Dry Eye

Dry eye disease is a common condition in which tears cannot keep the surface of the eye properly lubricated. This happens either because the eyes do not make enough tears, because tears evaporate off the eye too quickly, or because the tears that are produced are not the right quality to do their job. The medical term for this condition is keratoconjunctivitis sicca (KCS)—a Latin phrase meaning dryness and inflammation of the cornea and conjunctiva (the clear front surface of the eye and the thin membrane lining the inner eyelids). It is also sometimes called dry eye syndrome or dysfunctional tear syndrome.

A healthy tear film has three layers working together. The outermost layer is an oily film produced by small glands along the eyelid margins, called meibomian glands. This layer slows evaporation. The middle layer is a watery fluid made by the lacrimal glands, located above each eye. This is the thickest layer and carries nutrients and oxygen to the eye’s surface. The inner layer is a gel-like substance called mucin, produced by goblet cells on the inner surface of the eyelids. Mucin helps the tear film spread evenly across the eye and stick to the corneal surface. When any of these three layers is disrupted—whether from insufficient production, gland blockage, or surface inflammation—the entire tear film becomes unstable and dry eye disease can develop.

Dry eye disease is one of the most common eye conditions in the United States. Nearly 16.4 million Americans have been diagnosed with it, making it more prevalent than diabetes, heart disease, and cancer. Globally, estimates suggest that between 5 and 34% of people are affected, depending on the population and the diagnostic criteria used. Dry eye disease is chronic—meaning it is a long-term condition with no cure. It is managed rather than eliminated. Severity ranges from mild, occasional irritation to persistent discomfort that interferes with daily activities, work, and sleep. In severe cases, the corneal surface can be damaged, leading to scarring and vision loss. The condition has also been linked to higher rates of anxiety and depression because of the impact it has on quality of life.

In aqueous-deficient dry eye, the lacrimal glands do not produce enough of the watery middle layer of the tear film. Even if the oil and mucin layers are intact, there simply is not enough fluid to keep the eye’s surface wet. This type is divided into two subtypes based on the underlying cause.

• Sjögren’s syndrome dry eye: caused by an autoimmune attack on the lacrimal glands. The immune system mistakenly targets and destroys the gland tissue that makes tears. Sjögren’s syndrome is often associated with other autoimmune conditions such as rheumatoid arthritis, lupus, and scleroderma. It is one of the most severe forms of dry eye disease.
• Non-Sjögren’s syndrome dry eye: lacrimal gland deficiency from causes other than an autoimmune disease. This includes age-related decline in gland function, blockage of the tear ducts, reduced corneal nerve signaling (which can follow laser-assisted in situ keratomileusis—LASIK surgery or long-term contact lens wear), and side effects from certain medications.

In evaporative dry eye, the lacrimal glands are producing a normal amount of tears, but those tears evaporate off the eye too quickly. This is most often caused by a problem with the oil layer of the tear film, which normally acts as a barrier to slow evaporation. Evaporative dry eye is the most common form of dry eye disease. Causes are grouped into intrinsic (originating within the eye itself) and extrinsic (coming from outside the eye).

• Meibomian gland dysfunction (MGD): The most common single cause of dry eye disease. The meibomian glands become blocked or inflamed, reducing the quality and quantity of the oil layer. MGD is more common in people with rosacea (a chronic skin condition causing facial redness) and blepharitis (chronic eyelid inflammation).
• Reduced blink rate: Prolonged screen use, reading, and driving reduce how often a person blinks. Each blink spreads fresh tears across the eye, so fewer blinks means faster evaporation. Conditions like Parkinson’s disease, which reduce the frequency of blinking, have the same effect.
• Eyelid problems: Conditions that prevent the eyelid from fully closing, such as thyroid eye disease (which causes the eye to bulge forward) or facial nerve palsy (which can paralyze the closing muscles), expose the corneal surface to air and accelerate drying.
• Contact lens wear: Lenses sit on the tear film and can disrupt its stability, increasing evaporation from the surface.
• Preservatives in eye drops: Some eye drops, particularly those used to treat glaucoma, contain a preservative called benzalkonium chloride that can damage the ocular surface and worsen dry eye over time.
• Vitamin A deficiency: Vitamin A is essential for mucin production by goblet cells. Deficiency leads to loss of mucin and tear film instability.
• Allergic conjunctivitis: Chronic eye allergy inflames the conjunctival surface and can reduce the number of goblet cells, destabilizing the inner mucin layer of the tear film.

Many patients have both reduced tear production and excessive evaporation occurring at the same time. This is called mixed dry eye. Treatment in these cases must address both components. The boundary between the two major types is not rigid, and most patients fall somewhere on a spectrum rather than fitting neatly into one category.

Doctors also classify dry eye by how it developed and how severe it is. Dry eye that develops as a result of a medical procedure—such as LASIK surgery, cataract surgery, or using continuous positive airway pressure (CPAP) equipment for sleep apnea—is sometimes called iatrogenic dry eye (dry eye caused by treatment). Dry eye is also rated by severity—mild, moderate, or severe—based on the patient’s symptoms, how quickly the tear film breaks down, and the degree of surface damage visible during an eye exam. Severity classification guides the treatment plan.

Dry eye disease develops when the tear film loses its normal balance—a state doctors call homeostasis. This imbalance leads to tears that are too concentrated (a condition called hyperosmolarity), which in turn triggers inflammation on the surface of the eye. Once inflammation begins, it damages the cells that produce tears and mucin, which makes the tear film even more unstable. This creates a self-reinforcing loop—sometimes called the vicious cycle of dry eye—where each step makes the next step worse.

The specific causes that start this process fall into two main categories: those that reduce how much tear fluid is produced, and those that cause tears to evaporate too quickly.

• Aging: Lacrimal gland function declines naturally with age. Tear production decreases, and the composition of tears changes. This is one of the most common reasons dry eye becomes more prevalent in older adults.
• Autoimmune diseases: In Sjögren’s syndrome, rheumatoid arthritis, lupus, scleroderma, and graft-versus-host disease, the immune system attacks the lacrimal glands. Over time, gland tissue is destroyed, and tear production falls significantly.
• Medications: A wide range of commonly used medicines can reduce tear secretion as a side effect. These include antihistamines (allergy medicines), decongestants, antidepressants, beta-blockers (blood pressure medicines), diuretics (water pills), hormone replacement therapy, oral contraceptives, and retinoids (vitamin A-derived skin medicines). If you take any of these and have dry eye symptoms, talk to your doctor—adjusting your medication may help.
• Corneal nerve damage: The lacrimal glands receive signals through corneal nerves telling them when to produce tears. When those nerves are damaged—by herpes keratitis, LASIK surgery, long-term contact lens wear, or diabetic neuropathy—the signaling is disrupted and tear production drops. This form of dry eye is usually temporary after LASIK, but can persist in some cases.
• Vitamin A deficiency: This essential nutrient supports the goblet cells that produce mucin (the inner layer of the tear film). A severe deficiency reduces mucin production and destabilizes tear film integrity.
• Radiation therapy to the head or neck: Radiation can damage lacrimal gland tissue and reduce tear production, sometimes permanently.

• Meibomian gland dysfunction (MGD): When the oil glands along the eyelid margins are blocked or inflamed, they produce inadequate or poor-quality oil. Without enough oil in the tear film’s outer layer, tears evaporate rapidly. MGD is the most common cause of dry eye disease overall.
• Reduced blink rate: Blinking is essential to spreading fresh tears across the eye. When blink rate drops—as it does during intensive screen use, reading, or driving—the tear film is not refreshed frequently enough and evaporation accelerates.
• Eyelid closure problems: Conditions that prevent the eyelid from fully covering the eye during a blink or during sleep expose the cornea to air. This dramatically accelerates evaporation from the exposed surface.
• Contact lens wear: Lenses disrupt the tear film’s layered structure and can accelerate evaporation, reduce oxygen flow to the cornea, and contribute to surface inflammation over time.
• Screen use and environment: Low humidity environments (air conditioning, heating, airplane cabins), wind, and smoke accelerate evaporation. Prolonged digital screen use reduces blink rate, compounding the problem.
• Preservatives in topical eye drops: Long-term use of preserved eye drops, especially those for glaucoma, can damage goblet cells on the conjunctival surface and disrupt the mucin layer.

Dry eye disease can affect anyone, but certain people are at significantly higher risk. Some risk factors—like age and sex—cannot be changed, while others—like screen habits and medication use—can be addressed to reduce severity.

• Older age: Dry eye prevalence rises steadily with age. About 2.7% of adults aged 18 to 34 are affected, compared with 5.0% at ages 45 to 54, 8.4% at ages 55 to 64, 11.5% at ages 65 to 74, and 18.6% of adults aged 75 and older.
• Female sex: Women develop dry eye disease at nearly twice the rate of men. About 8.8% of women are affected compared with 4.5% of men. Hormonal changes—especially the drop in estrogen and androgens (male hormones that also affect the eye in women) after menopause—contribute significantly to this difference.
• Postmenopausal status: Hormonal changes after menopause affect lacrimal and meibomian gland function. Postmenopausal women, particularly those who have used hormone replacement therapy with estrogen alone (without progesterone), have a higher rate of dry eye.

• Autoimmune diseases: Sjögren’s syndrome, rheumatoid arthritis, lupus, and scleroderma are strongly associated with aqueous-deficient dry eye. Thyroid eye disease is associated with evaporative dry eye through lid position and exposure.
• Diabetes mellitus: Diabetic neuropathy (nerve damage from long-term high blood sugar) can reduce corneal sensitivity, impairing the reflex signals that tell the lacrimal glands to produce tears.
• Rosacea: This chronic skin condition commonly affects the eyelids, causing meibomian gland dysfunction and evaporative dry eye.
• Blepharitis: Chronic inflammation of the eyelid margins affects meibomian gland function and is a major contributor to evaporative dry eye.
• Graft-versus-host disease: This can occur after bone marrow or stem cell transplant when donor immune cells attack the recipient’s tissue, including the lacrimal glands.
• Allergic conjunctivitis: Chronic eye allergy inflames the conjunctival surface and reduces goblet cell density, weakening the mucin layer.

• Antihistamines and decongestants: among the most common drug-related causes of dry eye. They dry out mucous membranes throughout the body, including the eyes.
• Antidepressants: Both tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) can reduce tear production.
• Beta-blockers: These are commonly used for blood pressure and heart conditions; can reduce lacrimal secretion.
• Diuretics (water pills): They reduce fluid volume throughout the body, including tear production.
• Hormone-based contraceptives and hormone replacement therapy: These, particularly estrogen-only formulations, have been associated with increased dry eye risk.
• Retinoids: These are used for acne and skin conditions; oral and topical retinoids can reduce meibomian gland function and goblet cell density.
• Glaucoma eye drops containing benzalkonium chloride: The preservative in many glaucoma drops accumulates on the ocular surface and damages epithelial and goblet cells with long-term use.

• Prolonged digital screen use: Screen use is one of the fastest-growing drivers of dry eye, particularly in younger adults. Reduced blink rate during screen use leads to faster tear evaporation.
• Contact lens wear: Long-term contact lens wear disrupts the tear film and is a recognized risk factor for both evaporative and aqueous-deficient dry eye.
• Low-humidity environments: Air conditioning, forced-air heating, airplane cabins, and dry climates accelerate tear evaporation.
• Smoking: Cigarette smoke is directly toxic to the ocular surface and meibomian glands.
• Prior eye surgery: LASIK and other refractive surgeries can damage corneal nerves that regulate tear production. Most patients experience temporary dry eye after these procedures; a smaller percentage develop chronic dry eye.

Dry eye disease is diagnosed and monitored through a series of tests performed during a comprehensive eye exam. There is no single definitive test—diagnosis typically relies on a combination of the patient’s reported symptoms, clinical findings, and objective measurements. Adults who have persistent eye irritation, burning, or blurry vision that comes and goes should discuss dry eye screening with their eye doctor. People with known risk factors—including older age, autoimmune disease, diabetes, heavy screen use, or use of drying medications—should be screened proactively.

• Symptom questionnaires: Standardized questionnaires such as the Ocular Surface Disease Index (OSDI) and the Dry Eye Questionnaire (DEQ-5) ask patients to rate the frequency and severity of their symptoms. These tools help classify the severity of dry eye and track changes over time.
• Tear break-up time (TBUT): After placing a small amount of fluorescein dye in the eye, the doctor uses a slit-lamp microscope and cobalt blue light to time how long it takes for the first dry spot to appear in the tear film after a blink. A time of less than 10 seconds indicates an unstable tear film.
• Schirmer test: A thin strip of filter paper is placed inside the lower eyelid. After five minutes, the doctor measures how far the paper has been wetted by tears. Less than 5 millimeters of wetting suggests reduced tear production.
• Tear osmolarity testing: A small sample of tears is collected and analyzed for salt concentration. A reading above 308 mOsm/L (milli-osmoles per liter) is a biomarker for dry eye disease. High tear osmolarity confirms hyperosmolarity—the key driver of the inflammatory cycle in dry eye.
• Fluorescein staining of the cornea: The doctor examines the corneal surface under blue light after applying dye. Damaged or missing surface cells absorb the dye and appear as bright stained dots. The pattern and extent of staining reflect the severity of surface damage.
• Lissamine green staining: A green dye highlights dead or dying cells on the conjunctival surface. It helps assess goblet cell loss and overall ocular surface health.
• Meibomian gland evaluation: The doctor examines the eyelid margins under the slit lamp and may gently press on the glands to observe the quality and quantity of oil they express. Meibography—infrared imaging of the eyelids—can show structural loss of meibomian glands.
• Matrix metalloproteinase-9 (MMP-9) testing: A point-of-care test (InflammaDry®) can detect elevated levels of MMP-9, an inflammatory enzyme in the tear film. A positive result supports the diagnosis of inflammatory dry eye disease.

Dry eye disease caused by aging, hormonal changes, or genetic predisposition cannot be fully prevented. However, many contributing factors can be managed to significantly reduce the risk of developing dry eye or slow its progression. The following steps are particularly useful for people who spend long hours at screens, live in dry environments, or use medications that affect tear production.

• Follow the 20-20-20 rule during screen use: Every 20 minutes, look at something at least 20 feet away for at least 20 seconds. This gives the eyes a break and helps restore normal blink rate.
• Blink consciously during screen use: Most people blink far less often while looking at screens. Making a deliberate effort to blink fully and frequently helps spread fresh tears across the eye.
• Use a humidifier: Adding moisture to the air in your home or office reduces the rate at which tears evaporate, especially in heated or air-conditioned spaces.
• Wear wraparound glasses or sunglasses outdoors: Shielding the eyes from wind, dust, and direct sun exposure reduces tear loss.
• Avoid smoke: Both direct smoking and secondhand smoke are directly toxic to the ocular surface. Quitting smoking reduces dry eye risk.
• Ask your doctor about drying medications: If you take antihistamines, antidepressants, or other medications linked to dry eye, ask your doctor whether alternatives with less impact on tear production are available.
• Use preservative-free eye drops when possible: For people who use artificial tears frequently, or who use prescription eye drops for conditions like glaucoma, choosing preservative-free formulations reduces ongoing damage to the ocular surface.
• Practice good lid hygiene: Gently cleaning the eyelid margins with a warm, damp cloth or commercially available eyelid wipes can help prevent meibomian gland blockage and reduce the risk of evaporative dry eye.

The hallmark of dry eye disease is persistent discomfort in one or both eyes—often described as a burning, stinging, or gritty feeling—combined with vision that fluctuates or blurs, particularly during tasks that require sustained visual focus. Symptoms are often worse at the end of the day, in dry or windy conditions, during screen use, and in heated or air-conditioned spaces. It may seem paradoxical, but excessive tearing is also a common symptom of dry eye—when the surface is irritated, the eye reflexively floods itself with watery tears that lack the proper balance of oils and mucin and drain away quickly without providing lasting relief.

• Burning or stinging: This is a persistent feeling of heat or irritation on the eye’s surface, ranging from mild to severe.
• Gritty or sandy sensation: This is the feeling that something is stuck in the eye, even when nothing is there.
•  Intermittent blurry vision: vision that becomes hazy during reading, screen use, or driving, then briefly clears after blinking. This happens because blinking temporarily refreshes the tear film.
• Eye redness: This presents as persistent redness or pinkness in the white of the eye from chronic irritation and inflammation.
• Light sensitivity (photophobia): This is discomfort or pain in bright light, particularly in moderate-to-severe dry eye.
• Eye fatigue: Patients may experience tiredness, heaviness, or aching in and around the eye, especially after prolonged visual tasks.
• Watery eyes (paradoxical tearing): The eye produces a flood of thin, watery tears in response to irritation. These reflex tears lack the proper lipid and mucin components and drain away quickly, providing little lasting relief.
• Stringy or mucus discharge: There may be thin strings or strands of mucus in or around the eye, particularly in the morning.
• Discomfort with contact lenses: Lenses become difficult to tolerate as dry eye progresses, with increasing irritation and shorter comfortable wearing time.
• Difficulty with nighttime driving: Glare and halos around headlights and streetlights are worsened by an unstable tear film.

In mild dry eye, symptoms are intermittent and often triggered by specific activities or environments, such as screen use or air travel. Discomfort is manageable and usually responds quickly to over-the-counter artificial tears.

In moderate dry eye, symptoms are more frequent and persistent. They affect daily activities such as reading, computer use, and driving. Over-the-counter drops may no longer provide sufficient relief, and prescription treatment may be needed. The corneal surface may show mild staining on examination.

In severe dry eye, symptoms are constant and significantly limit daily function. Painful blisters (bullae) may form on the corneal surface in the most advanced cases. Corneal scarring is possible if the condition is not adequately treated. Patients in this category typically require prescription anti-inflammatory medicines, punctal plugs, autologous serum drops, or scleral contact lenses.

• In younger adults (20s to 40s): Dry eye in this group is most often related to heavy screen use, contact lens wear, or post-LASIK surgery. Symptoms tend to appear during or after prolonged visual tasks and may be dismissed as eye strain.
• In middle-aged adults (40s to 60s): Prevalence rises significantly as hormonal changes occur. Women approaching or past menopause notice a meaningful increase in dryness and irritation. Meibomian gland dysfunction becomes more common in this age range. Dry eye may coexist with reading glasses needs, and symptoms can be mistaken for general age-related vision changes.
• In older adults (65 and over): Dry eye affects nearly one in five adults aged 75 and older. Multiple contributing factors often converge—age-related gland decline, medications for chronic conditions, reduced blink rate, and lower indoor humidity in winter months. Symptoms in this age group may be more severe and harder to treat because of the cumulative damage to gland tissue and the ocular surface.

An ophthalmologist (a medical doctor who specializes in eye diseases) or an optometrist (a licensed eye care provider) diagnoses dry eye disease. Because no single test can definitively diagnose dry eye, the process combines a careful review of a patient’s symptoms with several objective measurements taken during a clinical eye exam. Early diagnosis is important—the longer dry eye goes untreated, the more the ocular surface can be damaged, potentially making treatment more difficult.

The diagnosis can sometimes be challenging because dry eye symptoms overlap with those of other common eye conditions, including allergic conjunctivitis, blepharitis, and contact lens-related eye problems. A thorough history—including medications, medical conditions, screen time, contact lens use, and environmental exposures—is an essential part of the evaluation.

• Standardized questionnaires: The Ocular Surface Disease Index (OSDI) and the DEQ-5 are validated tools used to quantify how often symptoms occur and how much they affect daily activities. Scores help classify severity as mild, moderate, or severe and provide a baseline to measure treatment response over time.
• Medical and medication history: The doctor reviews all current medications, systemic health conditions, prior eye surgeries, and environmental and occupational exposures. This is critical for identifying contributing or modifiable causes.

• Slit-lamp biomicroscopy: a specialized microscope that provides a magnified, illuminated view of the entire front surface of the eye and eyelids. It is the primary tool for assessing tear film quality, eyelid margin health, conjunctival and corneal surface changes, and meibomian gland appearance.
• Tear break-up time (TBUT): Fluorescein dye is placed in the eye, and the doctor times how quickly the tear film develops dry spots after a blink. Less than 10 seconds indicates tear film instability. This is one of the most important diagnostic tests for evaporative dry eye.
• Fluorescein corneal staining: the fluorescein dye used for TBUT also highlights areas where the corneal surface cells have been damaged or lost. The doctor grades the pattern of staining to determine the severity of surface damage.
• Lissamine green conjunctival staining: a second dye that highlights devitalized or dead cells on the conjunctival surface. It reflects goblet cell loss and helps assess the extent and severity of dry eye disease across the entire ocular surface.
• Tear osmolarity measurement: A small sample of tears is analyzed for salt concentration using a device called the TearLab® Osmolarity System. A reading above 308 mOsm/L is abnormal. High variability between the two eyes can also be a diagnostic marker, even when average values are not dramatically elevated.
• MMP-9 point-of-care test (InflammaDry®): A rapid in-office test that detects elevated levels of the inflammatory enzyme matrix metalloproteinase-9 in the tear film. A positive result confirms the presence of surface inflammation and helps identify candidates for anti-inflammatory therapy.

• Schirmer test: A standardized paper strip placed inside the lower eyelid measures how much tear fluid the eye produces over five minutes. Wetting of less than 5 millimeters is considered abnormal and suggests insufficient tear production (aqueous-deficient dry eye).
• Phenol red thread test: a shorter, less irritating alternative to the Schirmer test that measures tear production using a cotton thread treated with a pH-sensitive dye. It is sometimes preferred for patients who find the Schirmer test uncomfortable.

• Meibomian gland expression: The doctor gently presses on the eyelid margin and grades the quality and ease of oil expression from the glands. In meibomian gland dysfunction, the oil may be thick, cloudy, or absent.
• Meibography: Infrared imaging of the eyelids captures the structure of the meibomian glands. This can reveal gland dropout (permanent loss of functional gland tissue), which is a marker of severity and helps predict prognosis and treatment response.

• Impression cytology: A filter paper sample is gently pressed onto the conjunctival surface to collect cells. Laboratory examination of these cells can confirm goblet cell loss and assess the degree of conjunctival surface damage.
• Nerve mapping with in vivo confocal microscopy: In patients with suspected neuropathic dry eye or reduced corneal sensation, this cellular-level imaging technique can visualize corneal nerve density and architecture. Nerve loss or abnormal nerve morphology can explain why some patients experience symptoms disproportionate to their clinical signs.
• Blood tests: In patients with suspected Sjögren’s syndrome or another systemic autoimmune cause, the doctor may order blood tests including anti-Ro (SSA) and anti-La (SSB) antibodies, antinuclear antibody (ANA) testing, and rheumatoid factor. A referral to a rheumatologist may follow.

There is currently no cure for dry eye disease, but it can be managed effectively. The goal of treatment is to restore as much tear film stability as possible, reduce inflammation on the ocular surface, relieve symptoms, and prevent further damage to the cornea and conjunctiva. Treatment is tailored to the type and severity of dry eye and often follows a stepwise approach—starting with simpler therapies and advancing to more intensive treatments if initial options are not enough. Your doctor will work with you to build a treatment plan that fits your specific situation.

Over-the-counter artificial tears are the first-line treatment for mild-to-moderate dry eye disease. They supplement the natural tear film, reduce friction on the ocular surface, and temporarily dilute the inflammatory proteins that accumulate in dry eye tears. Artificial tears come in drops, gels, and ointments. Drops are used during the day; thicker gels and ointments are better suited for overnight use because they blur vision temporarily

If you use artificial tears four or more times per day, choose a preservative-free formulation. Preservatives in multi-use bottles, particularly benzalkonium chloride, can accumulate on the ocular surface with frequent use and worsen inflammation. Single-use preservative-free vials are available in most pharmacies. Thicker, gel-based drops provide longer contact time on the eye and are preferred by patients whose symptoms are not controlled by standard drops.

For patients with moderate-to-severe dry eye, or those whose symptoms do not improve with lubricating drops alone, prescription medicines that reduce ocular surface inflammation are the cornerstone of long-term management.

• Restasis® (cyclosporine ophthalmic emulsion 0.05%): U.S. Food and Drug Administration (FDA)-approved in 2002. Cyclosporine is an immunosuppressive medicine that reduces the T-cell-driven inflammation that damages tear-producing cells and goblet cells on the ocular surface. Used twice daily. It may take three to six months of regular use before the full benefit is apparent.
• Cequa® (cyclosporine ophthalmic solution 0.09%): FDA-approved in 2018. A higher-concentration cyclosporine formulation using a nanomicellar (nanoscale particle) delivery technology that allows for better penetration into the ocular surface tissues. Used twice daily.
• Xiidra® (lifitegrast ophthalmic solution 5%): FDA-approved in 2016. Lifitegrast works differently from cyclosporine. It blocks a specific interaction between proteins on immune cells (LFA-1 and ICAM-1) that drives T-cell activation on the ocular surface. Some patients notice improvement in symptoms within two weeks, though full benefit may take three months. Used twice daily.
• Eysuvis® (loteprednol etabonate ophthalmic suspension 0.25%): A short-term topical corticosteroid (steroid) eye drop approved by the FDA in 2020 specifically for the short-term treatment of dry eye disease flares. It is designed to reduce inflammation rapidly with a lower risk of the side effects associated with longer-term steroid use, such as elevated eye pressure and cataract formation. Used four times daily for up to two weeks.

• Tyrvaya® (varenicline tartrate nasal spray 0.03 mg): FDA-approved in 2021. This is a nasal spray rather than an eye drop. It stimulates a parasympathetic nerve pathway—the trigeminal parasympathetic pathway—that tells all three layers of the tear glands to produce tears simultaneously. Two sprays (one in each nostril) twice daily. The most common side effect is sneezing at the time of administration.

• Miebo® (perfluorohexyloctane ophthalmic solution): FDA-approved in 2023. This is the first and only prescription treatment specifically approved to target evaporative dry eye. Unlike anti-inflammatory drops, Miebo® works by forming a thin, stable monolayer (a single molecular layer) on the outer surface of the tear film that physically slows evaporation. It does not treat inflammation directly. Used four times daily.

• Oxervate® (cenegermin-bkbj ophthalmic solution 0.002%): FDA-approved in 2018 for neurotrophic keratitis, the most severe form of dry eye caused by nerve damage. It is a laboratory-made version of human nerve growth factor (NGF), a protein that promotes the growth and repair of corneal nerves and surface cells. Applied six times per day for eight weeks. It is used in cases where the cornea has persistent non-healing wounds and surface breakdown.

For patients who do not respond well to drops alone or who have significant meibomian gland dysfunction, several in-office treatments are available.

• Punctal plugs: Small plugs made of silicone or collagen are inserted into the tiny drainage openings (puncta) at the inner corner of each eyelid. By partially blocking tear drainage, the plugs help keep more of the patient’s own tears on the eye’s surface. They are quick to insert, generally comfortable, and can be removed if needed. Used for moderate-to-severe aqueous-deficient dry eye.
• Thermal pulsation therapy (LipiFlow®): A device applies controlled heat to the inner surface of the eyelids while simultaneously applying gentle pressure to unclog blocked meibomian glands. A single treatment session lasts about 12 minutes per eye and can improve meibomian gland function for months to years in some patients.
• Intense pulsed light (IPL) therapy: Originally developed for skin conditions, IPL uses pulses of broad-spectrum light applied to the skin around the eyes. It reduces abnormal blood vessels that release inflammatory proteins near the eyelid margins and improves meibomian gland function. A series of treatments is typically needed. Best evidence is for patients with dry eye related to rosacea.
• Meibomian gland probing: A fine probe is used to physically open blocked meibomian glands in patients with severe gland obstruction. Usually performed under topical anesthesia in the office.
• Autologous serum eye drops: eye drops prepared from the patient’s own blood serum (the liquid part of blood after cells are removed). Serum contains growth factors, vitamins, and immunoglobulins that closely match the natural components of tears. Used for severe dry eye and non-healing corneal surface wounds that have not responded to standard treatments. Requires regular blood draws to prepare new batches.

For patients with severe dry eye that has not been controlled by other treatments, scleral contact lenses can be transformative. These are large-diameter, rigid gas-permeable lenses that vault completely over the cornea and rest on the white part of the eye (the sclera). The space between the lens and the cornea is filled with preservative-free saline solution, creating a continuous fluid reservoir that bathes the eye all day. Scleral lenses protect the corneal surface from exposure to air and eyelid friction while keeping the surface continuously hydrated. They require fitting by a specialist and take some time to adapt to, but they can restore comfortable, functional vision in patients for whom all other treatments have been insufficient.

Lifestyle changes are an important part of any dry eye treatment plan, regardless of severity. These modifications do not replace medical treatment but can significantly reduce symptom burden and slow progression.

• Apply warm compresses daily: Warming the eyelids for five to ten minutes softens the oil in the meibomian glands and helps it flow more easily onto the tear film. Gentle eyelid massage after warming can further improve oil expression.
• Follow the 20-20-20 rule: Every 20 minutes of screen use, look at an object 20 feet away for 20 seconds. This helps restore blink rate.
• Use a humidifier: Maintaining indoor humidity between 40 and 60% reduces the rate of tear evaporation significantly.
• Position screens below eye level: Viewing a screen that is positioned below eye level reduces the area of the cornea exposed between blinks.
• Stay hydrated: Adequate fluid intake supports overall tear film production.
• Consider dietary omega-3 fatty acids: Some evidence suggests that omega-3 supplements may have a mild anti-inflammatory effect that benefits the meibomian glands and tear film. The National Institutes of Health (NIH)-funded DREAM study found mixed results overall, but many eye doctors continue to recommend them as a safe adjunct. Talk to your doctor before starting any supplement.

• Blepharitis and lid hygiene: If blepharitis (chronic eyelid inflammation) is contributing to dry eye, treating the eyelids directly is essential. This involves regular lid cleaning with gentle wipes or baby shampoo diluted in warm water, in addition to warm compresses. Antibiotic ointments applied to the lid margins or short courses of oral antibiotics (such as doxycycline) may be prescribed for significant bacterial blepharitis.
• Sjögren’s syndrome and systemic autoimmune disease: Patients with Sjögren’s syndrome should be co-managed by an ophthalmologist and a rheumatologist. Systemic treatments for the underlying autoimmune disease—including hydroxychloroquine and biologics—may indirectly benefit ocular surface health.
• Allergy management: Treating allergic conjunctivitis with non-sedating antihistamine eye drops (rather than oral antihistamines, which dry the eyes) and mast cell stabilizers can reduce the conjunctival inflammation that contributes to goblet cell loss.
• Medication review: If a medication is identified as contributing to dry eye, your doctor may consider switching to an alternative. Never stop a prescribed medicine without discussing it with your prescribing doctor first.
• Corneal damage management: In patients with moderate-to-severe corneal staining or surface erosions, more intensive treatment to protect and heal the cornea is prioritized. Bandage contact lenses and amniotic membrane grafts may be used in severe cases.

Dry eye disease is a chronic condition that requires ongoing attention, but the large majority of people who have it can find a combination of treatments that brings their symptoms under control and lets them live full, active lives. Some people manage well with a daily routine of lubricating drops and good lid hygiene. Others—particularly those with moderate-to-severe disease or an underlying autoimmune condition—need prescription medicines and closer monitoring. The most important things you can do are stay consistent with your treatment plan, keep your scheduled eye appointments even when your symptoms feel stable, and tell your doctor promptly if your symptoms worsen or change. Dry eye disease can evolve over time, and your treatment plan may need to evolve with it. With the right care, most people with dry eye disease are able to work, use screens, wear contact lenses (if appropriate), drive, and do the things they value most.

To further your understanding of your diagnosis and to contribute to cutting-edge research, consider participating in a clinical trial so clinicians and scientists can learn more about causes, symptoms, treatment, and prevention of dry eye disease and related disorders. Clinical research uses human volunteers to help researchers learn more about a disorder and perhaps find better ways to safely detect, treat, or prevent disease.

All types of volunteers are needed—those who are healthy or may have an illness or disease—of all different ages, sexes, races, and ethnicities to ensure that study results apply to as many people as possible, and that treatments will be safe and effective for everyone who will use them.

To learn more about clinical trials and find studies that may be right for you, visit NIH Clinical Research Trials and You at www.nih.gov/health-information/nih-clinical-research-trials-you and ClinicalTrials.gov at www.clinicaltrials.gov to search active studies by condition, location, and age group.