Cornea & Ocular SurfaceOphthalmologyOptometry

Dry Eye Disease

Also known as: DED, Keratoconjunctivitis sicca, Ocular surface disease

Overview

Dry eye disease is a multifactorial disease of the ocular surface characterized by loss of tear film homeostasis, accompanied by ocular symptoms, in which tear film instability, hyperosmolarity, inflammation, and neurosensory abnormalities play etiological roles. It is among the most common reasons patients present to eyecare providers. Management is staged and targets the underlying subtype—aqueous-deficient, evaporative, or mixed.

Nature
Multifactorial ocular surface disease
Core mechanism
Tear film instability + hyperosmolarity
Main subtypes
Evaporative, aqueous-deficient, mixed
Framework
TFOS DEWS II

Key clinical points

  • Evaporative dry eye from meibomian gland dysfunction is the most common subtype.
  • Symptoms and signs frequently do not correlate, so evaluation combines questionnaires with objective testing.
  • Tear osmolarity and matrix metalloproteinase-9 testing support diagnosis and characterize inflammation.
  • Management is staged from lubricants and lid hygiene up to anti-inflammatories, secretagogues, and procedures.
  • Identifying and treating meibomian gland dysfunction is central to most evaporative disease.

Pathophysiology

The TFOS DEWS II report frames dry eye around a self-perpetuating vicious cycle: tear film instability and hyperosmolarity trigger ocular surface inflammation and damage, which further destabilizes the tear film. Neurosensory abnormalities can amplify symptoms and, in some patients, produce a mismatch between reported discomfort and visible signs.

Classifying disease along the evaporative–aqueous-deficient spectrum guides therapy. Most patients have a significant evaporative component driven by meibomian gland dysfunction.

Diagnosis

A validated symptom questionnaire (such as OSDI or DEQ-5) begins the workup. Objective tests include tear breakup time, ocular surface staining with fluorescein and lissamine green, meibomian gland expression and meibography, and Schirmer testing for aqueous production.

Point-of-care tear osmolarity and MMP-9 testing add objective measures of instability and inflammation. Because signs and symptoms often diverge, an integrated picture is more reliable than any single test.

Management

Treatment is staged. Foundational measures include artificial tears, lid hygiene, warm compresses, environmental modification, and addressing contributing medications and systemic disease. Meibomian gland dysfunction is treated with lid-warming therapies and, when needed, in-office thermal pulsation or intense pulsed light.

Persistent disease warrants anti-inflammatory therapy such as topical cyclosporine or lifitegrast, short pulses of topical corticosteroid, and secretagogues. Punctal occlusion conserves tears in aqueous-deficient disease, and autologous serum or scleral lenses are reserved for severe or refractory cases.

Dry Eye Disease videos

Frequently asked questions

Why don’t dry eye symptoms match the clinical signs?
Neurosensory abnormalities and corneal nerve sensitization can produce prominent symptoms with minimal signs, or vice versa. This is why guidelines recommend combining symptom questionnaires with objective testing.
What is the most common cause of dry eye?
Evaporative dry eye due to meibomian gland dysfunction is the most common form, so evaluating and treating the meibomian glands is central to management.
Do anti-inflammatory drops help dry eye?
Yes. Because inflammation drives the dry eye cycle, agents such as topical cyclosporine or lifitegrast, and brief courses of corticosteroid, are used to interrupt it in moderate to severe disease.

References & further reading

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