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Guide to diagnosis and management of dry eye

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Dr Ben Ashby
BOptom (Hons) PhD GradCertOcTher
Associate lecturer, School of Optometry and Vision Science, University of New South Wales

 

The International Dry Eye WorkShop (DEWS)1-4 is the definitive compilation of the epidemiology, diagnosis and management of dry eye disease. DEWS is an evidence-based summation produced by the collaboration of 70 luminaries in dry eye disease from academia, clinical practice and industry. This article is a summary of the key points from DEWS that can be applied in the optometric management of dry eye disease in a standard clinical setting.

Dry eye disease is defined by DEWS as ‘a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface.’ This evolving definition makes an important link with symptomology and identifies dry eye disease as an inflammatory condition driven primarily by a salty tear film.

DEWS adopts a triple classification system for dry eye disease that considers the aetiology, mechanism and severity. ‘Aqueous-deficient’ and ‘evaporative’ are the two aetiological groupings. Aqueous-deficient may then be further classed as Sjögren or non-Sjögren with the latter including lacrimal deficiency, lacrimal duct obstruction and reflex block. Evaporative causes are divided into ‘intrinsic’ and ‘extrinsic’.

Intrinsic sources originate from the lid as in meibomian gland dysfunction (MGD) and exposure while extrinsic causes are at the ocular surface such as contact lenses, preservatives, allergy and vitamin A deficiency. Aetiology also includes ‘internal’ and ‘external’ risk factors.

Internal risks refer to the physiological conditions of low blink rate, wide lid aperture, ageing, low androgen levels and systemic drugs while the external group are environmental triggers including low relative humidity, high air flow and occupational environment. Classification by mechanism identifies if the problem begins with tear hyperosmolarity or tear film instability. It is hypothesised that instability is only the initiating cause when extrinsic factors are involved.

Classification

The severity classification of dry eye disease has four increasing levels. To stage the severity of dry eye disease, use the highest grade in which at least one sign and one symptom fall (Table 1). DEWS then links the severity of dry eye disease directly to treatment recommendations.

TABLE 1

Table 1. DEWS dry eye severity classification

Level 1

A staged hierarchy of interventions is recommended by DEWS whereby management begins with level 1 treatment options and then progresses to the next level if control is inadequate with those measures. However, the authors do point out that this approach should be modified to account for individual patient profiles and clinical experience. Therapy for MGD is integral to effective dry eye disease control for many patients. It is recommended practitioners refer to the International MGD WorkShop for management of this condition.5

Key environmental strategies recommended to minimise dry eye disease include avoiding air conditioner drafts, humidifying the surroundings and good visual hygiene with visual display units positioned below eye level to reduce the interpalpebral aperture plus regular breaks from near tasks.

Our understanding of nutritional factors continues to evolve6 but it seems a low dietary intake of omega-3 fatty acids is associated with a higher prevalence of dry eye disease7 although supplementation with 7 g/day of fish oil is observed to provide only a small improvement after 12 weeks.8 Common oral medications that have been identified to contribute to dry eye disease include antihistamines, antidepressants, hormone replacement therapy, beta-blockers, vitamin A, diuretics and antispasmodics.

When frequent administration of a lubricant is required, the most important feature of the formulation is that it is non-preserved, with a rapidly degraded preservative the next best option, to avoid preservative toxicity that will exacerbate the inflammation. Other beneficial qualities in lubricants include the presence of bicarbonate to promote restoration of epithelial barrier function, a physiological potassium concentration to maintain corneal hydration and hypotonicity to promote goblet cell growth and reverse the hyperosmotic DED tear profile. Increasing viscosity may be of benefit to improve contact time; however, this needs to be weighed against reduced vision and retention of inflammatory mediators. When MGD is present, a formulation with lipid can reduce the evaporative component of the dry eye disease.

Levels 2 and above

For dry eye disease of stage 2 and above, anti-inflammatories are likely to form part of the management. High quality evidence supports the efficacy of a course of a non-preserved surface steroid, that is: minims prednisolone sodium phosphate 0.5% four drops/day.

Oral tetracyclines may also be of benefit, particularly in the presence of MGD, due to their anti-inflammatory, anti-microbial and anti-apoptotic properties. Doxycycline is the current drug of choice given at 50-100 mg once or twice per day although the potential dose-dependent side-effects of gastrointestinal upset, photosensitisation, headache and candidiasis should be considered. Cyclosporine-A is an inhibitor of T-cell activation and is also well supported for use in dry eye disease with increased aqueous production and increased goblet cell numbers reported. This medication has a slow onset with a dosage of 0.05% twice per day for a month required to begin to have an effect that then increases over six months, with burning commonly reported during the early stages of treatment.9 In Australia, this drug must be either compounded or imported as Restasis through the Special Access Scheme.

DEWS II is currently in the planning and fund-raising phase. It is expected this will be an update on dry eye disease epidemiology, classification and management based on research published since the release of the original DEWS in 2007.

Those interested in following the progress of this highly-anticipated workshop can do so at the Tear Film and Ocular Surface Society website www.tearfilm.org/.

 

  1. Management and therapy of dry eye disease: report of the Management and Therapy Subcommittee of the International Dry Eye WorkShop. Ocul Surf 2007; 5: 2: 163-178.
  2. Methodologies to diagnose and monitor dry eye disease: report of the Diagnostic Methodology Subcommittee of the International Dry Eye WorkShop. Ocul Surf 2007; 5: 2: 1081-52.
  3. The epidemiology of dry eye disease: report of the Epidemiology Subcommittee of the International Dry Eye WorkShop. Ocul Surf 2007; 5: 2: 93-107.
  4. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop. Ocul Surf 2007; 5: 2: 75-92.
  5. Geerling G et al. The international workshop on meibomian gland dysfunction: report of the subcommittee on management and treatment of meibomian gland dysfunction. Invest Ophthalmol Vis Sci 2011; 52: 4: 2050-2064.
  6. Jalbert I. Diet, nutraceuticals and the tear film. Exp Eye Res 2013; 117: 138-146.
  7. Miljanovic B et al. Relation between dietary n-3 and n-6 fatty acids and clinically diagnosed dry eye syndrome in women. Am J Clin Nutr 2005; 82: 4: 887-893.
  8. Kawakita T et al. Effects of dietary supplementation with fish oil on dry eye syndrome subjects: randomized controlled trial. Biomed Res 2013; 34: 5: 215-220.
  9. Kymionis GD et al. Treatment of chronic dry eye: focus on cyclosporine. Clin Ophthalmol 2008; 2: 4: 829-836.


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