What is dry eye disease?

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The Tear Film and Ocular Surface Society Dry Eye Workshop II defines DED 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 aetiological roles.5

DED  is classified as:3,13

  • Aqueous-deficient: involves damaged lacrimal glands, which lead to inadequate tear volume. Can be classified as Sjögren or non-Sjögren. Sjögren syndrome is an autoimmune condition caused by the infiltration of activated T-cells in the lacrimal and salivary glands, causing symptoms such as dry eye and dry mouth. Non-Sjögren aqueous deficient DED results from lacrimal gland insufficiency or duct obstruction.
  • Lipid deficient: more common and occurs when abnormally rapid tear evaporation occurs. This is usually caused by meibomian gland dysfunction (MGD) or an insufficient oil layer on the surface of the aqueous layer of tears.
  • Mixed: Research suggests 30% to 70% of patients with DED may have a hybrid of both forms.

Symptoms of DED

Several ocular surface conditions or diseases can cause the same symptoms, making diagnosing, treating, and managing the DED challenging and frustrating to both clinicians and patients.1

DED may lead to any of the following symptoms:3

  • Stinging, burning, or a feeling of pressure in the eyes. 
  • A sandy, gritty, or foreign body sensation.
  • Epiphora, or tearing, is a symptom that is often counterintuitive. This is due to dryness leading to pain or irritation that results in intermittent excess tearing, or epiphora.
  • Pain is a broad term, and sharp and dull pain can be described, which may be localised to some part of the eye, behind the eye, or even around the orbit.
  • Redness is a common complaint and is often made worse by the rebound effect of vasoconstrictors found in many over-the-counter eye drops designed to reduce redness. Vasoconstrictors may decrease redness for the short term by constricting the vessels of the episclera but can have a rebound effect and increased redness after the drops wear off in a relatively short period. 
  • Blurry vision, particularly intermittent blurry vision, is a common complaint and may also be described as glare or haloes around lights at night.
  • A sensation of heavy eyelids or difficulty opening the eyes. 
  • Dryness is a common problem for contact lens wearers, and irritation may make contact lenses uncomfortable or even impossible to wear.
  • Tired eyes. Closing the eyes may provide relief to some individuals with dry eyes.

What causes DED?

Obstructive meibomian gland dysfunction (MGD) is a major cause of evaporative dry eye. Meibomian glands are the main source of tear lipids, which are essential for the retardation of tear aqueous evaporation.1

MGD is characterised by terminal duct obstruction and/or qualitative/quantitative changes in glandular secretion. It may result in alteration of the tear film, symptoms of eye irritation, and clinically apparent inflammation.5

Apart from Sjögren's syndrome, other systemic factors that may cause MGD to include for example androgen deficiency, menopause, ageing, cholesterol levels, psoriasis, atopy, rosacea, hypertension, and benign prostatic hyperplasia.

Medications used in the treatment of these diseases as well as the use of antihistamines, antidepressants, and retinoids may also cause DED.5

Another common risk factor for DED symptoms is preservatives used in topical anti-glaucoma ophthalmic medications. Some non-preserved glaucoma medications may also have adverse effects on ocular surface health, resulting in a higher prevalence of ocular surface diseases among treated glaucoma patients.1

Laser-assisted in situ keratomileuses (LASIK), which injure the sub-basal nerve plexus during the lamellar cut, has also been implicated in the onset of DED. Nearly 50% of post-LASIK patients experience DED symptoms. Blink anomalies can significantly exacerbate post-LASIK dry eye symptoms. Some cases of post-LASIK DED are neuropathic in aetiology and warrant treatment of the underlying neuralgia rather than treatment of aqueous deficient or evaporative DED.1

Furthermore, exposure to computer work or other visually intensive working conditions has been shown to play a role in the development of DED. Low humidity and temperatures are well-known triggering factors for DED.6

A study by van Setten et al found that wind is the most commonly reported weather condition causing symptoms (71%), followed by sunshine (60%) and heat (42%).6

Cold weather was also reported to aggravate dry eye sensation by 34% of patients. The two seasons most commonly associated with DED are summer and winter (for 51% and 43% of patients, respectively).6

The impact of DED on patients’ QoL

DED symptoms negatively affect patients’ quality of life (QoL). According to a study by Guo et al, DED may result in in:8

  • Pain and discomfort.
  • Blurred vision or fluctuating vision as well as glare or haloes around lights at night.
  • Poor sleep quality. 
  • Poor body image and low self-esteem as a result of chronic red hyperaemic eyes. As a result, some patients develop comorbid anxiety disorders, depression, and social phobias.
  • Thinking, learning, memory, and concentration problems.
  • Decreased independence and social interaction.
  • Dependence on medicinal substances and aids.


Treatment aims to improve ocular symptoms, return the ocular surface, and tear film to its normal homeostatic state, and improve patients’ QoL.7

Treatment for DED often begins with patient education and environmental modifications (see box 1), as well as over-the-counter artificial tears (lubricants), with patients progressing to pharmacologic treatments if non-pharmacologic options are inadequate.7,9

Other treatment options include tear retention (eg punctal plugs), tear stimulation (secretagogues), biological tear substitutes (non-pharmaceutical fluids eg serum), anti-inflammatories (eg cyclosporine, corticosteroids), essential fatty acids (eg omega-3), and environmental strategies. Treatment should be based on disease severity.7

10 benefits of PEG/PG/HP guar artificial tears

The efficacy and safety of various topical pharmacologic therapies, which inhibit ocular surface inflammation that can lead to DED symptoms, have been shown in studies.9

Artificial tears are topical eye formulations used to lubricate dry eyes and help in maintaining the moisture on the outer surface of the eyes. They are used traditionally in all stages of DED treatment as a first-line therapy to improve symptoms by protecting and lubricating the mucous membrane, preventing drying, and cracking, respectively.10

In addition to the above function, they replenish the deficiency of the tear film components, wettability, and spreading. Also, artificial tears reduce the osmolarity of the ocular surface through the dilution of the inflammatory cytokines and lower the susceptibility of the ocular surface to inflammation.10

Srinivasan and Manoj recently reviewed a decade of evidence supporting the efficacy and safety of PEG/PG/HP guar artificial tears in the management of DED. Their review found that PEG/PG/HP guar artificial tears offer the following benefits:11

  • Provides optimal ocular surface protection and lubrication to heal damaged areas of the cornea caused by DED and, therefore, is recommended for patients with both aqueous and/or mucin layer deficiencies
  • Mimics the mucin in the tear film and reduces the friction between the eyelid and ocular surface during blinks
  • Binds to desiccated or damaged hydrophobic regions of the cornea, allowing the protective layer to limit further damage and time for surface epithelial cells to undergo repair and renewal
  • Significantly reduces conjunctival and temporal corneal staining. Patients report a reduction in DED symptoms in the morning and evening, lower frequencies of foreign body sensation, and felt their eyes were ‘refreshed longer’
  • Significantly reduces tear osmolarity scores used for three weeks (four times a day). Unlike other hypotonic drops, the reduction in tear osmolarity was observed even 15 minutes after instillation
  • Improves adherence and retention to treatment
  • Improves tear stability and tissue hydration, and minimises tear evaporation, thereby lowering tear osmolarity and corneal dryness to provide long-lasting relief from DED symptoms
  • Contains no harmful preservatives.
  • Available in convenient, single-use sterile vials that provide immediate and long-lasting DED symptom relief. A multi-dose preservative-free version, which uses PureFlow technology and is also available.
  • Offers protective effects against exposure to adverse environmental conditions, according to Gokul et al.12

Patient education and environmental modifications

Patient education remains the cornerstone of management, write Engel and Abraham. Patients should be made aware that long-term treatment is needed and that potential triggers such as cigarette smoke and air conditioning should be avoided.7

Using humidifiers, avoiding dry environments, wearing glasses to decrease tear evaporation, and taking regular breaks from reading and computer use may alleviate symptoms. Dietary modifications, specifically to increase intake of omega-3 fatty acids and to decrease alcohol consumption may also be helpful.7


Dry eye


  1. Lin MC, Asbell PA, Margolis T, et al. Dry Eye Disease. Optometry and Vision Science, 2015.
  2. Akowuah PK, Kobia-Acquah E. Prevalence of Dry Eye Disease in Africa: A Systematic Review and Meta-analysis. Optom Vis Sci, 2020.
  3. Golden MI, Meyer JJ, Patel BC. Dry Eye Syndrome. [Updated 2022 Jun 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
  4. Craig  JP, Nichols  KK, Akpek  EK, et al. TFOS DEWS II definition, and classification report.   Ocul Surf, 2017.
  5. Nichols KK, Foulks GN, Bron AJ, et al. The International Workshop on Meibomian Gland Dysfunction: Executive Summary. IVOS, 2011
  6. Van Setten G, Labetoulle M, Baudouin C, et al. Evidence of seasonality and effects of psychrometry in dry eye disease. Acta Ophthalmalogica, 2016.
  7. Engler D and Abraham V. Dry eyes. S Afr Pharm J, 2019.
  8. Guo OD LW, Akpek E. The negative effects of dry eye disease on quality of life and visual function. Turk J Med Sci. 2020.
  9. Shen LB, Toyos M, Karpecki P, et al. Selective Pharmacologic Therapies for Dry Eye Disease Treatment: Efficacy, Tolerability, and Safety Data Review from Preclinical Studies and Pivotal Trials. Ophthalmol Ther, 2022.
  10. Basma HBM, El-Hamid NA, Fathalla HD, et al. Current trends in pharmaceutical treatment of dry eye disease: A review. European Journal of Pharmaceutical Sciences, 2022.
  11. Srinivasan S, Manoj V. A Decade of Effective Dry Eye Disease Management with Systane Ultra (Polyethylene Glycol/Propylene Glycol with Hydroxypropyl Guar) Lubricant Eye Drops. Clin Ophthalmol, 2021.
  12. Gokul A, Wang MTM, Craig JP. Tear lipid supplement prophylaxis against dry eye in adverse environments. Cont Lens Anterior Eye, 2018.
  13. Kwak DH. Mixed DED: A Chimera in Your Chair. What is it and how can you diagnose and manage patients who have it? Review of Optometry, 2018.

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