Review on the possible pathophysiological mechanisms underlying visual display terminal-associated dry eye disease

Abstract

Background: Visual display terminal (VDT) use is a key risk factor for dry eye disease (DED). Visual display terminal (VDT) use reduces the blink rate and increases the number of incomplete blinks. However, the exact mechanisms causing DED development from VDT use have yet to be clearly described.

Purpose: The purpose of the study was to conduct a review on pathophysiological mechanisms promoting VDT-associated DED.

Methods: A PubMed search of the literature investigating the relationship between dry eye and VDT was performed, and relevance to pathophysiology of DED was evaluated.

Findings: Fifty-five articles met the inclusion criteria. Several pathophysiological mechanisms were examined, and multiple hypotheses were extracted from the articles. Visual display terminal (VDT) use causes DED mainly through impaired blinking patterns. Changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, were proposed in some studies but lack sufficient scientific support. Together, these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development.

Conclusion: 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. 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.

Keywords: DED; VDT; VDT-associated dry eye; dry eye disease; pathophysiology; tear film.

Fig. 1

Tear film and important associated structures. Meibomian glands, the lacrimal gland and goblet cells are essential for maintaining the homeostasis of the tear film. Copyright Sara Tellefsen Nøland.

Fig. 2

Interblink interval (IBI) and tear film break‐up time (TBUT) in two different settings. The IBI increases and the TBUT decreases with visual display terminal (VDT) use. This leaves the ocular surface epithelium exposed for longer. Copyright Sara Tellefsen Nøland.

Fig. 3

Flowchart of the stepwise search strategy and methodology.

Fig. 4

Possible mechanisms involved in visual display terminal (VDT)‐associated dry eye development. Visual display terminal (VDT) use causes decreased blink frequency, increased incomplete blinks and exposure to blue light. This may induce excessive evaporation and several noxious reactions in the goblet cells, meibomian glands and lacrimal glands, feeding into the vicious cycle of dry eye disease. These reactions can be exacerbated by several factors, including contact lens wear and air conditioning. Copyright Sara Tellefsen Nøland.

Fig. 5

Ocular protection index (OPI) is the ratio between the tear film break‐up time (TBUT) and the interblink interval (IBI). Both tear film break‐up time and interblink interval worsen during visual display terminal (VDT) use. Copyright Sara Tellefsen Nøland.

Fig. 6

Possible effects of blue light on the ocular surface. Blue light emitted by visual display terminal (VDT) devices is shown to have direct cytotoxic effects on the corneal and conjunctival cells in vitro. Copyright Sara Tellefsen Nøland.