Dry Eye Disease (Keratoconjunctivitis Sicca)

Updated: Oct 09, 2017
  • Author: C Stephen Foster, MD, FACS, FACR, FAAO, FARVO; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Overview

Practice Essentials

Dry eye disease (DED), also known as dry eye syndrome (DES), keratoconjunctivitis sicca (KCS), and keratitis sicca, is a multifactorial disease of the tears and the ocular surface that results in discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. [1] Dry eye disease is a common form of ocular surface disease (OSD) and may overlap with other causes of OSD, such as ocular allergy and meibomian gland dysfunction (MGD).

The ocular surface is an integrated anatomical unit consisting of 7 key interactive and interdependent components: the tear film, the lacrimal and accessory lacrimal apparatus, the nasolacrimal drainage system, the eyelids, the bulbar and tarsal conjunctiva, cranial nerve V, and cranial nerve VII. [2] Abnormalities or deficiencies in any of the 7 ocular surface components may worsen dry eye disease, yet promise opportunities for effective therapeutic intervention.

The image below depicts the ocular surface anatomy.

Eye tear system anatomy, (Description) a. tear gla Eye tear system anatomy, (Description) a. tear gland / lacrimal gland, b. superior lacrimal punctum, c. superior lacrimal canal, d. tear sac / lacrimal sac, e. inferior lacrimal punctum, f. inferior lacrimal canal, g. nasolacrimal canal.

Dry eye disease may be subdivided into 2 main types as follows:

  • Dry eye disease associated with Sjögren syndrome (SS)
  • Dry eye disease unassociated with SS (non-SS KCS)

Dry eye disease can also be subdivided into pure aqueous deficiency dry eye and evaporative dry eye. [3] Eighty-six percent of patients with dry eye disease also have signs of meibomian gland dysfunction.

Signs and symptoms

The following are the most common complaints associated with dry eye disease:

  • Foreign-body sensation and ocular dryness and grittiness
  • Hyperemia
  • Mucoid discharge
  • Ocular irritation
  • Excessive tearing (secondary to reflex secretion)
  • Photophobia
  • Fluctuating or blurry vision

See Clinical Presentation for more detail.

Diagnosis

Studies that may be used for diagnosis include the following:

  • Vital staining of corneal and conjunctival epithelium with fluorescein, lissamine green, or rose bengal
  • Tear film osmolarity
  • Ocular surface matrix metalloproteinase 9 (MMP-9)
  • Measurement of tear breakup time (TBUT)
  • The Schirmer test
  • Tear meniscus height
  • Quantification of tear components through analysis of tear proteins
  • Impression cytology to monitor progression of ocular surface changes

Additional tests that may be used in a research workup include:

  • The tear stability analysis system (TSAS)
  • The tear function index (TFI; Liverpool modification)
  • The tear ferning test (TFT)

Criteria for a diagnosis of dry eye disease associated with Sjögren syndrome (SS) include the following:

  • Abnormally low Schirmer test result
  • Objective evidence of low salivary flow
  • Biopsy-proven lymphocytic infiltration of the labial salivary glands
  • Dysfunction of the immune system, as manifested by the presence of serum autoantibodies (eg, antinuclear antibody [ANA], rheumatoid factor [RF], and anti-Ro [SS-A] and anti-La [SS-B] antibodies)

See Workup for more detail.

Management

Early detection and aggressive treatment of dry eye disease, or keratoconjunctivitis sicca (KCS), may help prevent corneal ulcers and scarring.

Pharmacologic therapy

Lubricating supplements are the medications most commonly used to treat dry eye disease. Agents that have been used to treat dry eye disease include the following:

  • Artificial tear substitutes
  • Gels, emulsions and ointments
  • Topical anti-inflammatory agents: Topical cyclosporine, [4, 5] topical corticosteroids
  • Topical or systemic omega-3 fatty acids: Omega-3 fatty acids inhibit the synthesis of lipid mediators and block the production of interleukin (IL)–1 and tumor necrosis factor alpha (TNF-α)
  • Topical or systemic tetracyclines
  • Secretagogues: Diquafosol, which is approved in Japan [6, 7] but not in the United States
  • Topical hyaluronic acid, which is also approved in Japan [8]
  • Autologous or umbilical cord serum
  • Systemic immunosuppressants

Therapeutic eyewear

Specially made glasses known as moisture chamber spectacles, which wrap around the eyes to retain moisture and protect against irritants, may be helpful in some cases of dry eye disease. Therapeutic contact lenses may also be helpful.

Surgical intervention

Punctal plugs are often used in the treatment of dry eye disease. Available types include the following:

  • Absorbable plugs
  • Nonabsorbable plugs
  • Thermoplastic plugs
  • Hydrogel plugs

Other advanced or surgical options include the following:

  • Sealing of the perforation or descemetocele with corneal cyanoacrylate tissue adhesive
  • Corneal or corneoscleral patching for an impending or frank perforation
  • Lateral tarsorrhaphy - Temporary tarsorrhaphy (50%) is indicated in patients with dry eye disease secondary to exposure keratitis after facial nerve paralysis and after trigeminal nerve lesions that give rise to dry eye disease secondary to loss of corneal sensation
  • Conjunctival flap
  • Conjunctivoplasty excision of symptomatic conjunctivochalasis
  • Surgical cautery occlusion of the lacrimal drainage system
  • Mucous membrane grafting
  • Salivary gland duct transposition
  • Amniotic membrane transplantation or amniotic membrane contact lens therapy
  • Prosthetic replacement of the ocular surface ecosystem (PROSE) lens therapy

See Treatment and Medication for more detail.

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Background

Dry eye disease (DED), also known as dry eye syndrome (DES), keratoconjunctivitis sicca (KCS), and keratitis sicca, is a multifactorial disease of the tears and the ocular surface that results in discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. [1] It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface. Multiple causes can produce either inadequate tear production or abnormal tear film constitution, resulting in excessively fast evaporation or premature destruction of the tear film.

Dry eye disease may be subdivided into 2 main types as follows:

  • Dry eye disease associated with Sjögren syndrome (SS)
  • Dry eye disease unassociated with SS (non-SS KCS)

Patients with aqueous tear deficiency (ATD) have SS if they have associated xerostomia or connective tissue disease (CTD). Patients with primary SS have evidence of a systemic autoimmune disease, as manifested by the presence of serum autoantibodies and severe ATD and ocular surface disease. These patients, who are mostly women, do not have a separate, identifiable CTD. Subsets of patients with primary SS lack evidence of systemic immune dysfunction but have a similar clinical ocular presentation.

Secondary SS is defined as dry eye disease that is associated with a diagnosable CTD, which is most commonly rheumatoid arthritis (RA) but could also be systemic lupus erythematosus (SLE) or systemic sclerosis.

Non-SS dry eye disease is mostly found in postmenopausal women, women who are pregnant, women who are taking oral contraceptives, or women who are on hormone replacement therapy (especially estrogen-only pills). The common denominator is a decrease in androgens, from either reduced ovarian function (in postmenopausal women) or increased levels of the sex hormone–binding globulin (in women who are pregnant or are taking birth control pills).

Meibomian gland dysfunction is also a key component of dry eye disease, with a growing awareness among clinicians of the key role played by surface lipids. In Lemp et al’s cohort of 224 subjects with dry eye disease, 86% demonstrated signs of meibomian gland dysfunction based on an objective, composite, disease severity scale. The proportion of subjects exhibiting signs of evaporative dry eye resulting from meibomian gland dysfunction far outweighs that of subjects with pure aqueous deficiency dry eye in that general clinic-based patient cohort. [3]

Androgens are believed to be trophic for the lacrimal and meibomian glands. They also exert potent anti-inflammatory activity through the production of transforming growth factor beta (TGF-β), suppressing lymphocytic infiltration.

Dry eye disease is essentially a clinical diagnosis, made by combining information obtained from the history and from the physical examination and performing one or more tests to lend some objectivity to the diagnosis. No single test is sufficiently specific to permit an absolute diagnosis of dry eye disease.

Early detection and aggressive treatment of dry eye disease may help prevent corneal ulcers and scarring, as well as improve quality of life metrics. Treatment depends on the level of severity and may include medications, eye protection devices, and surgical interventions. The frequency of follow-up care depends on the severity of the signs and symptoms. Environment-related issues that may exacerbate dry eye disease should be discussed; alternatives may be needed.

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Anatomy

The tear film covers the normal ocular surface. It is generally considered to comprise the following 3 intertwined layers (see the image below):

  • A superficial thin lipid layer (0.11 µm) – This layer is produced by the meibomian glands, and its principal function is to retard tear evaporation and to assist in uniform tear spreading [9]
  • A middle thick aqueous layer (7 µm) – This layer is produced by the main lacrimal glands (reflex tearing), as well as by the accessory lacrimal glands of Krause and Wolfring (basic tearing)
  • An innermost hydrophilic mucin layer (0.02-0.05 µm) – This layer is produced by both the conjunctiva goblet cells and the ocular surface epithelium and associates itself with the ocular surface via its loose attachments to the glycocalyx of the microplicae of the epithelium; it is the hydrophilic quality of the mucin that allows the aqueous layer to spread over the corneal epithelium
  • Diagram of three layers of tear film layer. Diagram of three layers of tear film layer.

The lipid layer acts as a surfactant, constitutes an aqueous barrier, retards evaporation of the underlying aqueous layer, and provides a smooth optical surface. It may also act as a barrier against foreign particles, and it may possess some antimicrobial properties.

Because the meibomian glands are holocrine in nature, the secretions contain both polar lipids (aqueous-lipid interface) and nonpolar lipids (air-tear interface), as well as proteinaceous material. All of these are held together by ionic bonds, hydrogen bonds, and van der Waals forces. The secretions are subject to neuronal (parasympathetic, sympathetic, and sensory sources), hormonal (androgen and estrogen receptors), and vascular regulation. Evaporative loss is predominantly due to meibomian gland dysfunction (MGD).

The aqueous component includes about 60 different proteins, electrolytes, and water. Lysozyme, the most abundant (20-40% of total protein) and most alkaline of the tear proteins, is a glycolytic enzyme capable of breaking down bacterial cell walls. Lactoferrin has antibacterial and antioxidant functions, and epidermal growth factor (EGF) helps maintain the normal ocular surface and promote corneal wound healing. Other components include albumin, transferrin, immunoglobulin A (IgA), immunoglobulin M (IgM), and immunoglobulin G (IgG).

The secretion of the lacrimal gland is controlled by a neural reflex arc, with afferent nerves (trigeminal sensory fibers) in the cornea and the conjunctiva passing to the pons (superior salivary nucleus), from which efferent fibers pass in the nervus intermedius to the pterygopalatine ganglion and postganglionic sympathetic and parasympathetic nerves terminating in the lacrimal glands.

The glycocalyx of the corneal epithelium contains the transmembrane mucins (glycosylated glycoproteins present in the glycocalyx) MUC1, MUC4, and MUC16. These membrane mucins interact with soluble, secreted, gel-forming mucins produced by the goblet cells (MUC5AC) and also with others, such as MUC2. The lacrimal gland also secretes MUC7 into the tear film.

These soluble mucins move about freely in the tear film, a process facilitated by blinking and electrostatic repulsion from the negatively charged transmembrane mucins. Soluble mucins also function as cleanup proteins by picking up dirt, debris, and pathogens, holding fluids because of their hydrophilic nature, and harboring defense molecules produced by the lacrimal gland.

Transmembrane mucins prevent pathogen adherence and entrance. They also provide a smooth lubricating surface, allowing lid epithelia to glide over corneal epithelia with minimal friction during blinking and other eye movements. It has been suggested that the mucins are mixed throughout the aqueous layer of tears owing to their hydrophilic nature and, being soluble, move freely within this layer. 

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Pathophysiology

A genetic predisposition in SS-associated dry eye disease exists, as is evidenced by the high prevalence of human leukocyte antigen B8 (HLA-B8) haplotype in these patients.

This condition leads to a chronic inflammatory state, with the production of autoantibodies, including antinuclear antibody (ANA), rheumatoid factor (RF), fodrin (a cytoskeletal protein), the muscarinic M3 receptor, or SS-specific antibodies (eg, anti-RO [SS-A] and anti-LA [SS-B]); inflammatory cytokine release; and focal lymphocytic infiltration of the lacrimal and salivary gland, with glandular degeneration and induction of apoptosis in the conjunctiva and lacrimal glands. The lymphocytic infiltrates consist mainly of CD4+ T cells but also B cells.

This results in dysfunction of the lacrimal gland with reduced tear production, as well as loss of response to nerve stimulation and less reflex tearing. Active T-lymphocytic infiltrate in the conjunctiva has also been reported in non-SS dry eye disease.

Sex hormone deficiency

Both androgen and estrogen receptors are located in the lacrimal and meibomian glands. SS is more common in postmenopausal women. At menopause, a decrease in circulating sex hormones occurs, possibly affecting the functional and secretory aspect of the lacrimal gland. Initial interest in this area centered on evaluating estrogen or progesterone deficiency to explain the link between dry eye disease and menopause; subsequent research has tended to focus more on androgens (specifically, testosterone) or metabolites of androgens.

In meibomian gland dysfunction, androgen deficiency results in loss of the lipid layer—specifically, loss of triglycerides, cholesterol, monounsaturated essential fatty acids such as oleic acid, and polar lipids, including phosphatidylethanolamine and sphingomyelin. Loss of polar lipids, which are present at the aqueous-tear interface, exacerbates evaporative tear loss, and loss of unsaturated fatty acids raises the melting point of meibomian gland secretions, or meibum, leading to thicker, more viscous secretions that obstruct ductules and cause stagnation of secretions.

Patients on antiandrogenic therapy for prostate disease also have increased viscosity of meibum, decreased tear breakup time (TBUT), and increased tear film debris, all of which indicate a deficient or abnormal tear film.

Proinflammatory activity

Various proinflammatory cytokines that may cause cellular destruction, including interleukin (IL)–1, IL-6, IL-8, TGF-β, tumor necrosis factor alpha (TNF-α), and RANTES, are altered in patients with dry eye disease. IL-1β and TNF-α, which are present in the tears of patients with dry eye disease, cause the release of opioids that bind to opioid receptors on neural membranes and inhibit neurotransmitter release through production of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB).

IL-2 also binds to the delta opioid receptor and inhibits cAMP production and neuronal function. This loss of neuronal function diminishes normal neuronal tone, leading to sensory isolation of the lacrimal gland and eventual atrophy.

Proinflammatory neurotransmitters, such as substance P and calcitonin gene–related peptide (CGRP), are released, and these substances recruit and activate local lymphocytes. Studies suggest that dry eye severity is directly correlated with nerve growth factor (NGF) levels and inversely correlated with CGRP and neuropeptide Y (NPY) tear levels.

NGF tear levels point to a direct relation with conjunctival hyperemia and fluorescein staining results, suggesting that tear levels of NGF are more closely connected to corneal epithelial damage, perhaps as a reflection of attempted compensatory repair responses, and that the decreased tear levels of NPY and CGRP in dry eye disease are linked to impaired lacrimal function. [10] In one study, elevated NGF tear levels were decreased by giving 0.1% prednisolone. [11]

Substance P also acts via the nuclear factor of activated T cells (NF-AT) and through the NF-κB signaling pathway. This leads to expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), adhesion molecules that promote lymphocyte homing and chemotaxis to sites of inflammation.

Cyclosporine is a novel addition to the therapeutic armamentarium for dry eye, being used to treat both aqueous tear deficiency and meibomian gland dysfunction. It is a neurokinin (NK)–1 and NK-2 receptor inhibitor that can down-regulate these signaling molecules. It has been shown to improve goblet cell counts and to reduce the numbers of inflammatory cells and cytokines in the conjunctiva.

These cytokines, in addition to inhibiting neural function, may also convert androgens into estrogens, resulting in meibomian gland dysfunction. An increased rate of apoptosis is also seen in conjunctival and lacrimal acinar cells, perhaps owing to the cytokine cascade. Elevated levels of tissue-degrading enzymes called matrix metalloproteinases (MMPs) are also present in the epithelial cells.

Mucin deficiency

Mucin-synthesizing genes representing both transmembrane mucins and goblet cell–secreted soluble mucins have been isolated and designated MUC1 through MUC17. Their roles in hydration and stabilization of the tear film are being investigated in patients with KCS. Particularly significant is MUC5AC, which is expressed by stratified squamous cells of the conjunctiva and whose product is the predominant component of the mucous layer of tears. A defect in this and other mucin genes may be a factor in the development of dry eye disease.

Besides dry eye disease, other conditions may eventually lead to loss of goblet cells, including ocular cicatricial pemphigoid, Stevens-Johnson syndrome, and vitamin A deficiency. These conditions may lead to drying and eventual keratinization of the ocular epithelium. Both classes of mucins are decreased in these diseases, and, on a molecular level, mucin gene expression, translation, and posttranslational processing are altered.

Mucin deficiency leads to poor wetting of the corneal surface with subsequent desiccation and epithelial damage, even in the presence of adequate aqueous tear production.

Reduced tear protein production

Normal production of tear proteins, such as lysozyme, lactoferrin, lipocalin, and phospholipase A2, is decreased in dry eye disease.

Lipocalins, previously known as tear-specific prealbumin, are inducible lipid-binding proteins produced by the lacrimal glands and present in the mucous layer. They lower the surface tension of normal tears, which provides stability to the tear film and also explains the increase in surface tension seen in dry eye disease characterized by lacrimal gland deficiency. Lipocalin deficiency can lead to precipitation in the tear film, forming the characteristic mucous strands seen in patients with dry eye symptoms.

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Etiology

The International Dry Eye WorkShop (DEWS) developed a 3-part classification of dry eye based on etiology, mechanisms, and disease stage. [1] This classification system distinguishes 2 main categories (or causes) of dry eye states, as follows:

  • An evaporative state
  • An aqueous deficiency state

Evaporative loss due to meibomian gland dysfunction is the most common cause of dry eye. Causes of evaporative loss include the following:

  • Meibomian gland dysfunction
  • Disorders of lid aperture
  • Low blink rate
  • Drug action (eg, isotretinoin)
  • Vitamin A deficiency
  • Topical drugs and preservatives
  • Contact lens wear
  • Ocular surface disease (eg, allergy)

Aqueous tear deficiency (ATD) results from insufficient tear production. Causes of deficient aqueous production include the following:

  • SS dry eye (primary and secondary)
  • Lacrimal gland deficiency
  • Lacrimal gland duct obstruction
  • Reflex hyposecretion
  • Systemic drugs

Etiology: deficient aqueous production

Causes of deficient aqueous production can be further classified as related or unrelated to SS.

Non-Sjögren syndrome

Primary lacrimal gland deficiencies that may impair aqueous production include the following:

  • Idiopathic
  • Age-related dry eye
  • Congenital alacrima (eg, Riley-Day syndrome)
  • Familial dysautonomia

Secondary lacrimal gland deficiencies that may impair aqueous production include the following:

  • Lacrimal gland infiltration
  • Sarcoidosis
  • Lymphoma
  • AIDS
  • Graft vs host disease
  • Amyloidosis
  • Hemochromatosis
  • Lacrimal gland infectious diseases
  • HIV diffuse infiltrative lymphadenopathy syndrome
  • Trachoma
  • Systemic vitamin A deficiency (xerophthalmia) – Malnutrition, fat-free diets, intestinal malabsorption from inflammatory bowel disease, bowel resection, or chronic alcoholism
  • Lacrimal gland ablation
  • Lacrimal gland denervation

Lacrimal obstructive diseases that may impair aqueous production include the following:

  • Trachoma
  • Ocular cicatricial pemphigoid
  • Erythema multiforme and Stevens-Johnson syndrome
  • Chemical and thermal burns
  • Endocrine imbalance
  • Postirradiation fibrosis

Medications that may impair aqueous production include the following:

  • Antihistamines
  • Beta blockers
  • Phenothiazines
  • Atropine
  • Oral contraceptives
  • Anxiolytics
  • Antiparkinsonian agents
  • Diuretics
  • Anticholinergics
  • Antiarrhythmics
  • Topical preservatives in eye drops (eg, benzalkonium chloride [BAK], thimerosal)
  • Topical anesthetics
  • Isotretinoin

The following conditions may lead to reflex hyposecretion:

  • Neurotrophic keratitis – Cranial nerve (CN) V/ganglion section/injection/compression
  • Corneal surgery - Limbal incision (eg, extracapsular cataract extraction), keratoplasty, and refractive surgery
  • Infective - Herpes simplex keratitis and herpes zoster ophthalmicus
  • Topical agents - Topical anesthesia
  • Systemic medications – Beta blockers and atropinelike drugs
  • Chronic contact lens wear
  • Diabetes
  • Aging
  • Trichloroethylene toxicity
  • CN VII damage
  • Multiple neuromatosis

Sjögren syndrome

Primary SS has no associated CTD. Secondary SS may be associated with any of the following CTDs:

  • RA
  • SLE
  • Progressive systemic sclerosis (scleroderma)
  • Primary biliary cirrhosis
  • Interstitial nephritis
  • Polymyositis and dermatomyositis
  • Polyarteritis nodosa
  • Hashimoto thyroiditis
  • Lymphocytic interstitial pneumonitis
  • Idiopathic thrombocytopenic purpura
  • Hypergammaglobulinemia
  • Waldenstrom macroglobulinemia
  • Wegener granulomatosis

Etiology: evaporative loss

Causes of evaporative loss can be further classified as intrinsic or extrinsic.

Intrinsic causes

Meibomian gland disease may involve a reduced number of functioning glands, as in congenital deficiency or acquired meibomian gland dysfunction, or complete gland replacement, as in distichiasis, lymphedema-distichiasis syndrome, or metaplasia. Meibomian gland dysfunction may be divided into 3 subtypes, as follows: 

  • Hypersecretory - Meibomian seborrhea
  • Hyposecretory - Retinoid therapy
  • Obstructive - This may be simple, primary or secondary to local disease (eg, anterior blepharitis), systemic disease (eg, acne rosacea, seborrheic dermatitis, atopy, ichthyosis, or psoriasis), syndromes (eg, anhidrotic ectodermal dysplasia, ectrodactyly syndrome, or Turner syndrome), or systemic toxicity (eg, 13- cis retinoic acid or polychlorinated biphenyls); or it may be cicatricial, primary or secondary to local disease (eg, chemical burns, trachoma, pemphigoid, erythema multiforme, acne rosacea, vernal keratoconjunctivitis [VKC], or atopic keratoconjunctivitis [AKC])

Evaporative loss may result from a low blink rate caused by the following:

  • Physiologic phenomenon, such as may occur during performance of tasks that require concentration (eg, working at a computer or a microscope)
  • Extrapyramidal disorder, such as Parkinson disease (decreasing dopaminergic neuron pool)

Evaporative loss may result from the following disorders of eyelid aperture and eyelid-globe congruity:

  • Exposure (eg, craniostenosis, proptosis, exophthalmos, and high myopia)
  • Lid palsy
  • Ectropion
  • Lid coloboma

In addition, the actions of drugs such as isotretinoin may lead to evaporative loss.

Extrinsic causes

Vitamin A deficiency may cause dry eye as a consequence of the following:

  • Development disorder of goblet cells
  • Lacrimal acinar damage

Other extrinsic causes are as follows:

  • Topical drugs and preservatives that cause surface epithelial cell damage
  • Contact lens wear
  • Ocular surface disease (eg, allergy)

Mechanisms

A classification of dry eye on the basis of mechanisms includes tear hyperosmolarity and tear-film instability.

Severity

For classification of dry eye disease based on severity, the Delphi Panel Report was adopted and modified as a third component of the DEWS (see the Table below). [1, 12]

Table. Dry Eye Severity Levels (Open Table in a new window)

Variable Dry Eye Severity Level
1 2 3 4 (must have signs and symptoms)
Discomfort (severity and frequency) Mild, episodic; occurs under environmental stress Moderate, episodic or chronic; occurs with or without stress Severe, frequent or constant; occurs without stress Severe or disabling, constant
Visual symptoms None or episodic mild fatigue Annoying or activity-limiting, episodic Annoying, chronic or constant, activity-limiting Constant and possibly disabling
Conjunctival injection None to mild None to mild +/– +/++
Conjunctival staining None to mild Variable Moderate to marked Marked
Corneal staining (severity and location) None to mild Variable Marked central Severe punctate erosions
Corneal and tear signs None to mild Mild debris, decreased meniscus Filamentary keratitis, mucus clumping, increased tear debris Filamentary keratitis, mucus clumping, increased tear debris, ulceration
Lid and meibomian glands MGD variably present MGD variably present MGD frequent Trichiasis, keratinization, symblepharon
Tear breakup time Variable ≤ 10 s ≤ 5 s Immediate
Schirmer score Variable ≤ 10 mm/5 min ≤ 5 mm/5 min ≤ 2 mm/5 min
MGD=meibomian gland dysfunction.
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Epidemiology

Dry eye disease is very common in the United States, affecting a significant percentage of the population, especially those older than 40 years. Prevalence estimates range from approximately 10%-30% of the population. An estimated 3.23 million women and 1.68 million men aged 50 years and older are affected. [13]

As a consequence of the demographic pressure created by an aging population, meibomian gland dysfunction is expected to increase in prevalence and thus to impose a growing burden on ophthalmologic practices. [14] Development of thoughtful, effective strategies that involve the underlying mechanism of meibomian gland dysfunction is critical to the effective, patient-satisfying functioning of every ophthalmologist’s practice.

The reported frequency of dry eye in other countries closely parallels that in the United States.

Dry eye is more common in women. [13] Dry eye disease associated with SS is believed to affect 1%-2% of the population, and 90% of those affected are women. Data on race and ethnicity in dry eye disease are limited, but the frequency and the clinical diagnosis of dry eye appear to be greater in the Hispanic and Asian populations than in whites.

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Prognosis

The prognosis of dry eye disease varies depending on the severity of the condition. Most patients have mild-to-moderate cases, and they can be treated symptomatically with lubricants, providing adequate relief of symptoms. In general, the prognosis for visual acuity in patients with dry eye disease is good. Patients with SS or prolonged untreated dry eye represent a subgroup with a worse prognosis, requiring a longer course of treatment.

Dry eye may be complicated by sterile or infectious corneal ulceration, particularly in patients with SS. Ulcers are typically oval or circular, less than 3 mm in diameter, and located in the central or paracentral cornea. Occasionally, corneal perforation may occur. In rare cases, sterile or infectious corneal ulceration in dry eye disease can cause blindness. This risk is markedly increased with contact lens use, particularly with overnight wear.

Punctate epithelial defects (PEDs) may be present. Significant punctate epitheliopathy can lead to corneal erosions, both sterile and infectious corneal ulceration, corneal neovascularization, corneal scarring, corneal thinning, and even corneal perforation.

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Patient Education

A wide variety of educational materials are available for patients with dry eye disease, particularly online. For patients with SS, regular dental examinations are important because dry mouth or xerostomia, a component of SS, significantly increases the risk of dental problems. Women should receive regular checkups from their gynecologists.

Patients with SS can obtain up-to-date information from the Sjögren’s Syndrome Foundation, 6707 Democracy Boulevard, Suite 325, Bethesda, MD 20817; (301) 530-4420 or (800) 475-6473; fax, (301) 530-4415.

For patient education information, see the Eye and Vision Center, as well as Dry Eye Syndrome, Pink Eye, How to Instill Your Eyedrops, and Sjögren’s Syndrome. Websites include www.mydryeyes.com/ and www.dryeyeinfo.com/Disease. See also the following topics:

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