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UNSW SOVS Alumni evening: Dry Eye

31/10/2018By Lewis Williams PhD
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Earlier this year, UNSW’s School of Optometry and Vision Science (SOVS) held a special dry eye evening for its alumni. LEWIS WILLIAMS was on hand to record the latest updates from some of the world’s foremost dry eye experts.

Dry Eye (DE) is a topic that has gained great significance in UNSW’s School of Optometry and Vision Science (SOVS). The school has recently established a specialty Dry Eye Clinic, while eight staff members were on one or more Tear Film and Ocular Surface Society (TFOS) committees responsible for the release of its DEWS II series (Dry Eye Workshops II) of reports. All presenters were DEWS II committee members.

DEWS II

Professor Fiona Stapleton, SOVS’ outgoing Head of School and a member of more than one DEWS II committee – including chair of the epidemiology subcommittee – delivered an overview of last year’s report.

According to Stapleton, DEWS II set out to use an evidence base for its outcomes and tried to reuse as much of the earlier DEWS I output (2007) as was compatible with the group’s new positions.

New to DEWS II reports were the inclusion of neurological aspects of the disease, a broader, more encompassing definition of the disease, the inclusion of ‘normal’ in the spectrum of DE, and an attempt at preventative management. The new definition of DE embraces its multifactorial ocular surface disease nature, characterised by a loss of homeostasis of the tear film.

Included in signs are tear film instability and hyperosmolality, ocular surface inflammation and resulting damage, and neurosensory abnormalities. The latter is believed to play an aetiological role. Sjögren’s syndrome and other overlapping conditions are treated separately.

Importantly, all forms of DE are now presented as being part of a continuum of disease ranging from normal through aqueous-deficient, a mixture of aqueous-deficient and evaporative, to evaporative DE.

A problem identified with previous DE prevalence data relates to the variable criteria used to define DE, i.e., signs, symptoms, or both. DE is 1.9x more likely in females, twice as likely in Asians, and up to 15% of people aged 40 years or older are found to suffer from the disease.

While symptoms are equally likely to be reported by Asians and others, DE signs are 2.2x more likely to be seen in Asians. As people age, the prevalence of DE is likely to increase by 2–3% per decade. By way of contrast, there are smaller differences between the sexes in MGD.

Risk factors were assessed and divided along modifiable (e.g., lifestyle, diet, environment) and non-modifiable (e.g., sex, age, race) factors. DEWS II also identified the need for hypothesis-driven studies.

KEYNOTE SPEAKERS

Fiona Stapleton

Maria Markoulli

Blanka Golebiowski

Mark Willcox

Isabelle Jalbert

Eric Papas

A vicious circle

SOVS senior lecturer Dr Maria Markoulli provided a brief rundown on the pathophysiology and iatrogenic causes of DE. She described DE disease as a result of a vicious circle (illustrated above) between aqueous-deficient DE and evaporative DE, both contributing to tear film hyperosmolality, ocular surface stress, and lowered tear flow. The latter leads to further tear film hyperosmolality and around it goes.

MGD and chronic diffuse abnormalities of the meibomian glands were covered in a separate report, but keratinising of the gland duct orifices, continued secretions by meibocytes into the acini that feed into the ducts, and the resulting backpressure are factors that lead to meibomian gland dropouts.

It’s now accepted that gland dropouts result in reduced meibum products and an abnormal tear film.

Iatrogenic factors such as surgery and drugs, and subsequent possible allergic, toxic, immunological, and inflammatory consequences of their use have DE relevance. CL-induced DE also fits into this category.

CLs thin the tear film’s lipid layer, increase tear film instability, and decrease the basal tear volume. Corneal surgery including LASIK also induces DE, with some 50% of patients reporting DE at 1 week, 40% at 4 weeks, and 20–40% still reporting DE at 6 months. Other ocular surgery such as conjunctival, glaucoma, vitreoretinal, and strabismus can also be accompanied by complaints of DE.

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Sex, gender and hormones

SOVS staff member Dr Blanka Golebiowski presented details of the effects of sex, gender and hormones, and confirmed that being female is a significant DE risk factor.

In the case of Sjögren’s syndrome, the female/male ratio currently runs 9:1. There are also many other conditions that have significant differences between the sexes, mostly disadvantaging females.

In females, it has been shown that androgen has an overall positive effect on tear production, but the roles of progesterone and oestrogen are less clear, and appear to be dosage and target tissue-dependent. Ocular surface and adnexa regulation are also factors.

Other largely female issues are cosmetics applied on and near the eye, and the effects of ageing.

The related issues of ageing and pathology (ocular and other) present challenges and it can be difficult to tease-out and differentiate the contributions of each to a particular clinical presentation.

Tear film

The vicious circle of dry eye disease
The vicious circle of dry eye disease

Professor Mark Willcox spoke about tear film (TF) lipids and proteins. It’s been demonstrated that the TF’s lipid layer enhances TF stability and that disturbances of the lipid layer decreases TF stability and increases TF break-up (lower TBUT).

Willcox noted that laboratory studies (in vitro) have failed to confirm the long-held belief that the lipid layer played a significant anti-evaporative role in TF maintenance, but they did confirm that both the TF lipid and mucin components have central roles in TF stability. Polar lipids enhance the spreading and stability of the tears.

Despite their role in TF stability, mucins can also disrupt the TF suggesting their effects are complex. Research is ongoing to study protein biomarkers in the tears and what role(s) they might play in aqueous-deficient DE, MGD, Sjögren’s syndrome DE, blepharitis, and CL-related DE.

Diagnosis

Dr Isabelle Jalbert tackled the diagnosis of DE, noting from the outset that there was no single gold standard available. Jalbert advised that the first step to reducing diagnostic errors was to eliminate co-morbidities, especially keratitis, blepharitis, Sjögren’s syndrome, CL DE, and allergy.

Part of diagnosing DE is the assessment of its signs and symptoms, a known grey area for clinicians because of their seemingly disconnected or complex relationship. Compounding that difficulty are issues such as corneal staining, a sign that can be caused by many factors.

Attributing ‘blame’ is difficult or impossible. Questionnaires such as OSDI or DEQ-5 have validated utility but are probably seldom used outside research laboratories or specialised DE clinics. Jalbert summarised the key issues when diagnosing DE as non-invasive BUT of <10 seconds, a tear osmolality of 308 mOsm/L or more (mild to moderate DE) or 316 mOsm/L or more (moderate to severe DE).

She recommended lissamine green vital stain when assessing the cornea, conjunctiva, the lid wiper and Marx’s line. Tear prism height is an indirect analogue of tear volume, but it can be difficult to measure

Treatment

It was left to SOVS’s Professor Eric Papas to tackle the DE treatment issue. Overall, his recommendation was to take a staged approach based on the severity of DE.

 


 

Stage 1:

  • Educate
  • Change environment(s)
  • Modify diet (increase omega-3 intake) and monitor water intake
  • Alter external factors, e.g., medications
  • Use ocular lubricants (tear replacement and lipid supplementation)
  • Initiate lid hygiene measures including lid warming.

Stage 2:

  • Unpreserved ocular lubricant
  • Demodex sp. treatment
  • Tear conservation (punctal occlusion [plugs], moisture chambers)
  • Tear stimulation (using the nasal mucosa – not yet available in Australia)
  • In-office MGD treatment, e.g., LipiFlow, IPL, manual expression
  • Prescription drugs – topical and/or oral

Stage 3:

  • Oral secretagogues, e.g., pilocarpine
  • Autologous/allogenic serum eye drops
  • Bandage SCLs
  • Rigid scleral/miniscleral CLs

Stage 4:

  • Topical steroids
  • Surgical punctal occlusion

 


 

Other possible aids include Manuka honey (medical grade, hyperosmotic, used as a post-meibomian gland-expression therapy), meibomian gland ‘milking’, and hydration therapy.

Counterintuitively, it was reported that oestrogen therapy and HRT make DE worse, leading to a double whammy for menopausal/post-menopausal women on oestrogen therapy or HRT. Furthermore, fish oil capsules were reported to be inferior to eating the real thing, olive oil was described as ‘problematic’, and the Mediterranean diet was still supported by science.

Examining the lid wiper, and staining and assessing Marx’s line subsequently, were also recommended clinical procedures. Post gland-expression treatments (in addition to Manuka honey) included ocular lubricants and TF lipid enhancers.

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