By: Paul M. Karpecki, OD, FAAO
Director of Education – PECAA
Today, dry eye is considered one of the leading causes of patient visits to eye care providers (ECPs) in the US. 1 Depending on the study anywhere from 20-30 million people have early signs and symptoms of dry eye. Yet only 8 million patients utilize artificial tears at a minimum of treatment options. 2 And a much lower percentage are actually being therapeutically treated for the disease. Studies around the world show similar numbers although certain regions like Asia may have as much as 33% of the population with significant dry eye. It is the number one medical reason that patients see their ECP and will only increase for the next 40 years. The primary predisposing factors that will likely make this disease increase in prevalence are digital device use, systemic diseases like diabetes and the aging population with a greater life expectancy. Studies show that the average American spends 3-5 hours on electronic devices per day. 3 Diabetes as one example of a systemic disease with a significant association to dry eye is expected to increase from 29 million Americans in 2012 to 54 million in 2050. 4 5 Likewise the population greater than 65 is expected to increase from 14% in 2013 to 20% in 2050. 6
Yet the patient data on dry eye disease is quite disturbing with almost 80% of patients classifying their dry eye disease as moderate or severe and thus affecting their quality of life and yet 65% do not classify this as a disease but more of a nuisance. Unfortunately new research is showing that dry eye is not only a chronic disease but actually a progressive disease. 7 So these patients that may see it as a nuisance are less likely to be treated until the condition has advanced too far. For many it may mean that meibomian glands have shown atrophy and/ or lacrimal glands have scarred. Neither of these are reversible. It has also been shown that our subbasal corneal nerves shorten in the presence of long-standing dry eye disease and this has also not been shown to reverse. To make matters worse, only 45% of patient known that there are even tests for dry eye disease screening like osmolarity, tear break-up, corneal staining etc.
To add to this data, the average time of treatment from the point of early signs and symptoms of dry eye disease to initial treatment is almost 8 years! That’s a lot of disease progression!
But the part of the data from this Gfk Chronic Dry Eye Patient A&U data that took place as recently as 2014 is that only 29% of patients surveyed felt that their optometrist was very effective in managing their condition. Wow – that means we have a lot of work to do but what a wonderful opportunity! There are more patients with dry eye disease than any other ocular disease and those doctors that are doing a great job can truly thrive over the next two decades.
Let’s look at the history of our more recent understanding of dry eye disease:
Along the historic path there were some great insights that impact how the disease is diagnosed or managed today. For example the first mention of increased tear osmolarity occurred in 1941 by Von Bahr and colleagues. 8 The problem is that osmolarity requires two keys: acquisition or accumulation of tears into a reservoir and then measurement. Those capabilities were not available until just 3 years ago – but it is available today and is the most accurate test for dry eye. Still it shouldn’t be used in isolation but combined with other findings.
In the early 1960’s it was discovered that a decrease in lacrimal gland secretion lead to ocular surface desiccation. 9 In the 1970s the ocular surface was seen as an integrated functional unit. This is significant for today as we try to manage the conjunctival and cornea and lacrimal and/ or meibomian glands as being part of a functional unit. In the late 1970’s the first mention of the role of meibomian glands was implicated in the pathogenesis of evaporative tear loss. 10 Finally the role of the lipid layer in preventing the loss of aqueous tears was identified soon afterwards.11 These clinical findings have significantly affected how we manage dry eye disease to this day and play a key role in the testing and treatments being administered. And yet there is no ‘gold standard’ for the diagnosis of dry eye disease meaning that the interpretation of multiple testing results should be incorporated.
Even the way we diagnose dry eye today must change- the fundamental piece of the puzzle is that it must be looked at like the diagnosis of glaucoma. In glaucoma we use tonometry, pachymetry, hysteresis, optic nerve evaluation, visual fields and OCT’s to help determine the diagnosis.
In dry eye disease osmolarity testing would be analogous to tonometry, corneal staining is similar to visual field testing as central corneal staining seems to be a late stage sign similar to how visual field defects occur late in the disease process. Optic Nerve evaluations would be analogous to examining the meibomian glands and their secretions and OCT might be meibography in the future, ONH photography would of course be anterior segment photography in DED. The combination of this as well as other key findings like MMP-9, blink analysis, eye lid apposition and symptomatology will all be combined to help determine a diagnosis of dry eye disease. Part of the reason we have to employ multiple tests in the diagnosis of DED is because signs and symptoms are poorly correlated. 12 13 In fact many patients with significant symptoms may have milder forms or dry eye and as the nerves down regulate and signs become more apparent, the symptoms decrease. In fact one study showed that less than 60% of dry eye patients based on objective signs were actually symptomatic. 14 So objective findings including advances like meibography, osmolarity, MG expression, inflammatory marker testing (InflammaDry), lid margin evaluation, vital dye staining, blink analysis and lid apposition are more important than ever because of the progressive nature of this disease. 15
Two very recent areas of research have become landmark in our understanding of ocular surface disease and will greatly affect our treatment understanding. One study found that variability between eyes was a hallmark sign of DED. Patients who have normal ocular surface homeostasis show little to no signs and findings are very similar between the two eyes. For example osmolarity would be within 5mOsmol/L between the eyes and both eyes would have readings under 300mOsmol/L. The second critical new finding also published in late 2014 was that increased osmolarity – inflammation tear film instability – rapid tear film break-up time – change in VA – eventually other symptoms and signs. Another landmark paper looked at the effect of desiccating stress on the mouse meibomian gland function. Mice placed in low humidity – chronic evaporative stress – increased meibocyte production > oil production – dilation of ducts extensive and possible obstructionshort maturation time = increase in protein/lipid ratio – Tear film stability impaired = or > evaporative stress.
All of these studies were published in 2014 and will have major implications to how we manage DED going forward. And given the progression noted of the disease, one might surmise that the most appropriate future model might be that of the dental model. In that analogy patients -especially those with early symptoms such as end of day contact lens discomfort or decreased wear time, should be evaluated and managed to prevent future damage or loss of glands. 150 years ago people didn’t know to brush their teeth and the eventually lost them. Today because of the use of electronic devices in particular, patients are loosing their meibomian glands. We should be assessing this every year at a minimum and suggest that patients manage the early disease before it progresses. The tooth brush might be lid hygiene and cleansers and a commercial warm compress, cleaning in a doctors office might be a thermal pulsation treatment like LipiFlow, mechanical cleaning devices that remove biofilms (BlephEx), debridement/scaling of the lid margin and it’s not uncommon for a dentist to recommend treatments such as anti-inflammatory medications for gingivitis. Our eyelids are like our gums and they need to be managed daily and when inflamed treated with therapeutic medications like topical cyclosporine, topical topical corticosteroids, and in advanced cases, oral treatments like doxycycline.
We must embrace this new understanding of OSD to help our patients with the most common condition they will face for decades to come. Working to shorten the adoption lifecycle will have an amazing effect on not only dry eye disease patients and more advanced forms like Sjogrens Syndrome but also contact lens wearers, those who use electronic devices more than 3 hours a day and patients preparing for procedures such as cataract surgery. Getting involved now will help your practice but most importantly, your patient’s quality of life.
Excerpts were taken from the Dry Eye Summit which took place on December 12, 2014 in Dallas Fort Worth and involved over 30 of the top educators in Ocular Surface Disease.
Further excerpts were taken Review of Optometry Column on Ocular Surface Disease January 15, 2015 page 79.
1 Sullivan DA et al. Ocul Surf. 2012;10:108-116; 2 Dahl AA and Davis CP. Dry eye syndrome (dry eyes, keratoconjunctivitis sicca). Available at: http://www.medicinenet.com/script/main/art.asp?articlekey=43322. Accessed September 19, 2014. 3 U.S. Dept of Labor. American Time Use Survey Summary. Available at: http://www.bls.gov/news.release/atus.nr0.htm. Accessed October 1, 2014. 4 National Diabetes Statistics Report, 2014. Available at: http://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes- report-web.pdf 5 Centers for Disease Control. Number of Americans with Diabetes Projected to Double or Triple by 2050. Available at: http:// www.cdc.gov/media/pressrel/2010/r101022.html 6 Ortman JM et al. An Aging Nation: The Older Population in the United States. May 2014. Available at: www.census.gov/prod/ 2014pubs/p25-114.pdf. 7 Rao SN. Topical cyclosporine 0.05% for the prevention of dry eye disease progression. J Ocul Pharmacol Ther. 2010 Apr;26(2):157-64 8 Von Bahr G. Acta Ophthalmol (Copenh). 1941;19:125-134 9 Asbell PA and Lemp MA, eds. Dry Eye Disease: The Clinician’s Guide to Diagnosis and Treatment. Thieme Publications; 2006 10 Asbell PA and Lemp MA, eds. Dry Eye Disease: The Clinician’s Guide to Diagnosis and Treatment. Thieme Publications; 2006 11 Jester JV et al. Invest Ophthalmol Vis Sci. 1981;20:537-547 12 Nichols KK1, Nichols JJ, Mitchell GL. The lack of association between signs and symptoms in patients with dry eye disease. Cornea. 2004 Nov;23(8):762-70. 13 Sullivan BD et al. Acta Ophthalmol. 2014;92:161-166. Osm, osmolarity; TBUT, tear film breakup time; Sch, Schirmer’s test without anesthesia; Cor, fluorescein corneal staining; Conj, lissamine green conjunctival staining; Meib, Bron/Foulks meibomian gland grading; OSDI, Ocular Surface Disease Index. 14 Bron AJ et al. OculSurf. 2014;12(2 Suppl):S1-S31. 15 Rao SN. Topical cyclosporine 0.05% for the prevention of dry eye disease progression. J Ocul Pharmacol Ther. 2010 Apr;26(2):157-64.