At the completion of this article, the reader will be able to improve their management of dry eye disease and co-morbidities, including:
- Recall the pathophysiology of dry eye disease
- Recall the mechanism of action of the various dry eye treatment options
- Identify the causes of a patient’s symptoms of dry eye
- Implement effective management strategies for DED and co-morbidities.
Alissa Maillet
BOptom BSc(Hons) GCHETL FHEA
Lecturer in Optometry and Vision Science
Optometrist and contact lens practitioner
PhD candidate, Deakin University School of Medicine, Faculty of Health
Effective dry eye management relies on accurate identification of co-existing factors and implementing a patient-centred management plan. ALISSA MAILLET offers an up-to-date survey of the treatment considerations when dealing with co-morbidities.
Dry eye disease (DED) is a highly prevalent ocular disorder with significant effects on patient quality of life. In Australia, the prevalence of DED is reported to be in the range of 5-15% of the population.1 The condition is characterised by both patient-reported symptoms and clinical signs, resulting from inflammatory changes to the tear secreting glands and ocular surface causing a loss of tear film homeostasis. DED is chronic and worsening in nature due to the vicious cycle of inflammation impacting on tear film dynamics, with poor tear quality causing further inflammation.
The clinical presentation of DED varies greatly from patient-to-patient, but commonly involves symptoms of dryness, burning, stinging, with or without foreign body sensation.
Patient impact
In addition to the symptoms of ocular discomfort experienced in DED, since the tear film carries important optical characteristics, tear film instability has a significant impact on the vision. Light scattering, glare, photophobia, and loss of contrast sensitivity all contribute to difficulties with aspects of vision, colour perception, social functioning, and driving which can lead to a reduction in vision- and health-related quality-of-life (QoL).2
The impact of the disease has been shown to have a significant effect on the ability to conduct activities of daily living, and the symptoms and ocular pain experienced lead to feelings of frustration, depression, and anxiety. Additionally, the time and energy required to manage and treat the condition can be stressful and overwhelming, further contributing to mental health issues.
Risk factors
Evidence from large clinical trials indicates that the risk of disease increases with age and for female gender as tear production decreases with ageing and hormonal changes. Screen-based near work and contact lens wear are also shown to increase the prevalence of dry eye symptomatology especially in younger age populations.3
Health-related associations
Many common chronic health conditions have associations with DED. Autoimmune conditions such as Sjogren’s syndrome, rheumatoid arthritis, lupus, sarcoidosis, and immune disorders such as diabetes and thyroid dysfunction cause decreased tear production via interrupted metabolic activity of the lacrimal and meibomian glands and corneal nerve damage.4
Asthma and atopic disease both predispose to DED via increased presence of inflammatory cytokines and cells on the ocular surface.5 Recent studies have also suggested that affective disorders such as anxiety and depression and chronic pain conditions such as irritable bowel syndrome and fibromyalgia are linked to DED symptomatology, with both cause-and-effect relationships being found.6
Further, medications commonly taken on a regular basis by these at-risk populations such as antihistamines, antidepressants, hormone replacement therapy, and blood pressure medications further exacerbate the symptoms of dry eye.7
Ocular co-morbidities
Anterior blepharitis, meibomian gland dysfunction, and Demodex infection exist as co-morbidities with DED. In anterior blepharitis, the sebaceous glands secrete too much oil causing increased shedding of skin cells, which in turn provides a commensal environment for bacteria.
The progressive biofilm maturation along eye lid margin or the presence of Demodex mites results in increased inflammation and lipase activity which changes the composition of meibum. Thickened meibomian gland secretion eventually leads to obstruction of the meibomian glands, keratinisation of ductal system, meibum stasis and eventual gland atrophy.
Effective management strategies
Historically, and generally (even today) the management of DED has been relatively conservative and has focused on treating symptoms, with little regard to classification, the underlying causes and correlates of the disease.
The underlying principles for effective dry eye disease management are: 1) treating the contributing eyelid or ocular surface inflammation; 2) conserving tears; and 3) improving tear quality and production.
Reducing ocular surface inflammation
Both pharmacological and non-pharmacological interventions can be used to break the ‘vicious cycle’ of inflammation associated with DED. Topical steroids are used as short-term treatment courses initially of two to six weeks to interrupt the inflammatory cycle when and when flare-ups occur.
Longer term inflammatory control can be achieved by using topical immunomodulators such as cyclosporine A and lifitegrast or oral tetracyclines. Cyclosporine A is especially indicated when treating dry eye patients with associated autoimmune disease. Co-existing allergy should be controlled and treated with topical antihistamines or mast cell stabilisers in preference to oral antihistamines where possible.
Lid cleansing products
The removal of lid debris and scurf generated in anterior blepharitis to reduce bioburden, and Demodex mites is necessary to control eyelid inflammation. Historically, practitioners have recommended diluted baby shampoo as lid cleansing product; however, baby shampoo may have a detrimental effect on meibomian glands and goblet cell health. Greater reduction in symptomatology can achieved with dedicated eyelid hygiene product, specifically those containing anti-microbial agents such as tea tree oil, terpinen-4-ol, 0.1% hypochlorous acid (HOCl) or okra polysaccharide complexes. All products are shown to have similar efficacy but HOCl and okra are less toxic to ocular surface, which can lead to greater compliance because they are more comfortable for the patient to use.
Eyelid exfoliation
Lid scrubs only achieve eyelid cleaning. That said, multiple studies suggest that in-office eyelid exfoliation treatment combined with eyelid hygiene is more effective than lid scrubs alone.8 The aim of in-office treatment is the reduction of lid margin bioburden and debris, epithelial keratinisation, and meibomian gland capping.
Eyelid debridement-scaling (LDS) using a golf spud or purpose-designed debrider involves physical removal of mucous, hyper-keratinised tissue at the mucocutaneous junction, and meibomian gland blockages from the lid margin via physical scraping.
Microblepharoexfoliation (MBE), using instruments such as BlephEx, NuLids, or single-use Ocusoft SwabStix, uses detergent-based cleansers and friction to remove excess oils, scaling, and scurf from the lash line. MBE is better than LDS for decreased in bioburden and lipase activity, whereas LDS is better than MBE for improving MG expressibility.8 Where MGD and anterior blepharitis co-exist, LDS can be followed by MBE for maximum effectiveness.
Topical antibiotic and manuka honey ointments
Where recalcitrant anterior blepharitis is present, and eyelid inflammation is not adequately controlled by a combination of in-office lid treatment and home lid hygiene, topical antibiotic or manuka honey-based ointment can be used on the lid margin.9,10 A short course of topical antibiotics (at night for two weeks) is usually sufficient to break the acute inflammatory cycle, whereas manuka honey ointment can be used longer term (three months or ongoing).
Eyelid warming for MGD
Eyelid warming is a mainstay of treatment for MGD, used to soften or liquefy secretions in obstructed glands. For optimal effect, compresses should be heated to approximately 45°C and applied for five to 15 minutes. These conditions are difficult to achieve with hot towels, so heat-bead or electric warming eye masks, where temperature is easier to standardise and maintain, should be used in preference, and may result in greater patient compliance due to ease of use and reduced preparation.
Due to lack of uniformity of manufacture, consistent temperature and heating times are still difficult ensure, so patients who demonstrate low compliance or fail to achieve lasting improvement with self-treatment can be offered the option of undertaking treatment with in-office thermal systems (Blephasteam, LipiFlow, TearCare, iLux, etc.). In-office treatments have been shown to be more effective than home therapy, and symptomatic improvement may be maintained for up to nine months after treatment.11
Meibomian gland expression
In-office thermal treatments are shown to be most effective for treatment of MGD when followed by therapeutic expression of meibomian glands using a Mastrota paddle or forceps.
Clinical signs and patient symptoms (conjunctival injection, blink rate and Ocular Surface Disease Index (OSDI) Scores) can improve for up to two months after treatment, even when the quality of the expressed meibum is not visually changed, most likely due to the reduction in lipophilic bacteria concentrations in newly produced meibum.12
Intense pulsed light (IPL)
IPL treatment helps to improve tear composition and stability in patients with MGD. IPL utilises light in the visible spectrum to induce thermolysis of melanin and haemoglobin resulting in reduced inflammation and telangiectasia along the lid margin and improved cellular function of the meibomian glands. Additionally, heating of the meibomian glands, liquefication of meibum, and reduction of bacteria and Demodex mites that results from treatment is beneficial.13
Treatment involves the application of brief light pulses with a high-output flash lamp, through an interfacing gel, in a radial pattern under the inferior eyelids, across the nose, and to the temples. Typically, an initial treatment course of three to four sessions over a three-month period is recommended, with further treatments conducted as required for recalcitrant disease or maintenance.Further, IPL can be used to resolve acute chalazia when performed direct-to-lid with metal corneal shields.
Conserving tears
Evidence suggests that silicone punctal plugs could provide symptomatic relief in severe aqueous-deficient DED. Tear retention is achieved by blocking puncta with silicone or gel-like plugs or via a surgical procedure that can permanently close the tear ducts. For a less permanent solution, dissolving collagen plugs can be trialled to determine effectiveness of tear retention in improving symptoms and clinical signs.
However, caution should be used in the presence of ocular surface inflammation because, theoretically, occlusion of tear outflow could prolong the presence of pro-inflammatory cytokines on the ocular surface. Potential complications are spontaneous plug loss, epiphora, ocular irritation and foreign body sensation, as well as inflammatory effects to the tissue surrounding the plugs which can result in permanent change to the lid anatomy when they are left in long term.
Improving tear quality and production
Meta-analysis showed improvement tear stability and tear secretion (TBUT and Schirmer test) in DED patients taking omega-3 fatty acid supplements (EPA and DHA fatty acids).14 Omega-3 fatty acids act by improving the lipid profile of meibum which results in a more stable tear film; and contain anti-inflammatory lipids which reduce inflammation in the lacrimal gland allowing for increased tear production and reduced ocular surface inflammation. Additionally, evidence suggests that supplements containing flax seed oil (ALA fatty acids) in addition to fish oils, may also improve symptoms (reported by OSDI) in addition to clinical measures.
Artificial tear supplements
Ocular lubricants are the mainstay of DED therapy. They act to increase tear volume and stabilise tear film which reduces corneal epithelium/palpebral conjunctiva friction, replace deficient tear components, reduce tear hyperosmolarity, and dilute tear inflammatory cytokines.
Non-preserved lubricants should be chosen to avoid preservatives (especially BAK), and formulations should be specifically recommended to suit the patient’s requirements with respect to viscosity, osmolarity and constituents.
Biological tear supplements
Biological fluids applied to the anterior ocular surface as tear replacement have potential advantages over artificial tear supplements in that they serve as not only a lacrimal substitute for lubrication purposes, but also contain other bioactive agents that mimic natural tears more closely and may promote healthy cell growth and healing of the ocular surface.
Autologous serum (AS) is blood serum purified from patient then diluted with saline (20% concentration most common) which can be accessed through ophthalmologist referral and subsidised by Medicare. The greatest effect is shown within the first three months of treatment; however, some patients report ongoing preference for AS over artificial tear supplements.
Conclusion
The historical approach of ocular lubricants and hot towel compresses is neither sufficient nor acceptable practice where so much evidence for the effectiveness of further management strategies exists.
Patients with DED should be reviewed monthly during initial treatment until significant improvement of signs and symptoms is achieved, then less frequently as the patient becomes comfortable and compliant with ongoing home therapy.
With so many people affected by DED, implementing effective management strategies and education in our practices gives the opportunity to increase patient satisfaction, loyalty and create word-of-mouth referrals to increase business and revenue.
More reading
IPL: A paradigm shift in the treatment of dry eye disease
Harnessing the benefits of hyaluronic acid in lubricating eye drops
Changes in cataract surgery, patient expectations and collaborative care
References
- Chia EM, Mitchell P, Rochtchina E, Lee AJ, Maroun R, Wang JJ. Prevalence and associations of dry eye syndrome in an older population: the Blue Mountains Eye Study. Clin Exp Ophthalmol. 2003; 31 (3): 229-32.
- Sayegh RR, Yu Y, Farrar JT, Kuklinski EJ, Shtein RM, Asbell PA, et al. Ocular Discomfort and Quality of Life Among Patients in the Dry Eye Assessment and Management Study. Cornea. 2021; 40 (7): 869-76.
- Qian L, Wei W. Identified risk factors for dry eye syndrome: A systematic review and meta-analysis. PLoS One. 2022; 17 (8): e0271267.
- Tang YL, Cheng YL, Ren YP, Yu XN, Shentu XC. Metabolic syndrome risk factors and dry eye syndrome: a Meta-analysis. Int J Ophthalmol. 2016; 9 (7): 1038-45.
- Woo YR, Cho M, Ju HJ, Bae JM, Cho SH, Lee JD, et al. Ocular Comorbidities in Rosacea: A Case-Control Study Based on Seven Institutions. J Clin Med. 2021; 10 (13).
- Labbe A, Wang YX, Jie Y, Baudouin C, Jonas JB, Xu L. Dry eye disease, dry eye symptoms and depression: the Beijing Eye Study. British Journal of Ophthalmology. 2013; 97 (11): 1399.
- Bielory L. Ocular toxicity of systemic asthma and allergy treatments. Curr Allergy Asthma Rep. 2006; 6 (4): 299-305.
- Ballesteros-Sánchez A, Gargallo-Martínez B, Gutiérrez-Ortega R, Sánchez-González JM. Eyelid Exfoliation Treatment Efficacy and Safety in Dry Eye Disease, Blepharitis, and Contact Lens Discomfort Patients: A Systematic Review. Asia Pac J Ophthalmol (Phila). 2023; 12 (3): 315-325.
- Vernhardsdottir RR, Magno MS, Hynnekleiv L, Lagali N, Dartt DA, Vehof J, et al. Antibiotic treatment for dry eye disease related to meibomian gland dysfunction and blepharitis – A review. The ocular surface. 2022; 26: 211-21.
- Craig JP, Cruzat A, Cheung IMY, Watters GA, Wang MTM. Randomized masked trial of the clinical efficacy of MGO Manuka Honey microemulsion eye cream for the treatment of blepharitis. The ocular surface. 2020; 18 (1): 170-7.
- Beining MW, Magnø MS, Moschowits E, Olafsson J, Vehof J, Dartt DA, et al. In-office thermal systems for the treatment of dry eye disease. Survey of ophthalmology. 2022; 67 (5): 1405-18.
- Kaiserman I, Rabina G, Mimouni M, Sadi Optom NB, Duvdevan N, Levartovsky S, et al. The Effect of Therapeutic Meibomian Glands Expression on Evaporative Dry Eye: A Prospective Randomized Controlled Trial. Current eye research. 2021; 46 (2): 195-201.
- Albietz JM, Schmid KL. Intense pulsed light treatment and meibomian gland expression for moderate to advanced meibomian gland dysfunction. CXO. 2018; 101 (1): 23-33.
- Giannaccare G, Pellegrini M, Sebastiani S, Bernabei F, Roda M, Taroni L, et al. Efficacy of Omega-3 Fatty Acid Supplementation for Treatment of Dry Eye Disease: A Meta-Analysis of Randomized Clinical Trials. Cornea. 2019; 38 (5): 565-73.