Quin’s Disease (Dry Eye Syndrome)

Overview

Quin’s disease, more commonly known as **dry eye syndrome (DES)**, is a chronic condition in which the eyes do not produce enough tears—or the tears evaporate too quickly—to keep the surface of the eye lubricated. Tears are essential for maintaining corneal health, providing clear vision, and protecting against infection. When the tear film is deficient, the ocular surface becomes inflamed and damaged, leading to a wide range of uncomfortable symptoms.

Who it affects: Dry eye can affect anyone, but it is most prevalent among

• Adults over 50 years of age
• Women (especially post‑menopausal)
• Contact‑lens wearers
• People who spend many hours in front of digital screens
• Individuals with autoimmune diseases (e.g., Sjögren’s syndrome, rheumatoid arthritis)

Prevalence: According to the CDC and the American Academy of Ophthalmology, dry eye affects roughly 5–30 % of the U.S. population, with higher rates (up to 40 %) reported in older adults. Worldwide, the International Dry Eye Workshop (DEWS II) estimates that more than 400 million people live with clinically significant dry eye.

Symptoms

Symptoms can range from mild irritation to severe pain and visual disturbance. They may fluctuate throughout the day and often worsen in dry, windy, or air‑conditioned environments.

• Foreign‑body sensation – a feeling that something is in the eye.
• Burning or stinging – often described as “heat” on the surface.
• Itching – can be associated with mild allergy‑type redness.
• Redness – especially around the cornea and conjunctiva.
• Blurred or fluctuating vision – tears are critical for a smooth optical surface; instability causes temporary blur, especially after reading or computer work.
• Excessive tearing (reflex tearing) – paradoxically, the eye may over‑produce watery tears in response to irritation, but these tears lack the oily layer needed for retention.
• Sensitivity to light (photophobia).
• Eye fatigue – a heavy or “tired” feeling after prolonged visual tasks.
• Stringy mucus discharge – especially upon waking.
• Difficulty wearing contact lenses – intolerance or increased discomfort.

Causes and Risk Factors

Primary mechanisms

1. Aqueous‑deficient dry eye – reduced production of the watery component by the lacrimal glands. Common in Sjögren’s syndrome and age‑related lacrimal gland atrophy.
2. Evaporative dry eye – excessive tear evaporation, usually due to Meibomian gland dysfunction (MGD) that compromises the oily lipid layer.
3. Mixed type – most patients have a combination of reduced production and increased evaporation.

Risk factors

• Age: Tear production declines with age; >50 % of people over 65 have some degree of DES.
• Sex hormones: Estrogen decline after menopause reduces tear stability.
• Autoimmune disease: Sjögren’s, rheumatoid arthritis, lupus, and thyroid eye disease.
• Medications: Antihistamines, decongestants, antidepressants, beta‑blockers, isotretinoin, and certain diuretics.
• Environmental exposure: Low humidity, wind, smoke, air‑conditioned or heated rooms.
• Digital device use: “Computer vision syndrome” reduces blink rate from ~15 blinks/min to 5–7.
• Contact lens wear: Particularly soft lenses that limit oxygenation.
• Refractive surgery: LASIK or PRK can disrupt corneal nerves, decreasing tear reflex.
• Blepharitis or eyelid malposition: Improper lid closure leads to tear film breakup.

Diagnosis

Diagnosis is clinical but supported by a series of objective tests to assess tear quantity, quality, and ocular surface health.

History and symptom questionnaire

• Ocular Surface Disease Index (OSDI) – a validated 12‑item questionnaire that quantifies symptom severity.

Clinical examinations

1. Schirmer test – a thin strip of filter paper placed under the lower eyelid for 5 minutes; < 5 mm indicates aqueous deficiency.
2. Tear Break‑Up Time (TBUT) – fluorescein dye is applied, and the time until first dry spot appears is measured; ≤10 seconds suggests tear instability.
3. Osmolarity testing – high tear osmolarity (>308 mOsm/L) is a marker of dry eye severity.
4. Meibomian gland assessment – infrared meibography visualizes gland dropout; expression evaluates lipid quality.
5. Corneal and conjunctival staining – fluorescein, lissamine green, or rose bengal highlight surface damage; graded by the Oxford or NEI scales.
6. Inflammatory markers – point‑of‑care tests for matrix metalloproteinase‑9 (MMP‑9) can identify ocular surface inflammation.

Additional work‑up when indicated

• Blood tests for autoimmune disease (ANA, RF, SSA/SSB antibodies).
• Imaging (e.g., dacryocystography) if tear drainage obstruction is suspected.

Treatment Options

Treatment is individualized, often beginning with lifestyle measures and advancing to prescription medications or procedures as needed.

Artificial tears and lubricants

• Preservative‑free drops – preferred for chronic use; apply 4–6 times daily.
• Gels and ointments – thicker formulations for nighttime use.
• Cyclosporine 0.05 % (Restasis®) or lifitegrast 5 % (Xiidra®) – prescription drops that reduce ocular surface inflammation and increase tear production.

Anti‑inflammatory therapies

• Short courses of topical corticosteroids (e.g., loteprednol) for acute flare‑ups.
• Oral tetracycline‑class antibiotics** (doxycycline 40‑100 mg daily) to improve Meibomian gland lipid quality.
• Omega‑3 fatty acid supplements (e.g., fish oil 1000 mg EPA/DHA) – modest benefit per meta‑analysis (Cochrane, 2022).