OP4.5 | Dry Eye Disease — Summary & Reflection

KEY TAKEAWAYS

The tear film is a trilaminar structure: outer lipid layer (meibomian glands — retards evaporation), middle aqueous layer (main lacrimal gland + accessory glands of Krause and Wolfring — bulk volume + antimicrobials + EGF), inner mucin layer (goblet cells — wets hydrophobic epithelium).

Dry eye disease (DED) classified by mechanism: Aqueous-deficient DED (ADDE) — Sjögren's syndrome-associated (primary: KCS + xerostomia + anti-Ro/SSA; secondary: in RA/SLE/scleroderma) and non-Sjögren's (age, lacrimal scarring, medications). Evaporative DED (EDE) — meibomian gland dysfunction (commonest), blepharitis, lagophthalmos, reduced blink, contact lens, environment.

Symptoms: burning, gritty sensation, redness, blurring worse with sustained tasks, paradoxical reflex tearing. Signs: reduced tear meniscus, punctate corneal staining in the interpalpebral zone, short TBUT, low Schirmer's.

Investigations: Schirmer I test (≥10 mm at 5 min normal; <5 mm severe ADDE), TBUT (<10 sec abnormal, indicates EDE), fluorescein/lissamine staining (Oxford grade 0-V).

Management stepwise: artificial tears (preservative-free if frequent use) → warm compresses/lid hygiene for MGD → cyclosporine 0.05% for inflammatory component → punctal occlusion → autologous serum drops/scleral lenses for severe cases.

REFLECT

Dry eye disease disproportionately affects women and older adults, yet is often dismissed as 'just dry eyes' by clinicians. After working through this module, reflect: how would your clinical approach to a patient presenting with 'watering eyes' change? Would you consider DED in the differential before referring for nasolacrimal duct obstruction? If you had a patient with confirmed Sjögren's syndrome dry eye, what would you say to her about the long-term goals of treatment — since there is no cure, only management? How does the 20-20-20 rule apply to your own study habits?