Dry Eyes: What Could Be Causing It

How the Tear Film Works (and Fails)

A stable tear film is a three-layer structure: an outer lipid layer secreted by meibomian glands, a middle aqueous layer from the lacrimal gland, and an inner mucin layer produced by conjunctival goblet cells. When any layer is compromised, the film destabilizes and symptoms appear within seconds of a blink.

The Lipid Layer and Meibomian Gland Dysfunction

The lipid layer is only about 100 nm thick, yet it prevents roughly 90% to 95% of tear evaporation [2]. Meibomian gland dysfunction (MGD) thickens or blocks the oily secretions, accelerating evaporation. A 2011 international workshop reported that MGD was present in approximately 86% of dry eye patients examined across multiple studies [2]. Risk factors for MGD include rosacea, demodex mite infestation, contact lens wear, and androgen deficiency.

The Aqueous Layer and Lacrimal Gland Output

The lacrimal gland produces the bulk of the watery tear component. Aqueous-deficient dry eye (ADDE) results when this gland is inflamed, fibrosed, or neurologically impaired. Sjogren syndrome is the prototypical cause: a 2017 meta-analysis published in the American Journal of Ophthalmology estimated Sjogren syndrome prevalence at 0.06% in the general population, but nearly 10% of patients presenting with significant dry eye meet Sjogren criteria on workup [5].

The Mucin Layer and Goblet Cell Loss

Goblet cells lining the conjunctiva produce mucins (MUC5AC in particular) that allow tears to spread evenly. Chronic inflammation, vitamin A deficiency, chemical burns, and Stevens-Johnson syndrome destroy goblet cells, producing a "wettability" defect even when aqueous volume is normal. Severe vitamin A deficiency remains a leading cause of dry eye and corneal blindness in low-income countries, according to WHO data [8].

Common Causes of Dry Eyes

Dry eye is rarely caused by a single factor. Most patients have overlapping contributors, and identifying each one is the key to effective treatment.

Age and Hormonal Changes

Tear production declines roughly 0.3 microliters per minute per decade after age 30 [3]. By age 65, basal tear secretion may be 60% of what it was at 18. Women are disproportionately affected: the Women's Health Study (N=25,444) found that 6.7% of women aged 50 and older reported clinically significant dry eye symptoms, with prevalence climbing with each decade [3]. Estrogen and androgen receptors on the lacrimal and meibomian glands partially explain the sex difference, and menopause accelerates the decline.

Screen Time and Blink Rate Suppression

The average blink rate drops from about 15 blinks per minute during conversation to 5 or fewer during concentrated screen use [4]. Each incomplete blink leaves the inferior cornea exposed to evaporation. A 2023 cross-sectional study in BMJ Open Ophthalmology (N=672) found that participants with more than 6 hours of daily screen use had significantly lower TBUT and higher Ocular Surface Disease Index (OSDI) scores than those with fewer than 2 hours [4].

Medications That Dry the Eyes

Dozens of drug classes reduce tear production or alter tear composition. The most common offenders, per the American Academy of Ophthalmology [6]:

• Antihistamines (diphenhydramine, cetirizine): anticholinergic blockade of lacrimal secretion
• SSRIs and SNRIs (sertraline, venlafaxine): serotonergic suppression of lacrimal gland activity
• Isotretinoin (Accutane): meibomian gland atrophy at doses as low as 10 mg/day
• Beta-blockers (atenolol, metoprolol): reduced basal tear secretion
• Oral contraceptives and HRT: altered androgen-to-estrogen ratio affecting meibomian gland lipid output
• Anticholinergics (oxybutynin, scopolamine): direct parasympathetic blockade
• Diuretics (hydrochlorothiazide): systemic dehydration effect

If symptoms started within weeks of a new prescription, the medication should be the first suspect.

Autoimmune and Systemic Diseases

Sjogren syndrome is the most recognized systemic cause, but it is not the only one. Rheumatoid arthritis, systemic lupus erythematosus, sarcoidosis, graft-versus-host disease (GVHD), and thyroid eye disease (Graves orbitopathy) all damage the lacrimal gland or ocular surface through distinct inflammatory pathways [5]. GVHD deserves special mention: up to 60% of allogeneic bone marrow transplant recipients develop chronic dry eye within 2 years post-transplant [9].

Contact Lens Wear

Roughly 50% of contact lens wearers report dry eye symptoms [10]. The lens splits the tear film, increases evaporation from the pre-lens surface, and may reduce corneal sensitivity over time. Daily disposable lenses and scleral lenses tend to produce fewer symptoms than extended-wear soft lenses.

Environmental Triggers

Low humidity, air conditioning, forced-air heating, airplane cabins (cabin humidity can drop below 10%), and windy outdoor conditions all accelerate evaporative loss. Occupational exposure to dust, chemical fumes, or solvent vapors adds a toxic component that damages goblet cells and meibomian glands.

How Dry Eyes Are Diagnosed

A diagnosis of dry eye disease rests on symptom questionnaires, clinical signs, and targeted tests. No single test is definitive; the TFOS DEWS II diagnostic methodology report recommends a combination approach [7].

Symptom Questionnaires

The OSDI (Ocular Surface Disease Index) is the most widely validated instrument. A score of 13 to 22 indicates mild dry eye, 23 to 32 moderate, and 33 to 100 severe. The DEQ-5 (Dry Eye Questionnaire-5) is a faster alternative used in screening.

Clinical Tests Your Doctor May Perform

• Tear breakup time (TBUT): Fluorescein is instilled and the tear film is observed under cobalt blue light. A TBUT of <10 seconds is abnormal [7].
• Schirmer test: A filter paper strip is placed in the lower fornix for 5 minutes. Wetting of <10 mm without anesthesia suggests aqueous deficiency [7].
• Corneal and conjunctival staining: Fluorescein or lissamine green dye reveals epithelial damage not visible to the naked eye.
• Meibography: Infrared imaging of the meibomian glands reveals gland dropout. Advanced devices like LipiView also measure lipid layer thickness.
• Tear osmolarity: A reading of 308 mOsm/L or higher, or an inter-eye difference of more than 8 mOsm/L, supports a DED diagnosis [7].

When Blood Work Is Needed

If your eye doctor suspects Sjogren syndrome, they will order anti-SSA (Ro) and anti-SSB (La) antibodies, rheumatoid factor, ANA, and inflammatory markers (ESR, CRP). A lip biopsy showing focal lymphocytic sialadenitis with a focus score of 1 or greater per 4 mm² confirms the diagnosis per the 2016 ACR/EULAR criteria [5].

When to Worry About Dry Eyes

Most dry eye is a chronic nuisance, not an emergency. But certain red flags warrant urgent evaluation.

Signs That Need Same-Day or Next-Day Care

Sudden severe pain with redness and light sensitivity may indicate a corneal ulcer, especially in contact lens wearers. Vision loss that does not clear with blinking could signal corneal melting or a neurotrophic ulcer. A white or gray spot on the cornea visible in a mirror is likely an infiltrate or infection. Any of these scenarios requires same-day ophthalmologic assessment.

Signals of a Systemic Condition

Dry eyes paired with a persistently dry mouth, unexplained joint pain, skin rashes, or swollen parotid glands should prompt Sjogren syndrome screening. Bulging eyes with lid retraction point to thyroid eye disease. Dry eye appearing within months of a bone marrow transplant raises concern for GVHD [9].

Evidence-Based Treatment Options

The TFOS DEWS II management and therapy report outlines a stepwise approach, from lifestyle modification through advanced interventions [11]. Treatment should target the specific mechanism identified during diagnosis.

Step 1: Lifestyle and Over-the-Counter Measures

Preservative-free artificial tears remain first-line therapy. A 2019 Cochrane review found that all major tear formulations (carboxymethylcellulose, hyaluronic acid, polyethylene glycol) improved symptoms over no treatment, with no single formulation showing clear superiority [12]. Apply them 2 to 4 times daily. Lipid-based drops (such as those containing mineral oil or castor oil) are preferred when MGD is the dominant mechanism.

Other step-1 measures:

• The 20-20-20 rule: every 20 minutes, look at something 20 feet away for 20 seconds
• Humidifier use, especially in winter
• Omega-3 fatty acid supplementation (though the DREAM study, N=535, found no significant benefit of omega-3 over olive oil placebo at 12 months for moderate-to-severe DED [13])
• Warm compresses and lid hygiene for MGD (5 to 10 minutes daily)

Step 2: Prescription Anti-Inflammatory Drops

When artificial tears alone are insufficient, anti-inflammatory agents target the underlying ocular surface inflammation.

Cyclosporine 0.05% ophthalmic emulsion (Restasis): FDA-approved in 2003, cyclosporine inhibits T-cell activation on the conjunctival surface. In a phase 3 trial (N=877), 15% of cyclosporine-treated patients achieved a 10 mm or greater increase in Schirmer score at 6 months vs. 5% on vehicle (P<0.01) [14].

Lifitegrast 5% ophthalmic solution (Xiidra): Approved in 2016, lifitegrast blocks lymphocyte function-associated antigen-1 (LFA-1) interaction with ICAM-1. The OPUS-2 trial (N=711) showed statistically significant improvement in eye dryness score at day 84 compared with placebo [15].

Varenicline nasal spray 0.03 mg (Tyrvaya): Approved in 2021, this nicotinic acetylcholine receptor agonist stimulates the trigeminal parasympathetic pathway to boost natural tear production. The ONSET-2 trial (N=758) demonstrated that 47% of patients achieved a 10 mm or greater Schirmer improvement vs. 28% on placebo at week 4 (P<0.0001) [16].

Step 3: Procedural Interventions

• Punctal plugs: Silicone or collagen plugs inserted into the tear drainage puncta retain tears on the surface longer. Best suited for aqueous-deficient dry eye after inflammation is controlled.
• Intense pulsed light (IPL): Treats MGD-related ocular rosacea by reducing periocular inflammation and demodex populations. A 2020 meta-analysis of 8 studies found significant improvement in TBUT and meibomian gland expressibility after 3 to 4 sessions [17].
• Thermal pulsation (LipiFlow): Applies controlled heat and pressure to the eyelids to express blocked meibomian glands. A randomized trial (N=200) showed sustained symptom improvement at 12 months vs. Warm compresses alone [18].

Step 4: Advanced and Biologic Therapies

Autologous serum tears (20% concentration) provide growth factors and anti-inflammatory proteins not found in commercial drops. They are typically reserved for severe DED refractory to steps 1 through 3. Amniotic membrane grafting and scleral contact lenses are options for the most severe cases, including neurotrophic keratopathy and GVHD-related dry eye [11].

Dry Eye and Refractive Surgery

LASIK is the most studied surgical risk factor for dry eye. The procedure severs corneal nerves during flap creation, reducing reflex tearing for 3 to 6 months (and occasionally longer). A prospective study by Toda et al. Found that 95% of post-LASIK patients had some dry eye symptoms at 1 week, declining to 60% at 1 month and about 20% at 6 months [19]. PRK (photorefractive keratectomy) and SMILE (small incision lenticule extraction) sever fewer nerves and may carry lower dry eye risk, though head-to-head data remain limited.

Pre-Surgical Screening Matters

The AAO Preferred Practice Pattern recommends comprehensive dry eye screening before any corneal refractive surgery [6]. Patients with pre-existing moderate-to-severe DED, Sjogren syndrome, or low Schirmer scores (<5 mm at 5 minutes) are generally poor LASIK candidates.

The Role of Inflammation in Dry Eye Disease

Chronic dry eye is now understood as a self-perpetuating inflammatory cycle. Dr. Stephen Pflugfelder of Baylor College of Medicine has described it this way: "Tear film instability triggers epithelial stress, which releases inflammatory cytokines, which recruit T cells, which damage the lacrimal functional unit, which further destabilizes the tear film" [11]. Breaking this cycle is the rationale behind anti-inflammatory therapies like cyclosporine and lifitegrast.

A 2022 study in The Ocular Surface measured elevated levels of interleukin-6 (IL-6), IL-1 beta, tumor necrosis factor-alpha (TNF-alpha), and matrix metalloproteinase-9 (MMP-9) in the tears of DED patients vs. Controls [20]. MMP-9 point-of-care testing (InflammaDry) is now used in many clinics as a rapid biomarker for ocular surface inflammation.

The 2017 TFOS DEWS II pathophysiology report states: "Inflammation is a core mechanism in DED, though its prominence varies among patients, and treatment should be tailored to the individual inflammatory burden" [7].

Preventing Dry Eyes Before They Start

You cannot stop aging or change your genetics. But several modifiable factors reduce dry eye risk or slow its progression.

Digital Hygiene

Position screens slightly below eye level (this narrows the palpebral aperture and reduces exposed surface area). Increase font size to reduce squinting. Blink deliberately during screen breaks.

Nutritional Factors

Despite the neutral DREAM trial result for omega-3 supplements [13], dietary patterns rich in omega-3 fatty acids (fatty fish, flaxseed, walnuts) are associated with lower dry eye prevalence in epidemiologic studies. Adequate vitamin A intake (700 to 900 mcg RAE per day for adults) is protective against goblet cell loss [8].

Environmental Modifications

Use a humidifier to keep indoor humidity between 40% and 60%. Avoid direct airflow from fans, heaters, or car vents toward the face. Wrap-around glasses or moisture-chamber spectacles help in extreme conditions.