Dry Eye Disease (DED), also known as Keratoconjunctivitis Sicca, is a common and often chronic condition characterized by insufficient tear production or excessive tear evaporation. This leads to inadequate lubrication and moisture on the surface of the eye. The resulting ocular surface inflammation and damage can cause significant discomfort, visual disturbances, and a negative impact on quality of life.
DED affects millions worldwide and is particularly prevalent among older adults, contact lens users, and individuals with certain systemic conditions such as autoimmune diseases. Environmental factors, digital screen use, and some medications can also contribute to the onset and severity of symptoms.
Understanding the underlying mechanisms whether aqueous-deficient, evaporative, or mixed is essential for accurate diagnosis and tailored treatment. Left untreated, dry eye can lead to complications including corneal injury and increased risk of eye infections.
Epidemiology
Dry eye disease (DED) is a highly prevalent condition in the United States, particularly among individuals over the age of 50. Estimates suggest that between 5% and 50% of the population may be affected. Approximately 3.23 million women and 1.68 million men aged 50 and older are estimated to have DED. In recent years, prevalence has also been rising among young adults aged 18-34, largely due to increased use of soft contact lenses and prolonged exposure to digital screens such as smartphones and computers.
DED is one of the most frequent reasons patients seek eye care. Its widespread impact has led to a substantial socioeconomic burden on the U.S. healthcare system. Factors contributing to this burden include lost productivity due to missed workdays, increasing treatment costs, and the social and emotional challenges faced by those living with chronic dry eye symptoms.
Anatomy
Pathophysiology
Dry Eye Disease (DED), or Keratoconjunctivitis Sicca, is a multifactorial disorder involving tear film instability and ocular surface inflammation. It is broadly classified into two main types: aqueous tear-deficient and evaporative dry eye. In aqueous-deficient DED, the lacrimal glands produce an insufficient volume of tears, often due to age-related decline, systemic medications, or autoimmune conditions such as Sjögren’s syndrome, where immune-mediated damage reduces tear secretion. In evaporative DED, tear production may be normal, but excessive evaporation primarily caused by meibomian gland dysfunction (MGD) compromises tear film stability. Other contributors to evaporative dry eye include environmental factors like low humidity, as well as behavioral habits such as reduced blinking during extended screen use.
Despite differing initial causes, both types share a common pathophysiological cascade. Tear film instability and hyperosmolarity lead to damage of the corneal and conjunctival epithelium, which in turn triggers an inflammatory response. Inflammatory mediators such as cytokines and matrix metalloproteinases further disrupt the lacrimal and meibomian glands, perpetuating a vicious cycle of inflammation and ocular surface damage. Additionally, neurosensory abnormalities, including reduced corneal sensitivity, may impair reflex tearing and blinking, compounding the issue. Over time, these changes compromise the protective and lubricating functions of the tear film, resulting in chronic symptoms and ocular surface disease.
Etiology
Dry Eye Disease (DED) arises from a variety of factors that disrupt the quantity or quality of the tear film. The etiology is typically divided into two primary categories: aqueous tear-deficient and evaporative dry eye, though many patients exhibit a combination of both.
Aqueous tear-deficient dry eye occurs when the lacrimal glands fail to produce sufficient tears. This can result from aging, which naturally reduces tear production, or from autoimmune conditions such as Sjögren’s syndrome, in which immune-mediated damage to the lacrimal glands leads to chronic dryness. Other causes include systemic diseases like rheumatoid arthritis, sarcoidosis, and diabetes mellitus, as well as the use of medications that reduce tear production, such as antihistamines, antidepressants, diuretics, and beta-blockers.
Evaporative dry eye, on the other hand, is primarily caused by meibomian gland dysfunction (MGD), which impairs the lipid layer of the tear film, resulting in increased evaporation. Other contributing factors include long-term contact lens wear, prolonged digital screen use, and environmental conditions such as wind, low humidity, or air conditioning. Incomplete blinking, often associated with screen time, can further exacerbate tear evaporation.
Additional etiologic factors include ocular surface diseases like allergic conjunctivitis, eyelid disorders such as lagophthalmos or blepharitis, hormonal changes (especially in postmenopausal women), and ocular surgeries like LASIK, which can affect corneal nerves and reduce tear reflexes. Ultimately, DED results from a complex interplay of intrinsic and extrinsic factors that compromise tear film stability and ocular surface integrity.
Genetics
Prognostic Factors
The prognosis of Dry Eye Disease (DED) depends on the underlying cause, severity, and individual patient factors. Chronic or severe cases, especially those linked to autoimmune conditions like Sjögren’s syndrome, tend to be more treatment-resistant and carry a higher risk of ocular surface damage. Patient adherence to treatment and avoidance of environmental triggers are crucial for symptom control. Prognosis is generally worse in the presence of meibomian gland dysfunction (MGD), older age, female sex, or neuropathic ocular pain. Early diagnosis and a personalized treatment approach improve long-term outcomes.
Clinical History
Age group
Dry Eye Disease (DED) affects a broad range of age groups but is most prevalent in individuals over the age of 50. Aging naturally leads to decreased tear production and meibomian gland function, making older adults more susceptible. Women, particularly postmenopausal, are disproportionately affected due to hormonal changes. However, DED is increasingly seen in younger populations (ages 18-34), largely driven by environmental factors and lifestyle habits such as prolonged digital screen use and contact lens wear.
Dry Eye Disease (DED) is linked to systemic conditions like Sjögren’s syndrome, rheumatoid arthritis, lupus, and diabetes mellitus, as well as ocular disorders such as blepharitis, meibomian gland dysfunction (MGD), and allergic conjunctivitis. Activities like prolonged screen time, contact lens wear, and exposure to dry environments can worsen symptoms. DED may also be triggered or aggravated by ocular surgeries (e.g., LASIK) and medications like antihistamines, antidepressants, and diuretics.
Physical Examination
In patients with Dry Eye Disease (DED), physical examination focuses on the ocular surface and tear film assessment. Key findings may include conjunctival redness, especially in the interpalpebral zone, and decreased tear meniscus height at the lower eyelid margin. The cornea may show punctate epithelial erosions or staining with fluorescein or lissamine green dye, indicating epithelial damage.
Eyelid examination often reveals signs of meibomian gland dysfunction (MGD) such as thickened, inflamed eyelid margins, capped orifices, and abnormal meibum quality. Blink rate and completeness should be assessed, as incomplete blinking can worsen tear evaporation. Tear film stability can be evaluated using the tear break-up time (TBUT) test, with a reduced TBUT suggesting increased tear evaporation.
Additional tests like the Schirmer test measure aqueous tear production and help differentiate between aqueous-deficient and evaporative dry eye. The presence of debris, mucus, or signs of inflammation on the ocular surface should also be noted. A thorough physical exam guides diagnosis and helps tailor appropriate management.
Age group
Associated comorbidity
Dry Eye Disease (DED) is linked to systemic conditions like Sjögren’s syndrome, rheumatoid arthritis, lupus, and diabetes mellitus, as well as ocular disorders such as blepharitis, meibomian gland dysfunction (MGD), and allergic conjunctivitis. Activities like prolonged screen time, contact lens wear, and exposure to dry environments can worsen symptoms. DED may also be triggered or aggravated by ocular surgeries (e.g., LASIK) and medications like antihistamines, antidepressants, and diuretics.
Associated activity
Acuity of presentation
Dry Eye Disease (DED) typically presents with a chronic, gradual onset of symptoms, although acute exacerbations can occur, especially with environmental exposure or contact lens use. Most patients experience intermittent or persistent irritation, dryness, redness, and blurred vision that worsen throughout the day. While symptoms often develop slowly over weeks to months, some cases such as those related to medication changes or sudden gland dysfunction may present more abruptly. Acute presentations may mimic other ocular surface conditions and require prompt evaluation to rule out infections or inflammation.
Differential Diagnoses
Several ocular conditions can mimic or coexist with Dry Eye Disease, making accurate diagnosis essential. Common differential diagnoses include allergic conjunctivitis, which presents with itching and redness but typically lacks tear film instability; blepharitis, characterized by eyelid inflammation and crusting; infectious conjunctivitis, which often involves discharge and discomfort; and ocular rosacea, associated with chronic eyelid and skin inflammation. Other conditions such as ocular surface inflammation from exposure keratopathy, contact lens-related irritation, and corneal neuropathic pain may present with similar symptoms. Systemic diseases like thyroid eye disease and autoimmune disorders can also cause ocular surface symptoms resembling dry eye. Careful clinical evaluation and appropriate testing help distinguish DED from these conditions.
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
The management of Dry Eye Disease (DED) follows a stepwise approach tailored to disease severity and underlying causes. Initial treatment focuses on environmental modifications and patient education, including avoiding dry or windy conditions, reducing screen time, and increasing humidity.
First-line therapies typically include lubricating artificial tears to restore tear film moisture and comfort. For patients with meibomian gland dysfunction (MGD), warm compresses and eyelid hygiene are essential to improve lipid secretion and reduce evaporation.
If symptoms persist or inflammation is evident, anti-inflammatory treatments such as topical cyclosporine or lifitegrast may be prescribed. Short-term use of topical corticosteroids can help during acute exacerbations. In cases of significant aqueous deficiency, punctal plugs may be considered to reduce tear drainage.
Advanced therapies include autologous serum eye drops and secretagogues for severe or refractory cases. Management also involves treating associated eyelid disorders and reviewing medications that may contribute to dryness.
Regular follow-up is important to monitor response and adjust treatment, aiming to break the vicious cycle of inflammation and ocular surface damage.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
role-of-environment-in-treating-dry-eye-disease
Environmental modifications are a crucial first step in managing Dry Eye Disease (DED). Patients are advised to avoid exposure to dry, windy, or smoky conditions that can increase tear evaporation. Using humidifiers in dry indoor environments helps maintain adequate moisture levels. During activities involving prolonged screen time or reading, frequent breaks and conscious blinking can reduce ocular surface dryness. Wearing protective eyewear such as wraparound glasses or moisture chamber goggles can shield the eyes from environmental irritants. Additionally, minimizing exposure to air conditioning and heating vents helps prevent excessive tear film evaporation. These simple lifestyle adjustments can significantly reduce symptoms and complement other therapeutic measures.
Role of Ophthalmic lubricants in treating dry eye disease
Artificial tears
Artificial tears (such as Advanced Eye Relief, Bion Tears, Hypo Tears, Murine Tears, and Tears Naturale II) are commonly used to increase eye lubrication and provide symptomatic relief in dry eye disease.
Hydroxypropyl cellulose (Lacrisert)
Hydroxypropyl cellulose (marketed as Lacrisert) works by stabilizing and thickening the tear film on the eye’s surface, helping to extend the tear breakup time (TBUT). It is administered as a small insert placed once or twice daily in the lower eyelid’s conjunctival sac, reducing the need for frequent use of traditional artificial tear drops.
Effectiveness of mucolytic agents in treating dry eye disease
Acetylcysteine
Mucolytic agents like acetylcysteine work by breaking down mucoproteins, which reduces the thickness and stickiness of mucus. These agents are particularly helpful in cases where there is excessive mucus discharge or the formation of mucus plaques on the ocular surface.
Cyclosporine Ophthalmic (Restasis, Cequa, Vevye)
Cyclosporine functions as an immunomodulatory agent, although its precise mechanism is not fully understood. It primarily works by suppressing T-cell activity and inhibiting the enzyme calcineurin. Importantly, the use of cyclosporine eye drops has not been linked to an increased risk of ocular or systemic infections.
role-of-management-in-treating-dry-eye-disease
The management of Dry Eye Disease (DED) typically progresses through several phases based on severity and treatment response. The initial phase focuses on patient education and environmental modifications, along with the use of artificial tears and lubricants to alleviate mild symptoms and restore tear film stability. In the second phase, if symptoms persist or inflammation is present, anti-inflammatory therapies such as topical cyclosporine or lifitegrast are introduced, alongside measures to improve meibomian gland function like warm compresses and eyelid hygiene.
For patients with moderate to severe disease, the third phase may involve more advanced interventions such as punctal occlusion to conserve tears, autologous serum eye drops, or secretagogues to stimulate tear production. In refractory cases, additional therapies including therapeutic contact lenses or systemic immunomodulators may be considered. Throughout all phases, regular follow-up and reassessment are essential to tailor treatment, monitor effectiveness, and prevent progression.
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Home » CAD » Dry Eye Disease (Keratoconjunctivitis Sicca)
Dry Eye Disease (Keratoconjunctivitis Sicca)
Updated :
December 15, 2025
Dry Eye Disease (DED), also known as Keratoconjunctivitis Sicca, is a common and often chronic condition characterized by insufficient tear production or excessive tear evaporation. This leads to inadequate lubrication and moisture on the surface of the eye. The resulting ocular surface inflammation and damage can cause significant discomfort, visual disturbances, and a negative impact on quality of life.
DED affects millions worldwide and is particularly prevalent among older adults, contact lens users, and individuals with certain systemic conditions such as autoimmune diseases. Environmental factors, digital screen use, and some medications can also contribute to the onset and severity of symptoms.
Understanding the underlying mechanisms whether aqueous-deficient, evaporative, or mixed is essential for accurate diagnosis and tailored treatment. Left untreated, dry eye can lead to complications including corneal injury and increased risk of eye infections.
Dry eye disease (DED) is a highly prevalent condition in the United States, particularly among individuals over the age of 50. Estimates suggest that between 5% and 50% of the population may be affected. Approximately 3.23 million women and 1.68 million men aged 50 and older are estimated to have DED. In recent years, prevalence has also been rising among young adults aged 18-34, largely due to increased use of soft contact lenses and prolonged exposure to digital screens such as smartphones and computers.
DED is one of the most frequent reasons patients seek eye care. Its widespread impact has led to a substantial socioeconomic burden on the U.S. healthcare system. Factors contributing to this burden include lost productivity due to missed workdays, increasing treatment costs, and the social and emotional challenges faced by those living with chronic dry eye symptoms.
Dry Eye Disease (DED), or Keratoconjunctivitis Sicca, is a multifactorial disorder involving tear film instability and ocular surface inflammation. It is broadly classified into two main types: aqueous tear-deficient and evaporative dry eye. In aqueous-deficient DED, the lacrimal glands produce an insufficient volume of tears, often due to age-related decline, systemic medications, or autoimmune conditions such as Sjögren’s syndrome, where immune-mediated damage reduces tear secretion. In evaporative DED, tear production may be normal, but excessive evaporation primarily caused by meibomian gland dysfunction (MGD) compromises tear film stability. Other contributors to evaporative dry eye include environmental factors like low humidity, as well as behavioral habits such as reduced blinking during extended screen use.
Despite differing initial causes, both types share a common pathophysiological cascade. Tear film instability and hyperosmolarity lead to damage of the corneal and conjunctival epithelium, which in turn triggers an inflammatory response. Inflammatory mediators such as cytokines and matrix metalloproteinases further disrupt the lacrimal and meibomian glands, perpetuating a vicious cycle of inflammation and ocular surface damage. Additionally, neurosensory abnormalities, including reduced corneal sensitivity, may impair reflex tearing and blinking, compounding the issue. Over time, these changes compromise the protective and lubricating functions of the tear film, resulting in chronic symptoms and ocular surface disease.
Dry Eye Disease (DED) arises from a variety of factors that disrupt the quantity or quality of the tear film. The etiology is typically divided into two primary categories: aqueous tear-deficient and evaporative dry eye, though many patients exhibit a combination of both.
Aqueous tear-deficient dry eye occurs when the lacrimal glands fail to produce sufficient tears. This can result from aging, which naturally reduces tear production, or from autoimmune conditions such as Sjögren’s syndrome, in which immune-mediated damage to the lacrimal glands leads to chronic dryness. Other causes include systemic diseases like rheumatoid arthritis, sarcoidosis, and diabetes mellitus, as well as the use of medications that reduce tear production, such as antihistamines, antidepressants, diuretics, and beta-blockers.
Evaporative dry eye, on the other hand, is primarily caused by meibomian gland dysfunction (MGD), which impairs the lipid layer of the tear film, resulting in increased evaporation. Other contributing factors include long-term contact lens wear, prolonged digital screen use, and environmental conditions such as wind, low humidity, or air conditioning. Incomplete blinking, often associated with screen time, can further exacerbate tear evaporation.
Additional etiologic factors include ocular surface diseases like allergic conjunctivitis, eyelid disorders such as lagophthalmos or blepharitis, hormonal changes (especially in postmenopausal women), and ocular surgeries like LASIK, which can affect corneal nerves and reduce tear reflexes. Ultimately, DED results from a complex interplay of intrinsic and extrinsic factors that compromise tear film stability and ocular surface integrity.
The prognosis of Dry Eye Disease (DED) depends on the underlying cause, severity, and individual patient factors. Chronic or severe cases, especially those linked to autoimmune conditions like Sjögren’s syndrome, tend to be more treatment-resistant and carry a higher risk of ocular surface damage. Patient adherence to treatment and avoidance of environmental triggers are crucial for symptom control. Prognosis is generally worse in the presence of meibomian gland dysfunction (MGD), older age, female sex, or neuropathic ocular pain. Early diagnosis and a personalized treatment approach improve long-term outcomes.
Age group
Dry Eye Disease (DED) affects a broad range of age groups but is most prevalent in individuals over the age of 50. Aging naturally leads to decreased tear production and meibomian gland function, making older adults more susceptible. Women, particularly postmenopausal, are disproportionately affected due to hormonal changes. However, DED is increasingly seen in younger populations (ages 18-34), largely driven by environmental factors and lifestyle habits such as prolonged digital screen use and contact lens wear.
Dry Eye Disease (DED) is linked to systemic conditions like Sjögren’s syndrome, rheumatoid arthritis, lupus, and diabetes mellitus, as well as ocular disorders such as blepharitis, meibomian gland dysfunction (MGD), and allergic conjunctivitis. Activities like prolonged screen time, contact lens wear, and exposure to dry environments can worsen symptoms. DED may also be triggered or aggravated by ocular surgeries (e.g., LASIK) and medications like antihistamines, antidepressants, and diuretics.
In patients with Dry Eye Disease (DED), physical examination focuses on the ocular surface and tear film assessment. Key findings may include conjunctival redness, especially in the interpalpebral zone, and decreased tear meniscus height at the lower eyelid margin. The cornea may show punctate epithelial erosions or staining with fluorescein or lissamine green dye, indicating epithelial damage.
Eyelid examination often reveals signs of meibomian gland dysfunction (MGD) such as thickened, inflamed eyelid margins, capped orifices, and abnormal meibum quality. Blink rate and completeness should be assessed, as incomplete blinking can worsen tear evaporation. Tear film stability can be evaluated using the tear break-up time (TBUT) test, with a reduced TBUT suggesting increased tear evaporation.
Additional tests like the Schirmer test measure aqueous tear production and help differentiate between aqueous-deficient and evaporative dry eye. The presence of debris, mucus, or signs of inflammation on the ocular surface should also be noted. A thorough physical exam guides diagnosis and helps tailor appropriate management.
Dry Eye Disease (DED) is linked to systemic conditions like Sjögren’s syndrome, rheumatoid arthritis, lupus, and diabetes mellitus, as well as ocular disorders such as blepharitis, meibomian gland dysfunction (MGD), and allergic conjunctivitis. Activities like prolonged screen time, contact lens wear, and exposure to dry environments can worsen symptoms. DED may also be triggered or aggravated by ocular surgeries (e.g., LASIK) and medications like antihistamines, antidepressants, and diuretics.
Dry Eye Disease (DED) typically presents with a chronic, gradual onset of symptoms, although acute exacerbations can occur, especially with environmental exposure or contact lens use. Most patients experience intermittent or persistent irritation, dryness, redness, and blurred vision that worsen throughout the day. While symptoms often develop slowly over weeks to months, some cases such as those related to medication changes or sudden gland dysfunction may present more abruptly. Acute presentations may mimic other ocular surface conditions and require prompt evaluation to rule out infections or inflammation.
Several ocular conditions can mimic or coexist with Dry Eye Disease, making accurate diagnosis essential. Common differential diagnoses include allergic conjunctivitis, which presents with itching and redness but typically lacks tear film instability; blepharitis, characterized by eyelid inflammation and crusting; infectious conjunctivitis, which often involves discharge and discomfort; and ocular rosacea, associated with chronic eyelid and skin inflammation. Other conditions such as ocular surface inflammation from exposure keratopathy, contact lens-related irritation, and corneal neuropathic pain may present with similar symptoms. Systemic diseases like thyroid eye disease and autoimmune disorders can also cause ocular surface symptoms resembling dry eye. Careful clinical evaluation and appropriate testing help distinguish DED from these conditions.
The management of Dry Eye Disease (DED) follows a stepwise approach tailored to disease severity and underlying causes. Initial treatment focuses on environmental modifications and patient education, including avoiding dry or windy conditions, reducing screen time, and increasing humidity.
First-line therapies typically include lubricating artificial tears to restore tear film moisture and comfort. For patients with meibomian gland dysfunction (MGD), warm compresses and eyelid hygiene are essential to improve lipid secretion and reduce evaporation.
If symptoms persist or inflammation is evident, anti-inflammatory treatments such as topical cyclosporine or lifitegrast may be prescribed. Short-term use of topical corticosteroids can help during acute exacerbations. In cases of significant aqueous deficiency, punctal plugs may be considered to reduce tear drainage.
Advanced therapies include autologous serum eye drops and secretagogues for severe or refractory cases. Management also involves treating associated eyelid disorders and reviewing medications that may contribute to dryness.
Regular follow-up is important to monitor response and adjust treatment, aiming to break the vicious cycle of inflammation and ocular surface damage.
Ophthalmology
Environmental modifications are a crucial first step in managing Dry Eye Disease (DED). Patients are advised to avoid exposure to dry, windy, or smoky conditions that can increase tear evaporation. Using humidifiers in dry indoor environments helps maintain adequate moisture levels. During activities involving prolonged screen time or reading, frequent breaks and conscious blinking can reduce ocular surface dryness. Wearing protective eyewear such as wraparound glasses or moisture chamber goggles can shield the eyes from environmental irritants. Additionally, minimizing exposure to air conditioning and heating vents helps prevent excessive tear film evaporation. These simple lifestyle adjustments can significantly reduce symptoms and complement other therapeutic measures.
Ophthalmology
Artificial tears
Artificial tears (such as Advanced Eye Relief, Bion Tears, Hypo Tears, Murine Tears, and Tears Naturale II) are commonly used to increase eye lubrication and provide symptomatic relief in dry eye disease.
Hydroxypropyl cellulose (Lacrisert)
Hydroxypropyl cellulose (marketed as Lacrisert) works by stabilizing and thickening the tear film on the eye’s surface, helping to extend the tear breakup time (TBUT). It is administered as a small insert placed once or twice daily in the lower eyelid’s conjunctival sac, reducing the need for frequent use of traditional artificial tear drops.
Ophthalmology
Acetylcysteine
Mucolytic agents like acetylcysteine work by breaking down mucoproteins, which reduces the thickness and stickiness of mucus. These agents are particularly helpful in cases where there is excessive mucus discharge or the formation of mucus plaques on the ocular surface.
Ophthalmology
Cyclosporine Ophthalmic (Restasis, Cequa, Vevye)
Cyclosporine functions as an immunomodulatory agent, although its precise mechanism is not fully understood. It primarily works by suppressing T-cell activity and inhibiting the enzyme calcineurin. Importantly, the use of cyclosporine eye drops has not been linked to an increased risk of ocular or systemic infections.
Ophthalmology
The management of Dry Eye Disease (DED) typically progresses through several phases based on severity and treatment response. The initial phase focuses on patient education and environmental modifications, along with the use of artificial tears and lubricants to alleviate mild symptoms and restore tear film stability. In the second phase, if symptoms persist or inflammation is present, anti-inflammatory therapies such as topical cyclosporine or lifitegrast are introduced, alongside measures to improve meibomian gland function like warm compresses and eyelid hygiene.
For patients with moderate to severe disease, the third phase may involve more advanced interventions such as punctal occlusion to conserve tears, autologous serum eye drops, or secretagogues to stimulate tear production. In refractory cases, additional therapies including therapeutic contact lenses or systemic immunomodulators may be considered. Throughout all phases, regular follow-up and reassessment are essential to tailor treatment, monitor effectiveness, and prevent progression.
Dry Eye Disease (DED), also known as Keratoconjunctivitis Sicca, is a common and often chronic condition characterized by insufficient tear production or excessive tear evaporation. This leads to inadequate lubrication and moisture on the surface of the eye. The resulting ocular surface inflammation and damage can cause significant discomfort, visual disturbances, and a negative impact on quality of life.
DED affects millions worldwide and is particularly prevalent among older adults, contact lens users, and individuals with certain systemic conditions such as autoimmune diseases. Environmental factors, digital screen use, and some medications can also contribute to the onset and severity of symptoms.
Understanding the underlying mechanisms whether aqueous-deficient, evaporative, or mixed is essential for accurate diagnosis and tailored treatment. Left untreated, dry eye can lead to complications including corneal injury and increased risk of eye infections.
Dry eye disease (DED) is a highly prevalent condition in the United States, particularly among individuals over the age of 50. Estimates suggest that between 5% and 50% of the population may be affected. Approximately 3.23 million women and 1.68 million men aged 50 and older are estimated to have DED. In recent years, prevalence has also been rising among young adults aged 18-34, largely due to increased use of soft contact lenses and prolonged exposure to digital screens such as smartphones and computers.
DED is one of the most frequent reasons patients seek eye care. Its widespread impact has led to a substantial socioeconomic burden on the U.S. healthcare system. Factors contributing to this burden include lost productivity due to missed workdays, increasing treatment costs, and the social and emotional challenges faced by those living with chronic dry eye symptoms.
Dry Eye Disease (DED), or Keratoconjunctivitis Sicca, is a multifactorial disorder involving tear film instability and ocular surface inflammation. It is broadly classified into two main types: aqueous tear-deficient and evaporative dry eye. In aqueous-deficient DED, the lacrimal glands produce an insufficient volume of tears, often due to age-related decline, systemic medications, or autoimmune conditions such as Sjögren’s syndrome, where immune-mediated damage reduces tear secretion. In evaporative DED, tear production may be normal, but excessive evaporation primarily caused by meibomian gland dysfunction (MGD) compromises tear film stability. Other contributors to evaporative dry eye include environmental factors like low humidity, as well as behavioral habits such as reduced blinking during extended screen use.
Despite differing initial causes, both types share a common pathophysiological cascade. Tear film instability and hyperosmolarity lead to damage of the corneal and conjunctival epithelium, which in turn triggers an inflammatory response. Inflammatory mediators such as cytokines and matrix metalloproteinases further disrupt the lacrimal and meibomian glands, perpetuating a vicious cycle of inflammation and ocular surface damage. Additionally, neurosensory abnormalities, including reduced corneal sensitivity, may impair reflex tearing and blinking, compounding the issue. Over time, these changes compromise the protective and lubricating functions of the tear film, resulting in chronic symptoms and ocular surface disease.
Dry Eye Disease (DED) arises from a variety of factors that disrupt the quantity or quality of the tear film. The etiology is typically divided into two primary categories: aqueous tear-deficient and evaporative dry eye, though many patients exhibit a combination of both.
Aqueous tear-deficient dry eye occurs when the lacrimal glands fail to produce sufficient tears. This can result from aging, which naturally reduces tear production, or from autoimmune conditions such as Sjögren’s syndrome, in which immune-mediated damage to the lacrimal glands leads to chronic dryness. Other causes include systemic diseases like rheumatoid arthritis, sarcoidosis, and diabetes mellitus, as well as the use of medications that reduce tear production, such as antihistamines, antidepressants, diuretics, and beta-blockers.
Evaporative dry eye, on the other hand, is primarily caused by meibomian gland dysfunction (MGD), which impairs the lipid layer of the tear film, resulting in increased evaporation. Other contributing factors include long-term contact lens wear, prolonged digital screen use, and environmental conditions such as wind, low humidity, or air conditioning. Incomplete blinking, often associated with screen time, can further exacerbate tear evaporation.
Additional etiologic factors include ocular surface diseases like allergic conjunctivitis, eyelid disorders such as lagophthalmos or blepharitis, hormonal changes (especially in postmenopausal women), and ocular surgeries like LASIK, which can affect corneal nerves and reduce tear reflexes. Ultimately, DED results from a complex interplay of intrinsic and extrinsic factors that compromise tear film stability and ocular surface integrity.
The prognosis of Dry Eye Disease (DED) depends on the underlying cause, severity, and individual patient factors. Chronic or severe cases, especially those linked to autoimmune conditions like Sjögren’s syndrome, tend to be more treatment-resistant and carry a higher risk of ocular surface damage. Patient adherence to treatment and avoidance of environmental triggers are crucial for symptom control. Prognosis is generally worse in the presence of meibomian gland dysfunction (MGD), older age, female sex, or neuropathic ocular pain. Early diagnosis and a personalized treatment approach improve long-term outcomes.
Age group
Dry Eye Disease (DED) affects a broad range of age groups but is most prevalent in individuals over the age of 50. Aging naturally leads to decreased tear production and meibomian gland function, making older adults more susceptible. Women, particularly postmenopausal, are disproportionately affected due to hormonal changes. However, DED is increasingly seen in younger populations (ages 18-34), largely driven by environmental factors and lifestyle habits such as prolonged digital screen use and contact lens wear.
Dry Eye Disease (DED) is linked to systemic conditions like Sjögren’s syndrome, rheumatoid arthritis, lupus, and diabetes mellitus, as well as ocular disorders such as blepharitis, meibomian gland dysfunction (MGD), and allergic conjunctivitis. Activities like prolonged screen time, contact lens wear, and exposure to dry environments can worsen symptoms. DED may also be triggered or aggravated by ocular surgeries (e.g., LASIK) and medications like antihistamines, antidepressants, and diuretics.
In patients with Dry Eye Disease (DED), physical examination focuses on the ocular surface and tear film assessment. Key findings may include conjunctival redness, especially in the interpalpebral zone, and decreased tear meniscus height at the lower eyelid margin. The cornea may show punctate epithelial erosions or staining with fluorescein or lissamine green dye, indicating epithelial damage.
Eyelid examination often reveals signs of meibomian gland dysfunction (MGD) such as thickened, inflamed eyelid margins, capped orifices, and abnormal meibum quality. Blink rate and completeness should be assessed, as incomplete blinking can worsen tear evaporation. Tear film stability can be evaluated using the tear break-up time (TBUT) test, with a reduced TBUT suggesting increased tear evaporation.
Additional tests like the Schirmer test measure aqueous tear production and help differentiate between aqueous-deficient and evaporative dry eye. The presence of debris, mucus, or signs of inflammation on the ocular surface should also be noted. A thorough physical exam guides diagnosis and helps tailor appropriate management.
Dry Eye Disease (DED) is linked to systemic conditions like Sjögren’s syndrome, rheumatoid arthritis, lupus, and diabetes mellitus, as well as ocular disorders such as blepharitis, meibomian gland dysfunction (MGD), and allergic conjunctivitis. Activities like prolonged screen time, contact lens wear, and exposure to dry environments can worsen symptoms. DED may also be triggered or aggravated by ocular surgeries (e.g., LASIK) and medications like antihistamines, antidepressants, and diuretics.
Dry Eye Disease (DED) typically presents with a chronic, gradual onset of symptoms, although acute exacerbations can occur, especially with environmental exposure or contact lens use. Most patients experience intermittent or persistent irritation, dryness, redness, and blurred vision that worsen throughout the day. While symptoms often develop slowly over weeks to months, some cases such as those related to medication changes or sudden gland dysfunction may present more abruptly. Acute presentations may mimic other ocular surface conditions and require prompt evaluation to rule out infections or inflammation.
Several ocular conditions can mimic or coexist with Dry Eye Disease, making accurate diagnosis essential. Common differential diagnoses include allergic conjunctivitis, which presents with itching and redness but typically lacks tear film instability; blepharitis, characterized by eyelid inflammation and crusting; infectious conjunctivitis, which often involves discharge and discomfort; and ocular rosacea, associated with chronic eyelid and skin inflammation. Other conditions such as ocular surface inflammation from exposure keratopathy, contact lens-related irritation, and corneal neuropathic pain may present with similar symptoms. Systemic diseases like thyroid eye disease and autoimmune disorders can also cause ocular surface symptoms resembling dry eye. Careful clinical evaluation and appropriate testing help distinguish DED from these conditions.
The management of Dry Eye Disease (DED) follows a stepwise approach tailored to disease severity and underlying causes. Initial treatment focuses on environmental modifications and patient education, including avoiding dry or windy conditions, reducing screen time, and increasing humidity.
First-line therapies typically include lubricating artificial tears to restore tear film moisture and comfort. For patients with meibomian gland dysfunction (MGD), warm compresses and eyelid hygiene are essential to improve lipid secretion and reduce evaporation.
If symptoms persist or inflammation is evident, anti-inflammatory treatments such as topical cyclosporine or lifitegrast may be prescribed. Short-term use of topical corticosteroids can help during acute exacerbations. In cases of significant aqueous deficiency, punctal plugs may be considered to reduce tear drainage.
Advanced therapies include autologous serum eye drops and secretagogues for severe or refractory cases. Management also involves treating associated eyelid disorders and reviewing medications that may contribute to dryness.
Regular follow-up is important to monitor response and adjust treatment, aiming to break the vicious cycle of inflammation and ocular surface damage.
Ophthalmology
Environmental modifications are a crucial first step in managing Dry Eye Disease (DED). Patients are advised to avoid exposure to dry, windy, or smoky conditions that can increase tear evaporation. Using humidifiers in dry indoor environments helps maintain adequate moisture levels. During activities involving prolonged screen time or reading, frequent breaks and conscious blinking can reduce ocular surface dryness. Wearing protective eyewear such as wraparound glasses or moisture chamber goggles can shield the eyes from environmental irritants. Additionally, minimizing exposure to air conditioning and heating vents helps prevent excessive tear film evaporation. These simple lifestyle adjustments can significantly reduce symptoms and complement other therapeutic measures.
Ophthalmology
Artificial tears
Artificial tears (such as Advanced Eye Relief, Bion Tears, Hypo Tears, Murine Tears, and Tears Naturale II) are commonly used to increase eye lubrication and provide symptomatic relief in dry eye disease.
Hydroxypropyl cellulose (Lacrisert)
Hydroxypropyl cellulose (marketed as Lacrisert) works by stabilizing and thickening the tear film on the eye’s surface, helping to extend the tear breakup time (TBUT). It is administered as a small insert placed once or twice daily in the lower eyelid’s conjunctival sac, reducing the need for frequent use of traditional artificial tear drops.
Ophthalmology
Acetylcysteine
Mucolytic agents like acetylcysteine work by breaking down mucoproteins, which reduces the thickness and stickiness of mucus. These agents are particularly helpful in cases where there is excessive mucus discharge or the formation of mucus plaques on the ocular surface.
Ophthalmology
Cyclosporine Ophthalmic (Restasis, Cequa, Vevye)
Cyclosporine functions as an immunomodulatory agent, although its precise mechanism is not fully understood. It primarily works by suppressing T-cell activity and inhibiting the enzyme calcineurin. Importantly, the use of cyclosporine eye drops has not been linked to an increased risk of ocular or systemic infections.
Ophthalmology
The management of Dry Eye Disease (DED) typically progresses through several phases based on severity and treatment response. The initial phase focuses on patient education and environmental modifications, along with the use of artificial tears and lubricants to alleviate mild symptoms and restore tear film stability. In the second phase, if symptoms persist or inflammation is present, anti-inflammatory therapies such as topical cyclosporine or lifitegrast are introduced, alongside measures to improve meibomian gland function like warm compresses and eyelid hygiene.
For patients with moderate to severe disease, the third phase may involve more advanced interventions such as punctal occlusion to conserve tears, autologous serum eye drops, or secretagogues to stimulate tear production. In refractory cases, additional therapies including therapeutic contact lenses or systemic immunomodulators may be considered. Throughout all phases, regular follow-up and reassessment are essential to tailor treatment, monitor effectiveness, and prevent progression.
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