Q5
LONG ANSWER
10M
★ High-yield
Describe dry eye disease with its classification, investigation and management.
Nature and Classification
Dry eye disease is a multifactorial disease of the ocular surface characterised by loss of homeostasis of the tear film, with tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormality.
- Two concepts IN that definition drive modern treatment: hyperosmolarity, which is the core mechanism damaging the epithelium and triggering inflammation; and inflammation, which is why anti-inflammatory treatment works and why lubricants alone often do not
- The vicious circle — reduced or unstable tears raise osmolarity; hyperosmolarity damages epithelial and goblet cells and releases inflammatory mediators; inflammation further damages the glands and the goblet cells and damages the corneal nerves; and the resulting reduction in reflex secretion perpetuates the cycle. Breaking the circle, not merely wetting the eye, is the aim
| Category | Causes |
|---|---|
| Aqueous-deficient — sjogren |
|
| Aqueous-deficient — non-sjogren | Age-related lacrimal gland atrophy. |
| Evaporative — lid-related | Meibomian gland dysfunction and blepharitis (the leading cause); lid aperture disorders — proptosis, lagophthalmos, ectropion; and a low blink rate with screen work, reading and in Parkinson disease |
| Evaporative — surface-related | Vitamin A deficiency, which causes mucin deficiency through goblet cell loss; topical drugs and preservatives; contact lens wear; and allergic eye disease |
| Iatrogenic and environmental | Systemic drugs — antihistamines, anticholinergics, beta-blockers, diuretics, isotretinoin, antidepressants and hormone therapy; refractive surgery. |
Symptoms, Signs and Investigation
- Symptoms — grittiness, burning, foreign-body sensation, itching, photophobia, fluctuating blurred vision that clears on blinking, contact lens intolerance, and — paradoxically — watering from reflex hypersecretion
- A characteristic feature is that symptoms exceed signs, particularly early; and in severe long-standing disease with corneal nerve damage the reverse may be true, with marked signs and few symptoms
- Symptoms are worse with reading, screen work, driving, air conditioning, wind and in the evening.
| Test | Method and interpretation |
|---|---|
| Tear break-UP time (TBUT) |
|
| Schirmer I test |
|
| Fluorescein staining | Stains areas of epithelial loss on the cornea; graded by the Oxford or NEI scheme |
| Lissamine green or rose bengal | Stain devitalised and unprotected cells, and are better for the conjunctiva. Rose bengal stings considerably; lissamine green is equally informative and comfortable, and has replaced it |
| Tear osmolarity | Raised above 308 mOsm/L; a direct measure of the core mechanism and useful for monitoring |
| Meibography and interferometry | Image gland dropout and the lipid layer thickness |
| Matrix metalloproteinase-9 | A point-of-care marker of ocular surface inflammation |
| Systemic tests | Anti-Ro and anti-La, rheumatoid factor, ANA, ESR; salivary gland biopsy where Sjogren is suspected |
Management
- Treatment is a ladder, and severity determines the rung:
- Step 1 — education and environment: explain that the condition is chronic and controllable rather than curable; take breaks from screen work and blink deliberately (the blink rate falls by more than half at a screen); lower the screen below eye level to reduce the exposed surface area; humidify; avoid direct air conditioning and fans; and review systemic drugs with the physician
- Step 1 — lid hygiene with warm compresses and massage for meibomian dysfunction.
- Step 1 — tear substitutes: drops by day, gels and ointment at night. Preservative-free preparations are essential above about four instillations daily.
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