Dry eye disease
At a glance
Loss of tear-film homeostasis produces symptoms and ocular-surface dysfunction. Signs and symptoms may not correlate.
CAVE
- Marked unilateral pain, photophobia, focal infiltrate or reduced vision needs another explanation.
- Ask about systemic dryness.
Clinical presentation
- Burning, fluctuating vision, foreign-body sensation and discomfort during sustained visual tasks.
Diagnosis & investigations
- Start with symptoms and their functional impact, using a consistent questionnaire where helpful. Examine blink completeness, lid closure, lid margins, meibum and tear meniscus. Test tear stability, preferably non-invasive breakup before instilling drops, then corneal/conjunctival staining. Add osmolarity or Schirmer testing when it answers a specific question.
- Interpret findings together: tear-film instability, hyperosmolarity and surface damage support loss of homeostasis, but no single test describes every phenotype. Look for allergy, exposure, medication toxicity and neuropathic pain. Marked aqueous deficiency with dry mouth or systemic features warrants Sjögren evaluation.
Differential diagnosis
- Allergy, exposure, blepharitis, toxicity, neuropathic pain and infectious keratitis.
Treatment
- Explain the dominant mechanism and agree a manageable daily regimen. Modify drying airflow, screen-related incomplete blinking and aggravating medications where feasible; avoid preserved drops when frequent dosing or toxicity makes them unsuitable.
- Select treatment by phenotype rather than prescribing every step to every patient. Control inflammation and lid disease before relying on tear retention alone. Persistent epithelial defects, filaments or exposure require a more intensive corneal plan.
| Finding | Action | Timing / detail |
|---|---|---|
| Evaporative disease / MGD | Lid warming and hygiene, blink/environment measures and lipid-containing lubrication; treat associated rosacea/blepharitis | Document gland expression and tear stability; device treatments are selected options, not mandatory first steps |
| Aqueous deficiency | Preservative-free tear replacement; assess lacrimal deficiency, medications and possible Sjögren disease | Consider tear conservation after assessing surface inflammation; severe disease may need serum tears or scleral lenses |
| Persistent inflammatory surface disease | Consider a short monitored topical steroid course or longer-term immunomodulation with an authorised agent | Exclude infection; check IOP with steroid use and explain that ciclosporin response is not immediate |
| Severe pain with few surface signs, or marked signs with little pain | Reassess neuropathic pain or reduced corneal sensation/neurotrophic disease | Do not escalate lubricants indefinitely without rechecking the diagnosis |
Follow-up
- Agree a response review, often at 4–8 weeks for uncomplicated disease, using the same symptom measure and key surface findings. Review earlier for steroid monitoring, epithelial defects, pain or visual decline. If symptoms persist, check technique, adherence, exposure and diagnosis before simply adding another lubricant.
Risk factors & context
- Consider meibomian gland dysfunction, reduced tear secretion, exposure, medication effects and contact-lens wear.
- Several drivers often coexist.
Complications
- Persistent epithelial damage and unstable vision.
- Severe surface disease can impair contact-lens tolerance and the reliability of preoperative measurements.
When to refer
- Escalate for epithelial breakdown, suspected autoimmune disease or severe pain unexplained by examination.
References 2
- TFOS DEWS III · Diagnostic Methodology ↗2025 · Diagnosis; differential diagnosis; subclassification
- TFOS DEWS III · Management and Therapy / official report summaries ↗2025 · Management and Therapy report
Adapt to the patient, local pathways and authorised product information.