Visual Display Terminal may induce Dry Eye Disease through both direct and indirect routes

VDT use has been shown to decrease TBUT and increase interblink interval. However, much is still unknown regarding the adverse effects of VDT use on the ocular surface. Therefore, Dr Ketil Fjærvoll and his team conducted a review on pathophysiological mechanisms promoting VDT-associated DED.

In this review, the researchers searched PubMed for literature investigating the relationship between dry eye and VDT. They evaluated the relevance to the pathophysiology of DED. They included a total of fifty-five articles and examined the pathophysiological mechanisms and multiple hypotheses.

Key findings of the study:

• The researchers noted that visual display terminal (VDT) use causes DED mainly through impaired blinking patterns.
• Although some studies reported changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, they noted that the studies lack sufficient scientific support.
• They highlighted that these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development.

The authors concluded, "Visual display terminal (VDT) use appears to induce DED through both direct and indirect routes. Decreased blink rates and increased incomplete blinks increase the exposed ocular evaporative area and inhibit lipid distribution from meibomian glands."

They further added, "Although not adequately investigated, changes in parasympathetic signalling may impair lacrimal gland and goblet cell function, promoting tear film instability. More studies are needed to better target and improve the treatment and prevention of VDT-associated DED".

For further information:

DOI: https://doi.org/10.1111/aos.15150