 47-62g was generated by the Proview™. Baseline IOP was stable at 14.4±3.3mmHg. Repeatability (2.77 x within-subject standard deviation) from 3 baseline measurements was 2.4mmHg. Three subjects with IOP rise <2.4mmHg immediately after ocular compression were excluded. IOP was elevated to 28.0±8.3mmHg in 23 subjects (baseline: 14.2±3.4mmHg) and dropped to 24.0±7.9mmHg, immediately after and at 60-second during ocular compression, respectively. IOP returned to 13.3±3.6mmHg when the force was released. Subjects were divided into high (<-6D spherical equivalent) and non-high myopes. Although high myopes had slightly higher baseline IOP then non-high myopes, both groups had similar IOP rise immediately after ocular compression (Fig 2). High myopes had elevated IOP maintained for 30 seconds then dropped while non-high myopes had IOP dropped quickly. After the force was released, high myopes had greater IOP drop which took 3 minutes for it to return to the baseline level. The non-high myopes had IOP returned to the baseline level immediately.

Conclusions : Non-high myopes had elevated IOP dropped quickly during ocular compression that may indicate a better aqueous outflow. Further studies with subjects taking medication to enhance aqueous outflow, and with glaucoma patients are warranted.

This is a 2020 ARVO Annual Meeting abstract.

 

A Proview™ eye pressure monitor pressed on the lower eyelid of a subject

A Proview™ eye pressure monitor pressed on the lower eyelid of a subject

 

Intraocular pressure at different sessions of High and Non-High myopes

Intraocular pressure at different sessions of High and Non-High myopes

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