Dry Eye
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Direct answer
Foreign-body grittiness that grows worse as the day goes on, with burning and fluctuating vision, is the classic complaint of dry eye disease — a multifactorial condition of tear film instability and hyperosmolarity with ocular surface inflammation and neurosensory changes, per the TFOS DEWS II definition that replaced the simple "lack of tears" idea. Two mechanisms dominate: aqueous-deficient dry eye (lacrimal gland failure, as in Sjogren syndrome) and evaporative dry eye from meibomian gland dysfunction, which is the commoner cause worldwide. Testing pairs symptoms with signs — Schirmer strip wetting, tear film break-up time, and ocular surface staining with fluorescein or lissamine green — and management climbs a ladder from education and preservative-free artificial tears to anti-inflammatory drops such as cyclosporine, punctal plugs and treatment of lid disease.
What you must remember
- Tear film layers: outer lipid from meibomian glands (retards evaporation), middle aqueous from main and accessory lacrimal glands, inner mucin from goblet cells anchoring the aqueous to hydrophobic epithelium.
- Two subtypes, two mechanisms: aqueous-deficient (Sjogren syndrome — primary, or with rheumatoid arthritis and other connective disease as secondary; graft-versus-host disease; lacrimal gland removal) versus evaporative (meibomian gland dysfunction, blepharitis, contact lens wear, incomplete blinking — the commonest).
- Schirmer test: strip in the lateral lower fornix for 5 minutes; less than 10 mm of wetting is abnormal and less than 5 mm suggests severe aqueous deficiency (values vary with or without anaesthesia).
- Tear film break-up time: fluorescein-instilled tear film; break-up under 10 seconds indicates instability; the test is repeated and averaged.
- Staining patterns: fluorescein marks epithelial defects on the cornea; rose bengal and lissamine green stain devitalised conjunctival cells in a nasal interpalpebral pattern typical of dry eye.
- The paradox: reflex tearing means a "watering" patient can actually be dry — ask about evening grittiness and screen use (blink rate halves at a monitor).
- Treatment ladder: warm compresses and lid hygiene for meibomian disease, preservative-free artificial tear substitutes, topical cyclosporine 0.05 per cent (an immunomodulator that increases tear production), short-course topical steroids under supervision, punctal plugs after adequate lubrication, autologous serum drops for severe disease, and management of systemic causes.
- Systemic interrogation: bilateral dry eye with dry mouth (xerostomia) and joint pains warrants anti-Ro and anti-La antibodies and rheumatology referral for Sjogren syndrome.
Working through a gritty eye in clinic
A 52-year-old teacher reports two years of burning in both eyes, worst by evening and after long chalk-and-computer days; over-the-counter drops give only minutes of relief. Examine first. Her lid margins show capped meibomian orifices and telangiectasia — meibomian gland dysfunction at a glance. Tear meniscus is thin; tear film break-up time measures 6 seconds in each eye; Schirmer without anaesthesia shows 12 mm at 5 minutes, so aqueous production is borderline, not devastated. Lissamine green paints the nasal interpalpebral conjunctiva. The picture is predominantly evaporative dry eye on meibomian disease, with a contribution from infrequent blinking at work. Management begins mechanically: twice-daily warm compresses with lid massage and hygiene, and screen hygiene — the 20-20-20 habit. Preservative-free artificial tears four times a day treat the osmolar insult. If eight weeks of this fails to control symptoms, add cyclosporine 0.05 per cent — its benefit builds over weeks to months and it stings initially — and reserve punctal plugs for a confirmed aqueous-deficient component, since plugging tears that evaporate anyway adds no comfort. Should she later describe dry mouth and fatigue, the workup turns systemic, but the ocular ladder stays the same.
Where the exam frames it
Two vignettes recur. The first gives a postmenopausal woman with rheumatoid arthritis, grittiness and a Schirmer of 3 mm — severe aqueous deficiency with Sjogren syndrome — and asks for the next step, which is systemic workup plus lubrication, not just drops. The second gives a computer professional with normal Schirmer but reduced break-up time and lid margin disease — evaporative dry eye — where the mark-earning answer is lid hygiene and warm compresses first. Marks are lost by treating every dry eye with plugs (wrong when evaporation is the problem) or by forgetting that cyclosporine, not steroids, is the long-term anti-inflammatory of choice. The viva favourite is the paradoxical watering eye: a patient tearing while reading or in wind is usually dry, because irritation triggers reflex lacrimation that floods an unstable film.
Frequently asked questions
Which test distinguishes aqueous-deficient from evaporative dry eye?
The Schirmer test measures aqueous secretion (under 5 mm in 5 minutes suggests severe deficiency), while tear film break-up time assesses stability — prolonged break-up time loss with normal Schirmer points to evaporation.
What is meibomian gland dysfunction and why does it matter?
Obstruction and dysfunction of the lipid-secreting meibomian glands, causing tear film instability and faster evaporation — the commonest cause of evaporative dry eye.
When are punctal plugs indicated?
In aqueous-deficient dry eye that remains symptomatic despite frequent preservative-free lubricants; they conserve the patient's own tears and are best combined with anti-inflammatory treatment.
Why does dry eye cause watering?
Ocular surface irritation from an unstable, hyperosmolar tear film triggers reflex lacrimation, so paradoxical epiphora can mask dry eye disease.
What blood tests support Sjogren syndrome?
Anti-Ro (SSA) and anti-La (SSB) antibodies, usually with rheumatoid factor and antinuclear antibody, alongside xerostomia and salivary gland assessment.