Dry Eye Syndrome Reference Guide

Dry eye disease is a chronic, multifactorial condition marked by tear film instability, hyperosmolarity, inflammation, and neurosensory abnormalities. Patients report burning, grittiness, fluctuating vision, and fatigue that interfere with reading, computer work, and contact lens wear. Persistent surface irritation degrades quality of life and can erode trust in care if symptoms are dismissed as minor. Framing the condition as a controllable but ongoing disorder helps set realistic expectations for maintenance therapy and follow up.

Two dominant mechanisms drive most cases: reduced aqueous production and excessive evaporation. Autoimmune disease, aging, and systemic medications impair lacrimal secretion, while meibomian gland dysfunction, environmental stressors, and prolonged digital use destabilize the lipid layer. Many patients exhibit overlap, so identifying the primary driver guides whether to emphasize tear replacement, lipid restoration, or inflammation control. Document contributing factors such as hormone changes, eyelid margin disease, or prior ocular surgery to personalize care plans.

Tear film instability increases osmolarity and inflammatory cytokines, which damage epithelial cells and disrupt the smooth refractive surface of the cornea. Resulting punctate staining, filaments, and epithelial erosions reduce contrast sensitivity and create fluctuating acuity that patients often describe as foggy or smeared. Chronic inflammation can alter goblet cell density and meibomian gland architecture, making recovery slower and reinforcing the need for early, targeted therapy.

A structured workup includes TBUT for stability, Schirmer or phenol red thread for volume, corneal and conjunctival staining grades, osmolarity measurements, and meibography to assess gland dropout. Lid margin evaluation, expression quality, and symptom questionnaires (DEQ 5, OSDI) add context. Consistently recording these metrics allows staging severity, tracking response over time, and justifying escalation to prescription or procedural therapies when conservative care fails.

Begin with preservative free lubricants, environmental changes, and digital break strategies. Add topical immunomodulators such as cyclosporine or lifitegrast for inflammatory disease, short steroid pulses for flares, and oral secretagogues in severe aqueous deficiency. For evaporative disease, employ heat masks, manual expression, thermal pulsation, IPL with appropriate skin type screening, and omega 3 supplementation when indicated. Punctal occlusion, scleral lenses, or autologous serum drops offer relief in recalcitrant cases.

Set expectations that symptom improvement may take weeks and that maintenance therapy is often ongoing. Provide written routines, demonstrate lid hygiene and drop spacing, and review side effects such as initial burning with immunomodulators. Reevaluate staining patterns, TBUT, and gland function at regular intervals to adjust intensity or taper therapies. Clear documentation of stage, goals, and current regimen streamlines future visits and supports consistent care across providers.