A peer-level look at how eye-care professionals classify dry eye disease, decide what matters diagnostically, respond when first-line therapy is not enough, and manage the adherence, inflammatory, meibomian, autoimmune, and access barriers that complicate long-term care.
Audience: Ophthalmologists / Eye-Care HCPs
Countries: 6
Completion Rate: 83.6%
SGID: 9008491
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– Quick Read — Key Findings
Dry eye disease is often managed across overlapping tear-film, eyelid, inflammatory, environmental, autoimmune, medication-related, and neurosensory drivers rather than one isolated mechanism.
TFOS DEWS III now frames DED as a multifactorial symptomatic disease and emphasizes subclassification by etiologic drivers, fitting the MDForLives data, where mixed-mechanism disease dominates and persistent symptoms frequently trigger anti-inflammatory or meibomian-gland-directed escalation.
58.5% say mixed-mechanism dry eye most often drives their management approach, compared with 20.8% for evaporative disease, 18.9% for aqueous-deficient disease, and 1.9% for neuropathic ocular pain.
Mixed-mechanism disease dominates at 58.5%, supporting a phenotype-driven approach over one assumed mechanism: tear-film instability, meibomian gland dysfunction, aqueous deficiency, inflammation and neurosensory factors overlap, so one intervention may improve one component while leaving another active.
47.2% select ocular-surface staining as the finding that most influences their DED diagnosis. Tear-film breakup time follows at 22.6%, meibomian gland dysfunction at 18.9%, and Schirmer testing at 11.3%.
Ocular-surface staining carries the most diagnostic weight, and TFOS DEWS III likewise emphasizes objective evidence of homeostasis loss alongside symptoms. Staining is useful but sits within a wider framework of tear-film stability, osmolarity where available, eyelid and gland assessment, and differential diagnosis.
60.4% initiate preservative-free artificial tears first, while 26.4% begin with lid hygiene and warm compresses. Topical cyclosporine or lifitegrast accounts for 9.4%, and MGD-directed therapy for 3.8%.
Preservative-free artificial tears remain the most common starting point, consistent with a stepped approach: tear support and simple lid measures stay foundational, while prescription anti-inflammatory and procedure-based treatments are added when phenotype, severity or response warrant.
49.1% identify poor treatment adherence as the most common explanation for initial treatment failure, while 41.5% select persistent ocular-surface inflammation. Incorrect phenotype and uncontrolled environmental triggers are selected much less often.
Adherence and persistent inflammation explain most early failure, which reframes “treatment failure”: non-response may reflect a drug or device issue, but also treatment burden, delayed benefit, cost, technique or an inadequately controlled inflammatory driver.
When DED symptoms persist, 32.1% escalate topical anti-inflammatory therapy and 32.1% intensify MGD-directed treatment. Another 22.6% reassess the diagnosis and triggers, while 13.2% initiate advanced ocular-surface therapy.
Escalation splits between anti-inflammatory and meibomian-gland-directed treatment, reflecting the two common reasons symptoms persist despite lubrication: continuing inflammation and inadequately controlled meibomian gland dysfunction. Notably, more than one in five step back and reassess rather than simply adding another treatment.
Refractory meibomian gland dysfunction is the subgroup most often selected as changing treatment strategy, at 37.7%, followed by autoimmune-associated dry eye at 32.1%, severe aqueous deficiency at 18.9%, and neuropathic ocular pain at 11.3%.
Refractory meibomian gland dysfunction (37.7%) and autoimmune-associated disease (32.1%) are the subgroups that most change treatment, and the open cases reinforce the complexity: GVHD, persistent meibomitis, post-refractive neuropathic symptoms, Demodex, medication-related surface disease and insurance barriers.
The MDForLives findings describe a practice environment where mixed-mechanism disease is common, first-line lubrication remains important, and persistent symptoms quickly force clinicians to decide whether the next problem is inflammation, meibomian gland dysfunction, diagnosis, adherence, access or a less typical ocular-pain mechanism.
The data also show why symptom response and objective signs do not always move together: sustained symptom improvement is the outcome most used to support long-term treatment, yet some patients’ surface findings improve while discomfort persists, and others’ options are shaped as much by coverage and adherence as by phenotype.
The next phase of DED management may therefore depend on more consistent phenotyping, better recognition of refractory subgroups, realistic adherence support, and personalized algorithms that connect the right intervention to the right driver without losing sight of the patient’s lived symptom burden.
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