Etiology and Therapy of Dry Eye Syndrome in a Nutshell
Dry eye syndrome, the most common diagnosis in outpatient ophthalmology practice, is a multifactorial disease with varying severity of symptoms. It reduces the quality of life and can also affect the patient's visual functions. Therapy is individualized according to the primary trigger of the disease and aims to restore the homeostasis of the ocular surface and tear film. Due to the rapid pace of modernization associated with numerous extrinsic factors contributing to the development of dry eye syndrome, its incidence is rising, as well as the number of topical therapeutic options.
Introduction
Dry eye, also known as keratoconjunctivitis sicca, is a disease of the ocular surface caused by a loss of homeostasis of the tear film and accompanied by ocular symptoms that arise due to instability and hyperosmolarity of the tear film, inflammation and damage of the ocular surface, and neurosensory disturbances. Increased risk of dry eye syndrome (DES) is associated with older age, female gender, and many external and internal factors.
Intrinsic Factors
Autoimmune Basis
DES can be linked to several autoimmune diseases. In patients with Sjögren's syndrome, there is an increase in inflammatory cytokines in the tear film and a reduction in tear secretion due to excessive infiltration of lymphocytes and macrophages in the lacrimal glands. Graves' ophthalmopathy is characterized by an inflammatory response of orbital tissues to excessive production of thyroid hormones. It is a combination of mechanical damage to the eyelids, leading to reduced blink frequency, uneven distribution of the tear film and increased tear evaporation, and reduced tear production. In multiple sclerosis, poor conduction of sensory impulses by the cornea and decreased tear secretion are observed.
Hormonal Imbalance
The activity of lacrimal and Meibomian glands is influenced by androgenic hormones. Their deficiency can reduce the activity and size of lacrimal glands, thus reducing tear production.
Chronic Diseases
Diabetes mellitus is often associated with progressive damage to the epithelium of the cornea and conjunctiva and dysfunction of the lacrimal glands. DES is also part of xerophthalmia caused by vitamin A deficiency.
Genetic Disorders
Riley-Day syndrome is a rare genetic disorder that disrupts the development of specific sensory and autonomic neurons during embryogenesis, manifesting in childhood as optic neuropathy that progresses with age, along with an inability to produce tears.
Intestinal Dysbiosis
An imbalance of gut microbiota (specifically disrupted ratio of Firmicutes to Bacteroidetes) leads to the migration of dendritic cells and macrophages and the secretion of pro-inflammatory cytokines on the ocular surface and in the lacrimal glands. The heightened immune response results in decreased mucin and tear secretion.
Extrinsic Factors
Environmental Influences
The lacrimal functional unit of the eye can be disrupted by high air pollution, involving inorganic dust particles, dirt, soot, and organic allergens like pollen, molds, and microbial colonies. Excessive and prolonged exposure triggers a chronic inflammatory response and induces oxidative stress with cytotoxic effects on the eye's secretory cells.
Extreme weather conditions (strong wind, low humidity, high temperature, high altitude) reduce the stability of the lacrimal film and increase tear evaporation.
Lifestyle
Smoking traditional and electronic cigarettes affects eye function through smoke. Combustion by-products lead to inflammation and reduction in the quantity and quality of tears, along with damage to the ocular surface.
Long-term use of electronic display devices (computers, mobile phones, etc.) is associated with a lower blink frequency, which hinders the formation of a stable tear film and accelerates tear evaporation.
Contact Lenses
Wearing contact lenses over time causes mechanical friction and damage to the goblet cells of the ocular epithelium and Meibomian glands, accompanied by reduced lipid secretion, decreased tear film stability, and increased tear evaporation.
Ocular Surgery
Surgical corrections of refractive errors, such as laser-assisted in situ keratomileusis (LASIK), photorefractive keratectomy (PRK), and small-incision lenticule extraction (SMILE), are known risk factors for the development of DES. During these procedures, there is unavoidable damage to the eye's sensory nerves, which subsequently manifests as reduced blink frequency, decreased mucin and tear secretion, reduced lacrimal film stability, and increased tear evaporation.
Therapeutic Options
The key to treatment is identifying the primary trigger and subsequent therapy aimed at restoring the homeostasis of the ocular surface and tear film. Therapy for early and mild stages of DES is usually initiated with conventional over-the-counter products in the form of drops, ointments, or gels and consists of substituting natural tears. These substances can be combined with dexpanthenol or retinol, which support the regeneration of the ocular surface. To suppress the inflammatory component of DES, in some cases, corticosteroids or cyclosporine A can be applied locally.
Moisturizers
Moisturizing substances, known as artificial tears, are used for substitution therapy, especially for milder forms of dry eye. These substances include a range of low-viscosity molecules (e.g., povidone or polyvinylpyrrolidone /PVP/, polyvinyl alcohol /PVA/, hydroxypropyl methylcellulose /HPMC/, carboxymethylcellulose /CMC/) and high-viscosity molecules (e.g., hyaluronic acid, carbomer).
High-viscosity substances are characterized by beneficial moisturizing and bioadhesive properties and are also suitable for severe forms of dry eye syndrome. Hyaluronic acid (HA) appears highly effective in DES therapy with significant improvement in tear production, and HA-containing preparations are suitable for topical application more frequently than 4× a day. Carbomer creates a protective, viscoelastic environment on the ocular surface, helping to restore and stabilize the tear film.
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