Dry eye disease (DED) is one of the most prevalent ocular conditions encountered in clinical practice, affecting an estimated 16 million Americans with diagnosed disease and many millions more with undiagnosed symptoms. For the COA, dry eye management is a daily encounter — patients present with burning, grittiness, redness, blurred vision, and tearing (paradoxically, reflex tearing can occur with dry eye). Mastery of DED diagnostics is high-yield for both the COA exam and real-world practice.
The 2017 TFOS DEWS II (Tear Film and Ocular Surface Society Dry Eye Workshop II) report is the current evidence-based framework for understanding, diagnosing, and managing DED. Its definition: "Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation, and neurosensory abnormalities play etiological roles."
This guide covers the TFOS DEWS II classification (aqueous deficient vs. evaporative), all major diagnostic tests (TBUT, Schirmer, vital staining), questionnaire scoring (SPEED, OSDI), slit-lamp findings, meibomian gland dysfunction (MGD) and meibography, and the stepwise treatment pyramid the COA should know to support patient education.
TFOS DEWS II Classification: Aqueous Deficient vs. Evaporative
Aqueous-Deficient Dry Eye (ADDE)
Insufficient tear production from the lacrimal gland. Low tear volume and low tear meniscus height.
- Sjogren's syndrome DED: Primary (isolated) or secondary (associated with RA, lupus, other autoimmune). Systemic dry eye + dry mouth (sicca complex).
- Non-Sjogren's ADDE: Lacrimal gland disease, radiation, medications (antihistamines, antidepressants, anticholinergics, isotretinoin), reflex block.
- Diagnostic markers: Low Schirmer I (<5mm/5min), low TBUT, low tear meniscus height, positive vital staining cornea/conjunctiva.
Evaporative Dry Eye (EDE)
Normal aqueous production but excessive evaporation from inadequate lipid layer. Most common form (~65–80% of DED cases).
- Meibomian gland dysfunction (MGD): Most common cause of EDE. Inadequate meibum quantity or quality.
- Other causes: Low blink rate (computer use, Parkinson's), incomplete blink, vitamin A deficiency, contact lens wear, eye surgery.
- Diagnostic markers: Low TBUT, abnormal meibum expression, meibomian gland loss on meibography, normal or near-normal Schirmer.
Diagnostic Tests: What the COA Performs
Tear Break-Up Time (TBUT)
Procedure:
- Instill preservative-free fluorescein or wet a fluorescein strip (shake off excess)
- Patient blinks normally 2–3 times to distribute fluorescein
- Patient holds last blink open
- Start timer at last blink
- Observe with cobalt blue filter (broad beam, high magnification)
- Stop timer at first dark break or dry spot
- Repeat 3 times; record average
Interpretation: Normal >10 seconds; borderline 7–10 seconds; abnormal <5–7 seconds. Most sensitive test for evaporative DED. Avoid excess fluorescein — it dilutes the tear film and artifactually lengthens TBUT.
Schirmer Test
Procedure (Schirmer I, without anesthesia):
- Patient seated; dim room
- Fold strip at notch; place in inferior fornix at medial/middle third junction
- Patient closes eyes gently — do not squeeze
- Remove after exactly 5 minutes
- Measure wetting from the notch (not the fold)
- Record mm of wetting for each eye
Interpretation: Normal ≥10mm/5 minutes; borderline 6–9mm; abnormal (suggests ADDE) ≤5mm/5 minutes. Both eyes are tested simultaneously for comparison. Schirmer with anesthesia (basic secretion test) suppresses reflex tearing; normal ≥6mm/5 min with anesthetic.
Vital Staining of the Ocular Surface
| Dye | What It Stains | Clinical Notes |
|---|---|---|
| Fluorescein | Areas of epithelial disruption (broken tight junctions) | Bright green with cobalt blue filter. Inferior 1/3 corneal pattern = classic DED. Also used for TBUT. |
| Rose Bengal | Devitalized and dead cells, mucus | Triangular interpalpebral conjunctival staining classic for Sjogren's. Less used due to stinging. |
| Lissamine Green | Devitalized cells, dead cells, mucus | Similar to rose bengal but far less irritating. Preferred in practice for conjunctival assessment. |
Dry Eye Questionnaires: SPEED and OSDI
SPEED Questionnaire
Standard Patient Evaluation of Eye Dryness — 8 questions on symptom frequency and severity at different times of day. Score range: 0–28. Score ≥6 suggests symptomatic dry eye; ≥10 is significant. Quick to administer (~2–3 minutes). Practical for routine screening at check-in and tracking changes over time with treatment.
OSDI Questionnaire
Ocular Surface Disease Index — 12 questions covering ocular symptoms, vision-related function, and environmental triggers. Score range: 0–100 (0=no disability, 100=complete disability).
| OSDI Score | Classification |
|---|---|
| 0–12 | Normal |
| 13–22 | Mild DED |
| 23–32 | Moderate DED |
| 33–100 | Severe DED |
The OSDI is the gold standard patient-reported outcome measure in DED clinical trials. Takes approximately 5 minutes to complete. Remember: symptoms (OSDI/SPEED) and clinical signs (TBUT, staining) often do not correlate — TFOS DEWS II defines DED based on either symptoms OR signs.
Meibomian Gland Dysfunction (MGD)
MGD is the most common cause of dry eye disease worldwide and the primary reason TBUT is low even in patients with normal Schirmer values. MGD assessment is now a routine part of the dry eye workup.
Anatomy and Function
Meibomian glands (tarsal glands) are elongated sebaceous glands running vertically within the tarsal plate — approximately 25–30 in the upper lid and 20–25 in the lower lid. Each gland secretes meibum through an orifice at the posterior lid margin. Meibum forms the outermost lipid layer of the tear film, preventing evaporation and stabilizing tear film integrity.
Clinical Assessment
Slit-lamp lid margin findings: orifice capping/plugging (keratinized caps), orifice dropout or scarring, irregular lid margin (notching, scalloping), vascular engorgement (telangiectasia), foamy tears.
Gland expression: Apply digital pressure or a standardized expressibility device. Grade quality: clear oily = normal; cloudy = mild MGD; granular/paste-like = moderate; no expressible meibum = severe/end-stage. Grade number of expressible glands out of 5 central lower lid glands.
Meibography
Meibography is infrared imaging of the meibomian gland structure within the everted eyelid. Modern instruments (Oculus Keratograph, LipiView, Topcon Maestro) allow non-contact meibography with automated gland area analysis. Gland loss (dropout) appears as dark areas where gland tissue should be.
Meibography grade (0–3 scale): 0 = no gland loss; 1 = <1/3 gland area lost; 2 = 1/3 to 2/3 lost; 3 = >2/3 lost. Progressive gland loss correlates with more severe MGD and evaporative DED. Meibography is increasingly standard-of-care in comprehensive dry eye evaluations.
Slit-Lamp Findings in Dry Eye
| Finding | Significance | Assessment Method |
|---|---|---|
| Tear meniscus height (TMH) | Low (<0.20mm) suggests reduced aqueous production (ADDE) | Slit-beam 0.1mm comparison; keratograph quantification |
| Corneal fluorescein staining | Inferior 1/3 pattern = classic DED; superior = exposure/lagophthalmos | Cobalt blue illumination; Oxford staining scale 0–5 |
| Conjunctival staining | Nasal/temporal interpalpebral = DED; superior = superior limbic keratoconjunctivitis (SLK) | Broad beam; Van Bijsterveld scale |
| 3 and 9 o'clock staining | Fluorescein at 3 and 9 o'clock positions = soft contact lens-related DED | Cobalt blue filter; lens-bearing area |
| Bulbar conjunctival redness | Graded 0–4 (Efron scale); correlates with ocular surface inflammation | Slit-lamp direct illumination; standardized grading scale |
| Mucous filaments/strands | Filamentary keratitis — mucus anchored to corneal epithelium; severe DED | Direct illumination; fluorescein highlights filaments |
DED Treatment Pyramid: From Basics to Advanced
The TFOS DEWS II treatment pyramid organizes management stepwise from first-line conservative therapy to advanced interventions. The COA should understand this framework to support patient education and recognize which stage a patient is at in their management journey.
Step 1: Education and Lifestyle Modifications
Environmental modifications (humidifier, reduced screen time, blink exercises), dietary omega-3 supplementation (fish oil), elimination of offending systemic medications where possible, eyelid hygiene and warm compresses for MGD, over-the-counter lubricant eye drops (preservative-free preferred for frequent use >4×/day).
Step 2: Prescription Treatments
Topical anti-inflammatory agents: cyclosporine A 0.05% (Restasis, Cequa) and lifitegrast 5% (Xiidra) — both target T-cell-mediated ocular surface inflammation. Short-term topical corticosteroids (loteprednol, fluorometholone) for inflammatory flares. Punctal plugs (temporary collagen or permanent silicone) to reduce tear drainage and increase tear volume. Oral doxycycline for MGD (anti-inflammatory effect, not antibiotic).
Step 3: In-Office Procedures
Intense pulsed light (IPL) therapy — light energy applied to periocular skin improves meibomian gland function and reduces inflammation. LipiFlow thermal pulsation — applies vectored thermal pulse to the inner eyelid surface to liquefy and express meibomian gland content. Both are effective for evaporative DED secondary to MGD.
Step 4: Advanced Options
Autologous serum eye drops (patient's own blood serum containing growth factors and vitamins) for severe, refractory DED. Scleral contact lenses (large-diameter GP lenses that vault over the cornea and maintain a fluid reservoir) for severe DED with or without associated ocular surface disease. Surgical procedures (tarsorrhaphy, amniotic membrane transplant) for the most severe cases.