Dry Eye Syndrome: causes, symptoms, diagnosis and treatment

Dry Eye Syndrome (DS) (DED) belongs to the Ocular Surface Disease (OSD) group of disorders. It is one of the most common disorders that ophthalmologists deal with in daily practice. There are two forms of DED:

• caused by excessive evaporation of the tear film (Evaporative Dry Eye – EDE) – 80% of cases
• occurring due to deficiency of the aqueous component of the tear film (Aqueous-Deficient Dry Eye – ADDE) – 20% of cases

It is estimated that 10 to 18% of the population in Poland suffers from Dry Eye Syndrome, and up to 30% in some occupational and age groups. Among contact lens wearers, the percentage of sufferers rises to as much as 75%. The risk of developing AS increases with age and is higher in women. Dry Eye Syndrome is a multifactorial and multisymptomatic disorder. It is a chronic disease that starts out relatively mild, and over time the symptoms become so intractable that they result in visual disturbances and tear film instability, which can contribute to damage to the surface of the eye. This, in turn, induces the formation of inflammation, which affects the severity of the discomfort experienced by the patient.

The distinctions include:

• The so-called acute dry eye characterized by a specific profile of inflammatory biomarkers
• Age-related dry eye syndrome, where involutionary changes (related to aging) predominate

Dry Eye Syndrome, caused by a deficiency in the aqueous layer of the tear film, can occur either as a spontaneous condition/disorder or in the course of an autoimmune disease called Sjögren’s syndrome. According to a recent study, the incidence of Sjögren’s syndrome is increasing among patients with any autoimmune disease – currently it is about 8 percent of the general population, with up to 78 percent of this group being women.

The mechanism of pathophysiological changes on the ocular surface underlying dry eye associated with excessive evaporation is a vicious circle: deficiency of the lipid phase, results in tear film instability, increased evaporation and subsequent hyperosmolarity (water loss exceeding electrolyte loss), which implies inflammation leading to structural changes on the ocular surface.

Chronic and untreated AS can lead to corneal epithelial erosion, followed by bacterial or sterile corneal ulcers, which are conditions that threaten vision loss.

Risk factors for Dry Eye Syndrome

As can easily be seen, risk factors for AS include age, gender, contact lens wear and susceptibility to autoimmune diseases. Other factors include:

• Use of certain medications including antihistamines, antidepressants, anti-anxiety drugs and isotretinoin, cholinolytics, diuretics, beta-blockers, hormonal drugs
• surgical procedures on the eyeball including refractive surgery procedures
• endocrine disruptors
• dermatological diseases
• diabetes
• reduced levels of androgen hormones
• estrogen replacement therapy
• inflammation or tumors of the lacrimal gland
• Reduced layer of tear gland tissue or its absence (due to surgery)
• Obstruction of the outflow tract due to conjunctival scarring or conjunctival dysfunction
• horsetail
• connective tissue diseases (not just Sjögren’s syndrome)
• Environmental conditions: excessive computer use, being in air-conditioned rooms, low humidity and others)

Special attention should be paid to one of the causes of Dry Eye Syndrome – Meibomian Gland Dysfunction (MGD). About 80 percent of dry eye cases are precisely the form with excessive evaporation, induced mainly by abnormalities in the structure and function of the Meibomian glands. What are these glands?

Meibom’s glands are modified holocrine sebaceous glands lying in the mucocutaneous anastomosis of the eyelids. They are also called thyroid glands. They produce the so-called tear film, which consists of three layers: a mucin (mucous) layer directly covering the cornea, an aqueous phase and an outer lipid layer. The function of the tear film is to moisturize and protect the surface of the eye from infection, to nourish the cornea and keep its surface perfectly smooth for optimal visual acuity, and to create a moisturizing layer that protects against abrasion of the eye surface when blinking. The lipid layer of the tear film – whose stability depends precisely on the proper work of the Meibom’s glands – not only stabilizes the aqueous phase of the tear film, but also prevents the underlying aqueous layer from evaporating excessively and drying out the eyes. Meibom’s glands produce an oily secretion that is deposited as small droplets on the edge of the upper and lower eyelids. When we blink and the upper and lower eyelids come into contact (close), the secretion droplets combine and form a lipid film on the surface of the eye. When we open our eyelids, the lipid film forms an even layer over the tear film, and each time we blink, the lipid film is replenished.

When Meibom’s glands do not work properly, there is instability of the tear film, followed by irritation of the cornea, conjunctiva and eyelids. The risk of Dry Eye Syndrome is then very high.

Meibom’s gland insufficiency can be obstructive in nature (fatty secretions cannot escape from the gland channel) or productive in nature (no fatty secretions are produced in the gland). Depending on the nature of the lesions, management should be considered to change the state of fat blocking the Meibom’s gland outlets by using:

• hot compresses,
• Mechanical cleaning of the eyelid margins from dried secretions blocking the mouths of the glands,
• Mechanical expression of the eyelids using special tweezers.

In the case of overgrowth of Meibom’s gland mouths or obstruction of the gland channel, the procedure of choice is puncture and recanalization of Meibom’s glands with a Maskin needle.

Symptoms of Dry Eye Syndrome

Patients presenting to an ophthalmologist who are diagnosed with PE caused by excessive evaporation of the tear film most often complain of symptoms such as:

• pain,
• discomfort,
• Burning and pinching of the eyes,
• A feeling of a foreign body or sand under the eyelids,
• Transient/transient visual disturbances/foggy vision,
• Contact lens intolerance.

Patients presenting to an ophthalmologist who are diagnosed with PE with accompanying reduced tear production signal in turn:

• foreign body sensation in the eye
• conjunctival redness
• eyestrain
• hypersensitivity to light
• Excessive dryness of the mouth, dryness of the mucous membranes (NOTE: this symptom is also one of the symptoms that may suggest the existence of Sjögren’s syndrome and other autoimmune connective tissue diseases)

How the diagnosis of AS is carried out

A consultation with an ophthalmologist and specialized tests are required to diagnose and accurately determine the cause of ocular surface disorders.

The basic, simplest diagnostic test is the Tear Film Break-Up Time (BUT, Tear Film Break-Up Time), usually performed invasively after staining the surface of the eye with fluorescein. The doctor injects fluorescein (a yellow dye) into the patient’s conjunctival sac and asks the patient to blink several times and then stop blinking. He then evaluates in a slit lamp the time that has passed since the last blink until the dye breaks on the corneal surface. A tear film break time of less than 10 seconds is abnormal. BUT is not a highly sensitive test, the methodology requires several tests to be performed and an average to be drawn, and the fluorescein administered affects the stability of the tears, affecting the result.

Another test is the Schirmer Test, performed without anesthesia. It is performed using calibrated strips of blotting paper, which are placed in the inferior conjunctival fold. After waiting 5 minutes, the wetting level of the strip is read. The normal result is more than 15 mm. A result between 6-10 mm is borderline. A result below 6 mm indicates a tear secretion disorder. The test determines total tear secretion.

The Schirmer Test, on the other hand, performed after injecting anesthetic into the conjunctival sac, determines the basal secretion of tears (anesthesia eliminates their reflex secretion). The course of the test is the same as the version without anesthesia, while the normal results are lower (the norm is about 12 mm).

The diagnosis of MND includes not only tests that assess tear secretion in general and the evaluation of individual layers of the tear film, but also the evaluation of pro-inflammatory biomarkers in tears based on measurements of the level of extracellular metalloproteinase MMPs-9. The diagnosis of Meibom’s Gland Dysfunction is made on the basis of the characteristic clinical picture: morphology of the eyelid margins along with evaluation of gland secretions (MG expression).

If one suspects or wants to rule out AS as one of the symptoms from the Sjögren’s syndrome spectrum, one should test for anti-Lo, anti-Ra, RF and ANA antibodies. If the result for anti-Ro and anti-La antibodies is negative, and the patient has symptoms of severe dry eye syndrome, the patient should be further diagnosed.

Treatment of Dry Eye Syndrome

The mainstay in the treatment of Dry Eye Syndrome is the administration of moisturizers, which reduce friction between the structures of the eye surface and facilitate the distribution of the lipid layer. They also have the ability to cleanse the surface of the eye of toxins and pollutants, and reduce the concentration of pro-inflammatory proteins, including cytokines. Ophthalmologists most often turn to preparations containing sodium hyaluronate because, in addition to moisturizing, they can also stimulate the healing process of the conjunctival and corneal epithelium. Also available on the Polish market are preparations in the form of emulsions and oil-in-water cationic nanoemulsions, which provide substitution of all layers of the tear film and support regeneration of the corneal epithelium.

Treatment of dry eye syndrome, which is caused by the dysfunction of Meibom’s glands, can be carried out using specially developed devices for this purpose OptiLIGHT and E-EYE.