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Dry eye is caused by tear-film instability from decreased aqueous production, increased evaporation (most commonly from meibomian gland dysfunction), or a combination. Contributing factors include age, female hormones, autoimmune disease (eg, Sjögren's), systemic medications, contact lens use, environmental low humidity, and prolonged digital screen use.

Diagnosis combines patient symptom questionnaires (eg, OSDI), clinical tests such as tear breakup time (TBUT), corneal/conjunctival staining, Schirmer or tear osmolarity, and gland imaging (meibography) to phenotype aqueous-deficient vs evaporative disease. Accurate phenotyping guides targeted treatment rather than relying on symptoms alone.

Most dry eye is a chronic, relapsing disease that can be well-controlled but not permanently cured in many patients; however, treating the underlying cause (eg, autoimmune disease, eyelid disease) or reversible drivers (medication changes, environmental modification) can significantly reduce or resolve symptoms for some individuals. Procedural options and newer prescription treatments can produce durable improvement for certain phenotypes.

Artificial tears are a first-line symptomatic therapy; preservative-free formulations are preferred for frequent use, and lipid-containing drops are better for evaporative/meibomian gland dysfunction. Choice depends on symptom severity and phenotype — many patients need adjunctive therapies for meaningful, lasting benefit.

See a clinician if OTC drops don't improve symptoms within 2–4 weeks, if you have moderate-to-severe discomfort, fluctuating or blurred vision, pain, light sensitivity, recurrent corneal erosions, or are a contact lens wearer with reduced tolerance. Early evaluation is important when symptoms affect quality of life or when systemic autoimmune disease is suspected.

Yes — transient dry eye is a common post-LASIK complaint; up to 40–60% report short-term symptoms and about 10–20% may report persistent symptoms beyond 6 months depending on preoperative risk factors. Preoperative screening and perioperative dry eye management reduce risk and improve outcomes.

Prescription options include topical anti-inflammatories (cyclosporine, lifitegrast) and the intranasal nicotinic agent (varenicline nasal spray) to stimulate tear secretion. Procedural options targeting meibomian gland dysfunction and tear conservation include thermal pulsation (eg, LipiFlow), intense pulsed light (IPL), punctal occlusion (plugs), and autologous serum drops for severe surface disease.

Lifestyle measures — increased blinking, 20-20-20 screen breaks, humidifiers, warm compresses and lid hygiene — reliably reduce symptoms. Evidence for omega-3 supplements is mixed; they may help some patients but should be discussed with a clinician as part of a multimodal plan.

Punctal plugs can be an effective tear-conservation option for aqueous-deficient dry eye, with temporary (dissolvable) and longer-term removable plugs available; benefit is greatest when tear production is reduced but ocular surface inflammation is controlled. Risks include plug extrusion, local irritation, and in rare cases infectious complications, so they should be used selectively.

Topical immunomodulators like cyclosporine often require 4–12 weeks to show symptom and staining improvement, and full benefits may take several months; lifitegrast may provide earlier symptomatic relief in some patients. Clear expectations and follow-up improve adherence and allow timely escalation to procedural therapies if inadequate response occurs.