3. The role of increased friction in DED and its subsequent sequelae deserves further investigation. Inflammation of the ocular surface can cause inhibition of lacrimal secretion and loss of epithelial barrier function at the ocular surface.
4. Considering neuropathic pain in DED, TFOS DEWS II reports that it has been found that cold thermoreceptors continuously discharge nerve impulses at the normal ocular surface temperature, responding to warming or cooling and to osmolarity increases.
This likely contributes to reflex control of basal tear production and blinking. Studies to date suggest potential merit in exploring treatment strategies involving cold receptors to manage DED symptoms.
Restoration of tear film homeostasis is the ultimate goal in DED management. This involves breaking the vicious circle of the disease. Determining whether the major cause(s) of an individual’s DED pertains predominantly to aqueous tear deficiency or to evaporation—or both—is critical in helping select the most appropriate management strategy.
TFOS DEWS II researchers created a clinical algorithm for DED, which you can find in the downloadable report.