Key tests for diagnosing dry eye disease in general practice

As with many other conditions, early detection and treatment is key to prevent disease progression

Dry eye disease (DED) is a common and impactful condition, with global prevalence as high as 50 per cent.^1,2 It is a leading cause of patient visits to healthcare practitioners, and evidence-based diagnosis and treatment is often challenging. It presents a significant economic burden,³ with the annual cost of treating a patient with DED estimated to be approximately $1000.

DED can drastically impact quality of life,^4,5 with some studies showing mild DED affects QoL more than psoriasis, and severe DED has a QoL score worse than angina. Severe DED has also been linked with depression and suicide.^6,7 Therefore, there is a need for primary care health professionals to carefully consider their approach to DED, as early intervention often leads to better long-term outcomes.

Patients coming in to see their GP may mention they have eye dryness, and it can be easy and indeed tempting to ask the patient to buy some over-the-counter lubricants. However, as with many other conditions, early detection and treatment is key to prevent disease progression.

In 2017, the Report of the TFOS International Dry Eye Workshop II (TFOS DEWS II) was published. The workshop behind the report consisted of 12 subcommittees made up of 150 experts from 23 countries. The report was the result of two years of collaboration and is considered the main reference for practitioners in the dry eye field.

One of the main goals of the workshop was to put forth a consensus definition of DED, in order to focus research and clinical practice. Thus, DED was defined as “a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles”.⁸

The key takeaway from this definition is that dry eye is a disease of the ocular surface linked to inflammation and damage of the ocular surface. Hyperosmolarity and neurosensory abnormalities also play a role. DED can therefore be viewed as a chronic, inflammatory condition of the ocular surface.

When classifying DED, it is important to first distinguish between symptomatic and asymptomatic patients. To be diagnosed with DED, a patient must be symptomatic.

While symptoms can fluctuate, common symptoms of DED include:

• discomfort
• light sensitivity
• secondary reflex tearing
• visual symptoms
• anxiety and depression.

There are some symptoms that can be confused with dry eye. These include:

• itching (allergy)
• morning stinging (recurrent corneal erosion)
• localised area of discomfort (conjunctivochalasis).

A combination of symptoms and signs of ocular surface disease places the patient in the DED category. Asymptomatic patients with signs of dry eye are given the label of ocular surface disease but not DED. They have obvious signs of corneal damage but no accompanying dry eye symptoms.

Similarly, a patient with significant symptoms but no signs of ocular surface disease is classified as having ocular neuropathic pain and should be referred for pain management.

The ocular tear film has several functions. These include:

• cleansing and wetting the ocular surface
• providing optical stability
• providing bacteriostatic cover
• providing nutrients for the cornea.

The tear film consists of mucin, aqueous and lipid layers. The lipid layer is the outermost layer and protects the tear film from the atmosphere, limiting its evaporation. It is produced by the meibomian glands in the eyelids. The middle aqueous layer is secreted by the lacrimal glands, and the inner mucin layer is produced by goblet cells in the conjunctiva.

DED is the result of either a lack of aqueous production known as aqueous-deficient dry eye (ADDE), a lack of lipid production known as evaporative dry eye (EDE), or both (mixed dry eye).

ADDE is subdivided into Sjögren syndrome dry eye (SSDE) and non-Sjögren syndrome dry eye (NSDE):

• SSDE is a chronic autoimmune disorder that predominantly affects women. It is characterised by immune cell targeting of exocrine glands. The lacrimal and salivary glands are affected by an epitheliitis that leads to a destruction of these glands. This results in the key symptoms of dry eye and dry mouth (sicca symptoms). Therefore, patients with dry eye symptoms and a dry mouth should be investigated for Sjögren syndrome.
• NSDE is a rare subset of ADDE where the autoimmune features of Sjögren syndrome are not present. It is typically caused by congenital and acquired conditions, such as familial dysautonomia, age-related NSDE and congenital alacrima.

EDE is caused by a deficiency in the quality or quantity of the lipid layer of the tear film. This leads to more frequent evaporation of tears and an unstable tear film.

EDE is the most common type of DED and is linked to chronic blepharitis and its subsets, such as meibomian gland dysfunction, anterior blepharitis and ocular rosacea. Therefore, treatment of this condition focuses on treating the underlying lid disease.

To diagnose DED and exclude other conditions that can mimic it, a physician should begin with triaging questions:⁸

• How severe is the eye discomfort?
• Do you have any mouth dryness or enlarged glands? (Trigger for Sjögren syndrome investigation.)
• How long have your symptoms lasted and was there any triggering event?
• Is your vision affected and does it clear on blinking?
• Are the symptoms or any redness much worse in one eye than the other?
• Do the eyes itch, are they swollen or crusty, or have they given off any discharge?
• Do you wear contact lenses?
• Have you been diagnosed with any general health conditions (including recent respiratory infections) or are you taking any medication?

If DED is suspected, risk factor analysis should be done. These risk factors include:

Medications and treatments – antihistamines, antidepressants, anxiolytics and isotretinoin have consistently been linked with DED. Hormone replacement therapy and haematopoietic stem cell transplantation both have strong links with DED. Anticholinergics, diuretics and beta-blockers have a probable link with DED, while multivitamins and oral contraceptives have an inconsistent link.

Lifestyle factors – smoking, drinking alcohol, computer use and contact lens wear are all modifiable risk factors for DED. Environmental factors include pollution, air-conditioned offices and environments with low humidity.

Systemic conditions – connective tissue disorders, androgen deficiency and Sjögren syndrome have a strong link with DED. Diabetes, rosacea, viral infections, thyroid dysfunction and psychiatric conditions have a probable link with DED, while menopause, acne and sarcoidosis have an inconsistent link.

Not all factors listed above are modifiable. However, when risk factors are modifiable, the GP is in a prime position to reduce the effects of these risks to help their patient manage their DED.

To diagnose DED, a positive score on a dry eye questionnaire and clinical signs, such as a reduced tear break-up time or ocular surface staining, are needed. It is very easy to administer a dry eye questionnaire in a GP practice setting. The 5-item Dry Eye Questionnaire (DEQ-5), or the Ocular Surface Disease Index (OSDI) are the recommended options (see useful resources).

A tear break-up time test can be performed using a slit lamp and fluorescein – a break-up time of less than 10 seconds is indicative of DED. If a slit lamp isn’t available, then an attempt can be made to visualise ocular surface staining using fluorescein and a cobalt blue light with a direct ophthalmoscope or pen torch (see photo). A positive result is more than five corneal spots.

Once a DED diagnosis is made, a treatment plan can be formulated for the patient. This will be discussed in the follow-up article in September.

Ryan Mahmoud is an optometrist and a dry eye and contact lens specialist at NVision Eyecare; Mo Ziaei is a senior lecturer at the University of Auckland and a cataract, cornea and anterior segment specialist at Greenlane Clinical Centre and Re:Vision Laser & Cataract, Auckland