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Dry Eye Disease: Diagnosis and Treatment Algorithms

2T in Autralia | 2CD in New Zealand | 8 December 2018



Dry Eye Disease is increasing in awareness in both patients and healthcare professionals. Increased awareness combined with an increasing prevalence is forcing eyecare professionals to take a more proactive approach to the investigation and treatment of dry eye disease. Colette Parkinson, consultant to the Dry Eye Institute in Sydney, has written this article to provide you with a systematic approach to the diagnosis and management of dry eye disease with a focus on meibomian gland dysfunction. Understand which tests to conduct and how to use specific test results to build a specific treatment plan for your patients. Learn how to look for non-obvious meibomian gland dysfunction and how to use the full scope of lisamine green staining for a comprehensive dry eye investigation. Understand the importance of conducting a blink assessment and screening for poor lid seal. Review the role that inflammation plays in the vicious cycle of dry eye disease and how to incorporate inflammation management into your dry eye treatment plans. Review both high and low technology diagnosis and treatment options, including blinking exercises, omega3 supplements, BlephEX, IPL and LipiFLow, and understand how to combine treatments for optimal patient outcomes. Read the article and take the online MCQ test to build your confidence in developing protocols for dry eye management suitable for your clinic.

1. Understand what tests should be used to screen for and investigate dry eye disease and how to interpret the results
2. Review the various uses for lisamine green in the diagnosis of dry eye disease
3. Understand the role that inflammation plays in dry eye disease and how to manage this
4. Review the pathophysiology of dry eye disease
5. Review the mechanism of action of the various dry eye treatment options
6. Review the anatomy of the meibomian glands and how this relates to meibomian gland dysfunction.

Almost a quarter of patients have dry eye disease, yet few optometrists routinely screen for this debilitating condition. When this disease is identified, first line treatment is typically artificial tears, yet 32 per cent of patients who use these lubricants alone will experience dry eye disease progression at 12 months. So, where do you go from there?

Currently there are multiple progressive ocular diseases that optometrists routinely screen for in every eye examination. Some are symptomatic diseases, like macular degeneration and cataracts, while others are asymptomatic like glaucoma, retinal pigment epithelial lesions, and various retinopathies. It is commonly accepted that dry eye disease is a chronic progressive condition,1 yet screening, diagnosis, proactive and prophylactic treatment is not the standard of care in most optometry clinics. Many optometrists still rely on patient symptoms to initiate investigation and treatment, however dry eye disease has been shown to be present in 24.1 per cent of asymptomatic patients over the age of 40.2 Furthermore, first line treatment for many clinicians is artificial tears, however, even with compliant use of artificial tears, 32 per cent of patients who use lubricants alone will experience dry eye disease progression at 12 months.3

Like all chronic progressive diseases, taking the time to understand the pathophysiology of dry eye disease can help establish logical and systematic diagnosis and treatment protocols. The Tear Film and Ocular Surface Society (TFOS) DEWSII report describes the pathophysiology of dry eye disease as water loss from the ocular surface (tear film instability) causing hyperosmolar tissue damage. This damage occurs either directly from or by inducing inflammation, which causes loss of both epithelial and goblet cells. This cell loss decreases the wettability of the ocular surface, further increasing tear instability and osmolality, and the subsequent inflammatory vicious cycle that follows.1 Based on this definition, dry eye treatment protocols need to focus on improving the tear osmolarity and reducing inflammation.

Traditionally, optometrists have focussed on trying to make a diagnosis of either aqueous deficiency or evaporative dry eye and then, based on this diagnosis, have attempted to either improve meibomian
gland function or bulk up the tear volume. In a population of patients with dry eye disease, Lemp and colleagues found 14 per cent to have aqueous deficiency only, 50 per cent to have evaporative only and
35 per cent to have mixed.4 This can also be viewed as 50 per cent of patients to have an aqueous deficiency component and 86 per cent an evaporative component to their dry eye disease.4 Inflammation plays a significant role in both of these conditions and therefore, diagnosing and managing inflammation will almost always play a role in any dry eye disease protocol.

In aqueous deficient dry eye disease, inflammation may be the primary cause of lacrimal gland dysfunction, which then results in decreased tear production and subsequent hyperosmolar tears, causing more inflammation. Alternatively, lacrimal gland dysfunction may be caused by other factors like androgen deficiency, auto-immune disease, or medication. This decreases tear production followed by tear film hyperosmolarity, ocular inflammation, and augmentation of the vicious cycle.1

Evaporative dry eye is the result of meibomian gland dysfunction (MGD). MGD is the abnormal regulation of keratin metabolism within the meibomian glands.5 This abnormal regulation may be the result of age, androgen deficiency, autoimmune disease, rosacea, infection, poor lid hygiene, poor blinking, contact lens wear, poor diet, or medication. Abnormal keratin will eventually occlude the lumen and orifices, this increases the pressure within the ductal system causing dilation and eventually atrophic degeneration of the secretory acini.5 Inflammation may be a direct cause of hyperkeratinisation, it may be secondary to the increased pressure within the ductal system following obstruction, or it may be secondary to the hyperosmolarity that results from increased evaporation of tears. Like in aqueous deficiency, inflammation is a key contributor to the vicious cycle of evaporative dry eye disease.


Investigation of dry eye disease should be focussed on looking for the hall marks of the disease as well as early signs and risk factors. While symptoms should be evaluated, they do not always correlate with disease severity and can provide false negative results if used in isolation for diagnosis. Using quantitative assessments like the Standardised Patient Evaluation of Eye Dryness (SPEED) or Ocular Surface Disease Index (ODSI) are highly recommended. SPEED tends to be more effective at identifying and monitoring treatment for evaporative dry eye and ODSI for auto-immune related dry eye disease. Due to the differences between the tests, some practitioners may elect to perform both.

According to the definition of dry eye disease in the DEWSII report, investigation should look for  hyperosmolarity, tissue damage, and inflammation. Hyperosmolarity can be measured using devices like Tear Lab. A reading of above 308 mOsms/L is indicative of dry eye disease. The higher the osmolarity reading the more severe the disease. Osmolarity has been shown to have 75 per cent sensitivity in mild/moderate disease; and 95 per cent sensitivity in severe disease.6

Tissue damage is best assessed using lissamine green and fluorescein. Lissamine green stains dead and degenerate cells but will not stain healthy epithelial cells.7 Different lissamine green conjunctival staining patterns can indicate the progression of dry eye severity levels. Nasal only staining correlates with mild dry eye disease, both nasal and temporal staining indicates moderate disease and finally, severe cases will have corneal staining present as well.8 Fluorescein stains damaged tissue or pools in corneal defects where cell to cell junctions are compromised – it does not detect dead cells. Although fluorescein staining does not correlate directly with dry eye disease like lissamine green does, it is still helpful to assess for corneal punctate erosions, especially in contact lens wearers, and to assess for epithelial basement membrane dystrophy (EBMD). EBMD is prevalent in approximately 2 per cent to 6 per cent of patients.8 It presents as raised dots, maps, and fingerprints, which negatively stain. The elevations of the ocular surface associated with EBMD will show an immediate tear film break-up over the corresponding area. This differs from dry eye syndrome, which typically shows a delay in tear break-up.8

Inflammation can be diagnosed with simple observation, however not all patients will present with obvious signs of inflammation. In the absence of obvious signs InflammaDRY can be used as a diagnostic test. InflammaDRY takes a sample of tears from the palpebral conjunctiva and will produce a positive response if it detects 40 ng/mL or greater of matrix metalloprotease-9 (MMP-9). The test can also be used to assess the severity of inflammation, with the red positive line varying in intensity relative to the MMP-9 concentration. The test result can be graded as strong positive, positive, weak positive, trace, and negative. This test can be helpful to start the conversation with patients about the importance of managing inflammation in order to prevent disease. It may be used as an introduction to encourage diet changes or other lifestyle modifications in patients who are starting to show risk factors for dry eye but have not yet progressed into the vicious cycle of dry eye disease. For this reason, it is useful for both diagnosis and screening.


Designs for Vision; InflammaDRY



Assessing for the hallmark features of dry eye disease will help a practitioner produce an overarching diagnosis. Assessing the severity of these key features will provide a guide for how aggressive the patient’s management plan will need to be. In order to be able to provide an adequate management plan, a practitioner must be able to identify the underlying causes of tear film instability and inflammation. This requires assessment of medical, systemic or lifestyle risk factors, allergy, infection, MGD, and aqueous deficiency.

The list of medical, systemic, and lifestyle risk factors for dry eye is extensive. Medications may include betablockers, diuretics, anxiolytics, antidepressants, antipsychotics, antihistamines, decongestants, antispasmodics, narcotic analgesics, hormone therapies, incontinence medications, chemotherapy agents, and radiation.9 Systemic diseases include diabetes, thyroid dysfunction, hormone imbalances, and connective tissue disease including rheumatoid arthritis, sarcoidosis, Behcet’s disease, rosacea, and tuberculosis. Lifestyle risk factors include smoking, alcohol consumption, caffeine, computer use, make-up, and a high omega 6 diet. Management of these risk factors should be done in consultation with the patient’s general practitioner or specialist.

Facial rosacea is present in approximately 10 per cent of the adult population, with over 80 per cent of these patients suffering from concomitant MGD.14 Ocular rosacea precedes facial rosacea in 20 per cent of patients.14 More than 10 years ago, Rolando Toyos and colleagues who use the Lumenis M22 technology noticed that patients receiving IPL for facial rosacea also experienced dry eye disease symptom relief. Since then, the literature and use of IPL technology in dry eye disease has been rapidly increasing around the world. In Australia and New Zealand there are several technologies now available, however the Lumenis M22 is the only technology approved for the treatment of ocular rosacea. Ocular rosacea can be diagnosed using simple slit lamp observation of telangiectasia along the eyelid margins. These abnormal blood vessels release pro-inflammatory mediators throughout the orbital vasculature. The M22 treats rosacea via thrombosis/coagulation of abnormal facial blood vessels.

Testing for ocular allergy is an important part of the dry eye investigative process. TearScan can be used to measure both the presence and severity of allergy. TearScan measures the concentration of IgE in the tear film. Allergy is most commonly diagnosed following finding of both conjunctival papillae and symptoms of ocular itching. If allergy is diagnosed, treatment can be initiated with the use of antihistamines or mast-cell stabilisers. Patanol, which is available with a prescription, dosed twice daily, is highly effective at treating both the signs and symptoms of ocular allergy. Patients can continue Patanol for three months if required. If high levels of inflammation are present, a steroid such as FML or Flarex qid can be prescribed, which will address both the inflammation and allergic response.

Lumenis M22


Infection in dry eye disease will typically occur with blepharitis. The presence of blepharitis will almost always be associated with MGD and inflammation. Infection may be bacterial, demodex, or both. In all cases, debridement and mechanical cleaning of the eyelid surface with Blephex in office is recommended as a primary treatment with tea-tree oil based lid scrubs to be used daily at home. In both cases, debridement in office and at home will reduce the microbial load. The tea-tree oil will provide both antimicrobial and anti-inflammatory benefits. BlephEx is a small hand-held electronic debridement tool that can be purchased from Optimed.

The presence of cylindrical dandruff on the eyelashes is a sign that the patient has a demodex infection. In-office and home based treatments for blepharitis will only be effective against the mites present near the top of the gland. The mites deeper in the gland will continue to replicate and, in most cases, the signs and symptoms will eventually return. Demodex infection will likely require ongoing in-office Blephex treatments every three to six months. The removal of the demodex will help reduce the secondary inflammation that occurs as a result of the bacteria they release at the end of their lifecycle.

Optimed: BlephEx

Soap or foam in the tear film, especially if there is a history of styes or conjunctivitis, suggests that the patient has a bacterial infection. If a bacterial infection is suspected, a systemic antibiotic such as Doxycycline or Azithromycin, should be prescribed. These antibiotics are potent against gram-negative and gram-positive micro-organisms yet also have anti-inflammatory properties with the inhibition of pro-inflammatory cytokines, and have been shown to improve meibum quality. There is no universal standard, however Doxycycline 100mg twice daily for one month and Azithromycin 500mg stat and 250mg/d for four days, prescribed for the treatment for MGD, have been assessed in a randomised double-masked open-label clinical trial. Azithromycin was found to be more effective with 52 per cent of patients experiencing a clinical improvement at two months, compared to only 32 per cent of patients in the Doxycycline group. Only 6 per cent of patients in the Azithromycin group experienced side-effects, compared to 25 per cent with Doxycycline.10

An alternative treatment to oral antibiotics is Optimel, a Manuka honey-based eye drop which is available in a liquid (16 per cent Leptospermum species) and gel (98 per cent Leptospermum species) form. Optimel is distributed by Designs for Vision. Manuka honey has both antibacterial and anti-inflammatory properties. The mechanism of action is slightly different for different bacteria. For Staphylococcus Aureas it disrupts bacterial cell division15 whereas for Pseudomonas Aureginosa it inhibits flagellum production.16 The phenolic content provides anti-inflammatory properties by inhibition of the production of the inflammatory cytokine TNF-α.17 It is also believed that the hyperosmolarity of Optimel helps to draw meibum out of the glands. A study that evaluated the effectiveness of Optimel for the treatment of MGD found that both concentrations were effective at improving tear film break up time, corneal staining, tear osmolarity, meibum quality, bulbar, limbal and lid margin redness, as well as bacterial colony units. The gel was most effective at improving meibum quality and gland expressibility.18

Designs for Vision; Optimel


Diagnosis of meibomian gland dysfunction is a critical part of any dry eye evaluation and should be performed as a screening test as part of a routine eye examination. It is important to look for both obvious and non-obvious MGD (NOMGD). MGD is the abnormal regulation of keratin metabolism within the meibomian glands. Hyperkeratinisation eventually occludes the lumen and orifices, or the meibomian glands. Abnormal keratin metabolism can be assessed by grading the quality of the meibomian gland secretions.5 Healthy meibum should have the appearance of olive oil. Grading of meibum quality is typically done as clear, milky, toothpaste, or no secretions present. Obstruction of the glands can and should also be graded. The severity of this grading will decide what therapeutic and maintenance therapy is required. Many optometrists apply forced pressure to the eye lid margin and observe for secretions from the glands. The problem with this technique is that is does not correlate to the habitual environment of the patient. Day to day, the patient relies on from the glands. MGD assessment should therefore grade the number of glands producing liquid secretions under normal blinking conditions. Korb and Blackie noted that patients with less than six functional meibomian glands yielding liquid secretions were positive for dry eye symptoms.19

A meibomian gland Evalutor (MGE), designed by Donald Korb and sold by Johnson and Johnson, has been designed to exert the same amount of pressure as the blink (~1.25 g/mm2). The MGE is applied perpendicular to the lid margin and held in place for a few seconds. This is performed nasally, centrally, and temporally in both eyes. During each applanation, the number of glands producing secretions is noted along with the quality of the meibum. This will allow for approximately 15 glands in each eye to be evaluated. Treatment for MGD should be initiated if less than seven glands are yielding liquid secretions. Treatment should also be initiated if the quality of the meibum is classified as either milky, toothpaste, or no secretions present.

In addition to the use of an MGE, meibography is an extremely useful diagnostic tool. This is helpful to understand the current state of the disease, monitor progression, and help educate patients to your findings and why you are recommending a treatment plan. The use of meibography for the diagnosis and monitoring of MGD can be used, much like OCT imaging is in the management of glaucoma. There are a range of meibographers on the market. The better technologies use transillumination to gain higher quality images of the gland structures. The LipiView and LipiScan, previously from Johnson and Johnson, both use this technology.

Johnson & Johnson LipiView 2


Moderate MGD Atrophy (image supplied by Dry Eye Institute)


Well defined glads with upper truncation (image supplied by Dry Eye Institute)


Large scale drop out (image supplied by Dry Eye Institute)


Upper lid total atrophy, lower lid large scale atrophy - Severe (image supplied by Dry Eye Institute)


Johnson & Johnson; LipiScan

Another important diagnostic test for MGD is assessment of the patient’s blink quality and lid seal. The eyelid contains two muscles which surround the meibomian glands and contribute to normal gland function. The first is the Orbicularis muscle. This muscle surrounds the middle and lower areas of the meibomian glands. The second, and possibly the most important, is the Riolan muscle. This surrounds the superior part of the gland. In order to secrete meibum from the gland, this muscle needs to activate. The complete closure of the eyelids is required to activate this muscle. Poor blink quality and/or poor lid seal can lead to stagnation of the meibum within the glands, either directly causing or contributing to meibomian gland dysfunction. This can help to explain why we observe higher dry eye symptoms with screen use. Blink quality is assessed using a video camera. The footage can be slowed down and the number of incomplete blinks can be calculated as a percentage of total blinks in 30 seconds. There are plenty of options for recording patients blink quality, a high-tech option is the LipiView2 from Johnson & Johnson.

“Lagopthalmos” corneal staining (image supplied by Dry Eye Institute)

Blinking exercises should be prescribed to all patients who are displaying poor blink quality. Blinking exercises should be performed three times per day. Instruct the patient to gently close their eyes and then without scrunching their eyes, simply activate their eyelid muscles so they feel like they are forcing the superior and inferior eyelid margins to push against each other and hold this for two seconds. This should be repeated 10 times. It is also recommended to perform blinking exercises after the use of hot compresses.

Symptoms of dry eye upon waking should raise your suspicion of poor eye seal. Eye seal can be assessed using a transilluminator. Ask the patient to gently close their eyes as though they were sleeping. Apply the transilluminator to the superior eyelid and observe for light escaping between the eye-lashes. The amount of light can be graded from zero (complete lid seal) to three (excessive light seen). Eye-Eco Eye Seals, sold by Designs for Vision, can be provided to patients to wear at night while sleeping. These are highly effective and patients notice an instant relief in their symptoms.

Lisamine green staining is also helpful in the diagnosis and treatment of MGD. Lisamine green stains Marx line, which is visualised as a thin strip at the crest of the posterior lid border separating the keratinised cutaneous epithelium from the non-keratinised conjunctival epithelium.12 The position of Marx line is indicative of MGD13 and can be graded as:

0: entirely on the conjunctival side of the meibomian orifices (MOs);
1: part of ML touches the MOs;
2: ML runs through all of the MOs; and
3: ML runs on the eyelid-margin side of the MOs.13

As mentioned earlier, MGD is the abnormal regulation of keratin metabolism within the meibomian glands. Hyperkeratinisation eventually occludes the lumen and orifices of the meibomian glands. Ensuring the keratinised cutaneous epithelial cells do not make their way into the meibomian glands is an important part of your MGD management. If the position of Marx line is graded as one or above, then debridement of the eyelid margin is recommended.20 This can be performed using BlephEx or topical anaesthetic and a spud.

MGD Treatment Options

There are multiple options available for the treatment of MGD and the treatment of choice should be directly related to the clinical findings. Ocular rosacea, inflammation, and blepharitis management may be required. In most cases additional therapies will be required to increase the number of functional meibomian glands yielding liquid secretions. To achieve this, treatments must improve the regulation of keratin metabolism within the meibomian glands. Clearing of the hyperkeratinisation occluding the lumen and orifices of the meibomian glands is required to improve the regulation of keratin metabolism within the acini. The most effective way to achieve this is LipiFlow, initially designed by TearScience and recently acquired by Johnson & Johnson. LipiFlow is thermal pulsation technology, which heats both the inner and outer eyelids, combined with gentle massage. The treatment takes approximately 13 minutes and most patients find it very relaxing. Lipiflow will liquefy the meibum, completely draining the glands of stagnant meibum occlusions. The patient may feel worse for the initial one to two weeks as the glands start to upregulate their production of meibum. Supplementation with a lipid-based drop can help to manage symptoms during this initial time. Occasionally, a patient may require a mild steroid for additional relief. The regulation of keratin metabolism within the glands will take approximately six to12 weeks to normalise. Improvements in gland expressibility and meibum quality will continue over time with optimal levels seen at nine months post treatment. Studies have shown that LipiFlow improves meibomian gland secretions by three times 12 months post treatment, with symptoms decreasing by approximately 50 per cent.21 Gland secretion improvement can be sustained for three years post treatment22 and treatments in contact lens wearers can improve comfortable wearing time by four hours per day.23 For patients to support the long-term benefits of LipiFlow, hot compresses and omega3 supplements should be used as maintenance therapy.

LipiFlow, designed by TearScience and recently acquired by Johnson & Johnson

Hot compresses are a mainstream part of MGD treatment. Studies have shown that for hot compresses to be effective, the inner eyelid, where the meibomian glands are located, should be heated to 40 degrees Celsius and sustained for 10 minutes. This would require an external heating device to heat the outer eyelid to 45 degrees.24 In a study that evaluated 10 different hot compress techniques, the only device found to be effective was called the bundle method, which involves rolling or bundling several moist face cloths together and heating in the microwave.24 In general, hot compresses are not adequate to progress glands from not flowing to flowing. They can be very effective at maintaining flowing glands and therefore should be performed daily by all MGD patients in addition to other treatments. Patients should be encouraged to invest in a high quality hot compress mask that will maintain its temperate for at least 10 minutes. Eyelid massage following hot compresses is more or less discouraged due to the risk of corneal damage25 as well as damage to the delicate acini ducts. Blinking exercises following hot compresses should be recommended.


Diagnosis of aqueous deficiency requires assessment of tear volume. Tear meniscus height can be estimated with a slit lamp or measured using a tear film analyser or an optical coherence tomographer (OCT). A normal tear meniscus height is 300 microns. Abnormal lower tear meniscus height is <164 μm. This can be further supported using tests like Schirmer’s or Phenol Red Thread test. Schirmer’s test is considered normal if over 15mm of the strip is wet after five minutes, 7-14mm is borderline, 5-7mm is abnormal, and less than five is highly suspicious for Sjogrens syndrome. Using InflammaDRY to assess for inflammation is also useful as this will help guide treatment protocols.

Aqueous Deficiency Treatment Options

Treatment for aqueous deficiency should firstly consider any system associations as discussed previously. Artificial tears should be prescribed to increase tear film volume and reduce the osmolarity of the tear film. Punctal plugs can help to improve symptoms but should only be used if InflammaDRY is negative and osmolarity is normal. Amniotic membranes or bandage contact lenses should be considered if significant corneal staining is present. TruTear from Allergan, currently available in the United States, is a neurostimulator device for aqueous deficient patients. TruTear increases tear production by electrically stimulating the trigeminal nerve via the afferent ethmoid nerve in the nasal cavity. Omega3 supplements and management of inflammation with steroids or cyclosporin should also be incorporated into the treatment plan.

Plasma Rich in Growth Factors (PRGF) can be helpful for patients with aqueous deficient dry eye as well as those with significant corneal staining or recurrent corneal epithelial erosion. Currently the Dry Eye Institute in Sydney is the only facility in Australia and New Zealand to offer this technology. The patient has their blood drawn, which is placed into a centrifuge and activated with calcium to stabilise the platelets and release the growth factors. The benefit of this process, over autologous serum, is that neutrophils and leukocytes – known inflammatory mediators – are removed. The growth factor rich plasma is then removed and placed into vials which can be frozen and defrosted as required. Patients usually receive approximately three months of drops each time. PRGF supports tissue repair and reduces inflammation. In a study of 16 patients with moderate to severe dry eye unresponsive to other therapies, Autologous PRGF drops
resulted in improvement of symptoms as well as squamous cell metaplasia after three months.27

Management of inflammation is likely to play a significant role in the majority of patients with dry eye disease. Ocular surface stress causes the release of pro-inflammatory cytokines, Interleukin [IL]-1, IL-6, tumour necrosis factor-α, matrix metalloproteinases (MMP), and chemokines. These cytokines trigger an inflammatory cascade, which eventually leads to the production of CD4+ T helper cells in the lymph nodes, which migrate to the eye and secrete more pro-inflammatory cytokines including TNF-α. This causes goblet cell dysfunction28 and IL-17, which causes epithelial barrier disruption.29

Pre post PRGF Drops (image supplied by Dry Eye Institute)


2 month post PRGF drops (image supplied by Dry Eye Institute)


“Filamentary Keratiitis”: severe dry eye (image supplied by Dry Eye Institute)

Treatment options for inflammation will typically require either a steroid or cyclosporin supported by omega3 supplementation. Optimel and oral antibiotics may be sufficient in more mild cases where their use is also indicated by other clinical findings. PRGF may be required in more advanced cases.

Topical corticosteroids can be effective at breaking the vicious cycle. Corticosteroids suppress the inflammatory response associated with dry eye through inhibition of phospholipase A2, which forms the inflammatory mediators prostaglandins and leukotrienes. Steroids have been shown to be effective at reducing ocular surface staining and dry eye symptoms30,31 as well as improving both tear break up time and tear secretion.32 Treatment options include Prednisolone Forte, Maxidex, FML, and Flarex. For the treatment of ocular surface disease, FML is usually sufficient with less risks of systemic side effects. Dosing is usually four times daily for one to four weeks. For more severe cases a loading dose may be used.

Cyclosporine is an immunosuppressant. Cyclosporine reduces inflammation by the inhibition of T-lymphocyte activation and by reducing apoptosis in conjunctival epithelial cells.33 Cyclosporine 0.05 per cent has been shown to increase aqueous production34 and increase tear meniscus height.35 In a randomised, investigator-masked trial, one group of patients was provided artificial tears while the other was provided cyclosporin 0.05 per cent dosed twice daily. At 12 months only 6 per cent of the cyclosporin group had experienced dry eye disease progression, compared to 32 per cent in the artificial tear group.36

Omega3 supplements are an important part of any dry eye disease treatment plan due to their anti-inflammatory properties. Studies have shown omega3 supplementation to provide statistically significant improvements in tear osmolarity, tear breakup time, inflammatory markers (MMP-9 and osmolarity) as well as patient symptoms.37 Improvements to Schirmer’s test values have also been shown, although the benefits seem to be more marked in patients with blepharitis and meibomian gland dysfunction.38 Unfortunately, modern diets have a 15:1 Omega6:Omega3 ratio compared to an ideal ratio of 1:1. Eicosapentaenoic acid (EPA) and Docosahexaenoic (DHA) acid are the two vital omega 3s. They are found in fatty fish such as salmon, mackerel, sardines, trout, and tuna. Alpha-linolenic acid (ALA) is a plant-based Omega3, found in foods such as walnuts, chia seeds, and flax seeds. However, because ALA has to be broken down in the body and only then converted to EPA and DHA, much larger amounts of ALA are required to achieve the same therapeutic benefits. The biggest mistake with Omega3 supplementation is selection of a poor-quality product. Patients should be instructed to look for products that have 70 per cent+ purity with >1000mg combined DHA:EPA per daily dose in order to achieve therapeutic effects.


Dry Eye Disease is a multifactorial, choric, progressive disease. It requires long-term management plans supported by strong patient education. Both high and low technology diagnosis and treatment options are available. Eye care practitioners should be routinely screening all patients to identify early signs and prevent future disease progression.



Colette Parkinson graduated with a Bachelor of Optometry from the University of Auckland in 2006. After 7 years of clinical practice she joined Alcon to support clinical training of contact lenses and dry eye management. Colette eventually moved into marketing, during which time she managed multiple specialist portfolios including cataract and laser refractive surgery. In 2017 she was the consultant and project manager for the Dry Eye Institute in Sydney and in 2018 she planned and hosted the national Dry Eye Symposium conference.

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