Asking the right questions can lead to successful tailored treatment plans

By Leslie E O’Dell, OD, FAAO

One of the challenges we face in diagnosing our patients with dry eye disease is that clinical findings and the patient’s symptoms often do not correlate.1,2 There’s simply no definitive “one size fits all” approach.

In lieu of improving diagnostic tests, symptoms have been shown to be more repeatable than clinical findings.3 The challenge is our patients’ perception of dryness when using a subjective measure. This challenge in diagnosing dry eye parallels the challenges practitioners face when diagnosing glaucoma. We evaluate subjective and objective measures to develop a risk/benefit ratio for each patient that guides our clinical decision on when to treat. We do not and cannot use one test for making this diagnosis; the best diagnosis is made using a culmination of data points over time.

Defining normal for each patient

During a typical day seeing patients in our bustling practice, it’s surprising how many dry eye patients I encounter, but you wouldn’t know it by reviewing patient intake information. I’ve learned the phrase, “No complaints of dry eye” can’t always be accepted as gospel.

As I start my exam, there are several important signs I look for that indicate I may be dealing with a dry eye patient who doesn’t know she is one—yet. A quick introduction will show me any signs of redness to the eyelid margin or the ocular surface, and even the appearance of the patient’s face might show redness associated with rosacea.

During my refraction, visual fluctuations before and after blink can be apparent. From there, I get into the most crucial element of my evaluation: a thorough slit lamp exam.

I evaluate the lid, tear meniscus, tear break-up time, corneal and conjunctiva staining, and meibomian glands. I then take time to step back from the slit lamp and begin to ask questions that can quickly reveal if a patient is suffering from ocular surface disease.

I ask questions such as:

While optometrists are trained to know what dry eye symptoms are, we need to be cognizant that patients suffering these symptoms often accept them as a “new normal” and may not realize that dry eye disease is the cause.

Implementing a questionnaire

This disconnect with patient perception led our practice to shift from simply asking the patient if she has dry eyes to utilizing a detailed questionnaire that the patient fills out when he is checking into the office.

Several years back, I developed my own questionnaire based on past experience and would occasionally use the Ocular Surface Disease Index (OSDI) for patients already being treated for dry eye, aqueous deficient or evaporative.

About two years ago, we started to implement the Standard Patient Evaluation of Eye Dryness (SPEED) survey, a validated dry eye survey that like its name is fast.4,5 This helps immensely with patient (and staff) compliance. SPEED evaluates both the frequency and severity of symptoms in just eight questions. The patient grades the severity of her symptoms on a scale of zero to four with zero being no symptoms and four being intolerable symptoms. The numeric value for each answer is simply added with scores ranging from zero to 28. The questionnaire is set up to ask patients about their symptoms in the present and up to three months due to the variability of symptoms over time.6 The symptoms Korb and Blackie used for the survey help to quickly identify possible underlying causes. Grittiness is common complaint of patients with lid wiper epitheliopathy, while burning is often found in patients with partial blinks.6

The SPEED questionnaire is able to differentiate symptomatic from asymptomatic patients.7 Having a number from a questionnaire quickly helps me to identify and categorize dry eye patients.

For those with many symptoms greater than eight on the SPEED, their current treatment should be re-evaluated to gain better symptom control. For those asymptomatic, clinical signs that might indicate early stages of dry eye, especially meibomian gland dysfunction, should be evaluated. Start educating patients even when they are not complaining, less than six on the SPEED.

Current treatments may be more effective if we initiated them in early stages. We are in an evolving role presently; raising public awareness of ocular surface wellness starts with the optometrist. This challenge harkens back to the uphill battle dentistry faced years ago before annual and biannual evaluation were standard of care to prevent tooth decay and even that of dermatology prior to public awareness of the importance for sunscreen to prevent skin cancer. Changing public perception and industry practices related to dry eye disease will not be an easy or short-term process, but is a critical element in helping dry eye sufferers avoid symptoms and find relief.

Validated questionnaires

There are a wide variety of options of validated questionnaires to use in a clinical setting. OSDI, Dry Eye Questionnaire (DEQ), McMonnies Questionnaire (MQ), Subjective Evaluation of Symptoms of Dryness (SESoD), and now, SPEED. Studies have shown the SPEED questionnaire to be similar to the OSDI in determining symptomatic from asymptomatic patients.6 The OSDI is a great tool for assessing the quality of life impact dry eye is having for a patient, which is a critical consideration.

Using a validated questionnaire as a routine part of your evaluation is one more tool that will guide your diagnosis and treatment. With the proven repeatability of these questionnaires, the results can also show outcomes for the treatment you have implemented. If the number on the SPEED survey is going down, rest assured your treatment is effective for the time being. If the number from the SPEED is stationary or on the rise, step back and re-evaluate.

The challenge

Start using a questionnaire for every patient you see, it’s fast and you may be surprised with the hidden number of dry eye patients. Then the real challenge begins. Take the extra time to talk to your patients and develop a treatment plan to not only relieve their symptoms but also slow the progression of the disease. And schedule a follow-up, even if you are simply starting artificial tears. A follow-up not only allows you to re-evaluate the therapy and repeat the SPEED but also validates the problem to your patients.

This article originally appeared in Optometry Times

  1. Begley CG, Chalmers RL, Abetz L, et al. The relationship between habitual patient-reported symptoms and clinical signs among patients with dry eye of varying severity. Invest Ophthalmol Vis Sci. 2003 Nov;44(11):4753-61.
  2. Sullivan BD, Crews LA, Sonmez B, et al. Clinical utility of objective test for dry eye disease: variability over time and implications for clinical trials and disease management. Cornea. 2012 Sep;31(9):1000-8.
  3. Nichols KK, Nichols JJ, Mitchell FL. The lack of association between signs and symptoms in patients with dry eye disease. Cornea. 2004 Nov;23(8):762-770.
  4. Korb DR, Herman JP, Greiner JV, et al. Lid wiper epitheliopathy and dry eye symptoms. Eye Contact Lens. 2005 Jan;31(1):2-8.
  5. Korb DR, Scaffidi RC, Greiner JV, et al. The effect of two novel lubricant eye drops on tear film lipid layer thickness in subjects with dry eye symptoms. Optom Vis Sci. 2005 Jul;82(7):594-601.
  6. Blackie C, Albou-Ganem C, Korb D. Questionnaire assists in dry eye disease diagnosis. Four-question survey helps evaluate patients’ dry eye symptoms to improve screening. Ocular Surgery News Europe Edition. November 2012.
  7. Ngo WSitu PKeir N, et al. Psychometric properties and validation of the Standard Patient Evaluation of Eye Dryness questionnaire. Cornea. 2013 Sep;32(9):1204-10.

Can one progressive eye disease teach us how to best treat another?

By Leslie O’Dell, OD, FAAO

Dry eye disease (DED) and glaucoma: though fundamentally different in many ways, their similarities are more numerous than you might expect. Both are chronic, progressive diseases with an age-related increase in prevalence. Both require diligent medication compliance from patients. Both can be confounded by a mismatch between the subjective and objective findings. And neither is likely to ever be “cured,” instead subjecting patients to a lifelong management regimen and some diminution of quality of life.

While advanced diagnosis and treatment of ocular surface disease is still in its infancy, a lot can be learned from earlier developments made in the field of glaucoma—from obtaining a definitive diagnosis and driving progressive research to developing effective treatment options and raising public awareness.

Early in my career in private practice, I realized ocular surface disease was the driving force behind many patient complaints and emergency visits. Patients with red, itchy, irritated eyes were a common occurrence, so much so that I dreaded these patients at first. However, as I learned the nuances of how to make the right diagnosis and subsequently developed best-practice treatments, my confidence and patient outcomes both improved. Today, my patient base is strong—both from colleague referrals for glaucoma evaluation and patient self-referrals for dry eye consultations.

Fig. 1. Disease progression in glaucoma (left) and dry eye (right). Photo: TearScience

Defining the Problem

Glaucoma took more than a century and a half to be truly understood. In the early 1970s, Drance developed the modern definition of glaucoma as a disease of optic neuropathy, not that of elevated IOP.1 Although the meibomian glands were initially defined by Heinrich Meibom in the 1600s, it wasn’t until 1980 that Korb and Henriquez defined meibomian gland dysfunction (MGD). Since then, we have gained a much better understanding of their role in ocular surface disease.2 In the last three decades, a paradigm shift has occurred with respect to DED, and meibomian gland dysfunction is now recognized as the main cause of patient symptoms as well as a dry eye cascade resulting in inflammation of the ocular surface.3,4 With the help of the Tear Film and Ocular Surface Society, the DEWS and MGD workshops have introduced definitions of DED and MGD, respectively:

  • Dry eye disease is defined 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.4
  • Meibomian gland dysfunction is defined as a chronic, diffuse abnormality of the meibomian glands, commonly characterized by terminal duct obstruction and/or qualitative and quantitative changes in the glandular secretion. It may result in alteration of the tear film, eye irritation, clinically apparent inflammation and ocular surface disease.5

These definitions are the first step in directing future research in this area. To properly treat patients with both glaucoma and ocular surface disease, their condition must first be defined. In glaucoma management, defining the disease’s primary and secondary forms helps when establishing a treatment plan. For a dry eye patient, differentiating aqueous deficient from evaporative or a combination lays the foundation to build an effective treatment plan.

Structure vs. Function

Both glaucoma and ocular surface disease are chronic, progressive ocular pathologies with an endstage that results in vision loss. In glaucoma, patient vision loss is due to progressive optic neuropathy, while in dry eye, corneal melts can cause loss of vision. Both groups of patients face increased depression as a result of their respective diseases.6

Both conditions pose the question: when should treatment be initiated with respect to structure vs. function?

Glaucoma specialists have been arguing for years over the clinical significance of structural changes of the optic nerve head (ONH) and retinal nerve fiber layer (RNFL) associated with visual field changes or functional vision loss, and it remains an important topic for research.7 In MGD, structural changes of the meibomian glands are associated with a change in the function or secretion of the gland, leading to alterations in the tear film and inflammation to the ocular surface.

In both cases, a change in structure affects function. So, should we as dry eye specialists adopt the thought process already used by our colleagues treating glaucoma—namely, to treat before symptoms emerge in hopes of delaying onset or at least dampening their impact?

Preventative exams are recommended twice a year in the dental profession to help reduce the risk of tooth decay, often well before symptoms like tooth sensitivity and pain appear. Similarly, dermatologists suggest applying sunscreen well before sun exposure to prevent skin damage. Clearly, preventative care works in other contexts. It stands to reason that an ocular wellness evaluation could be a beneficial part of every exam as well, as it may help identify nascent or subclinical pathology.

Much as the optic nerve and NFL can be evaluated using high-powered lenses and red-free settings without expensive OCT testing, evaluating the structure of the meibomian gland can be done simply with transillumination of the eyelid at the slit lamp. Additionally, manual gland expression can be performed to properly assess  function. Using a tool such as the meibomian gland evaluator (MGE), we can determine the number of glands producing clear, healthy oil under normal physiological blinking.8 This procedure is important to use, as dry eye can easily be missed by only looking at the lid margin without expressing the glands—a condition known as “non-obvious” MGD, which can become serious if not identified quick enough.9 Thus, evaluating and caring for meibomian glands early, before they atrophy, is likely the best course of action; however, further, large-scale research needs to support this concept.

Table 1. Similarities Between Glaucoma and Ocular Surface Disease

Research Is Key

Modern glaucoma management is based on several multicenter, randomized clinical studies.10-12 These findings have served as a seminal guide on how to slow disease progression and what the goal of treatment should be. The main risk factor for glaucoma progression and severity is intraocular pressure; treatment has primarily focused on this because it is the only modifiable risk factor. For glaucoma, the gold standard for progression has been optic nerve photographs and changes over time from baseline.

In the case of evaporative dry eye, the patient’s blink pattern and/or lipid layer thickness are the main modifiable risk factors. One limitation with current treatments and research, however, is that much of it is geared toward relieving symptoms, which can vary significantly with different contributing factors. Recent studies have also shown treatment can be challenging for some dry eye patients with low pain thresholds.13

When managing dry eye, the focus should be on rehabilitating the ocular surface. Patients should be informed that this process can be difficult, and may require many treatments and ongoing care. Studies are still somewhat lacking in the management of the ocular surface, but a few have offered some compelling insights. For example, Korb found debridement of the meibomian glands increased their function.14 Much like the dentistry model, scheduling routine exams to track overall ocular surface and meibomian gland health is a good first step; it can make a big difference in tackling symptoms.

When considering treatment methods, be sure to look at the data and research—not the cost of treatment. LipiFlow has been demonstrated to provide repeatable results and 79% to 88% symptom improvement for patients.15 These same studies also showed improved function of the meibomian glands.16-17 Additionally, new technologies like the MiBoFlo Thermoflo, which helps improve meibomian gland function, and at-home treatments like warm compresses or masks, are also emerging.

Focusing on the Correct Diagnostics

Much as with glaucoma, new diagnostic tools can provide the dry eye specialist with more key information we need to develop an integrated, clinical approach to making the best diagnosis. These tests will help improve diagnosis and progression analysis and hopefully continue to drive research forward towards better treatment methods.

For example, we now have questionnaires and history intake forms that provide information on modifiable factors, including environment, hormone changes, allergy and other medications, while TBUT has proven to be a valuable tool for evaluating tear stability. Tear volume can be evaluated with Schirmer testing, tear film meniscus and anterior segment OCT, while meibomian gland function, lid seal and blink are also important elements to consider. Finally, emerging blood tests like Sjö are demonstrating that Sjögren’s syndrome is far more common than once thought and can be associated with both aqueous and evaporative dry eye.

Personalize Your Approach to Care

All glaucoma patients receive an individualized treatment plan based on their unique risk factors, symptomatology and likelihood of progression. These personalized treatment plans are under constant scrutiny during follow-up exams to determine if the risk of progression has been completely halted or only significantly slowed, to prevent vision loss.

Treatments for these patients do not typically follow an all-or-none philosophy—some patients need multiple medications, while others require surgical intervention. In making these decisions for our patients, we develop our best treatment plans when we rely on pre-existing knowledge and ongoing research to guide us. The medications we prescribe all have pros and cons and do not always work for each patient, and even surgical interventions can fail.

Dry eye patients also need to be managed just like other chronic progressive disease patients. Planned follow-ups to continually reassess the ocular surface health and wellness of the eye are vital.

Schedule a follow-up exam whenever any treatment is initiated, even if it is only an artificial tear. Reassess the ocular surface and symptoms to determine if that treatment is effective and if not, reconsider what factors might still be contributing to the condition. Evaluating each patient’s disease and risk factors helps guide treatment plans to improve ocular health and patient comfort. Consider a patient with tear film instability to be a “dry eye suspect” (akin to a “glaucoma suspect” in similarly vulnerable patients) and follow patients with risk factors accordingly.

Follow-up exams after treatment is initiated also allow better assessment of adherence to therapy. Adherence is a fairly common problem when managing glaucoma, even with the threat of blindness.18 The same barriers to adherence are present for dry eye patients—cost, increased age and comorbidities such as dementia or arthritis that make it hard to use eye drops. Changing the concept of DED begins with the prescribing doctor’s attitude, so make it an important part of the general eye exam.

In any case, optometrists need to recognize one another as specialists and refer more within our profession. The eye is undoubedly very complex; to master every aspect is a challenge. According to Malcom Gladwell, it takes 10,000 hours of practice to master a field, making it an intimidating and unlikely goal to attempt to know everything there is to know about many subjects.18 Many fields often separate into subcategories—for example, there are at least nine specialties within ophthalmology, ranging from general ophthalmology to neuro-ophthalmology. Thus, it is important to know what subspecialties the other eye care professionals in your referring network might have so you can refer a patient before their condition progresses too far.

Work together with the appropriate specialist to initiate a treatment plan and achieve the goal of a healthy ocular surface. And as always, be sure to keep track of new dry eye research—change takes time, but the growing amount of interest in the area of ocular surface disease will likely continue to improve the understanding of the condition and the available treatments.

This article originally appeared in the Review of Optometry

  1. Morgan RW, Drance SM. Chronic open-angle glaucoma and ocular hypertension. Br J Ophthalmol. 1975;59(4):211-215.
  2. Korb DR, Henriquez AS. J Am Optom Assoc. 1980;51:243-251.
  3. Lemp MA, Crews LA, Bron AJ, Foulks GN, Sullivan BD. Distribution of aqueous-deficient and evaporative dry eye in a clinic-based patient cohort: a retrospective study. Cornea. 2012;31(5):472-478.
  4. Nichols KK, et al. The international workshop on meibomian gland dysfunction: executive summary. Invest Ophthalmol Vis Sci. 2011;30;52(4):1922-1909.
  5. The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye Workshop (2007). Ocul Surf. 2007;5(2):75-92.
  6. Kim KW1, Han SB, et al. Association between depression and dry eye disease in an elderly population. Invest Ophthalmol Vis Sci. 2011 Oct 10;52(11):7954-8.
  7. European Glaucoma Society. Terminology and guidelines for glaucoma. 3. Vol. 2008. Savona: Italy Editrice Dogma; 2008.
  8. Korb DR, Blackie CA. Meibomian gland diagnostic expressibility: correlation with dry eye symptoms and gland location. Cornea. 2008 Dec;27(10):1142-7.
  9. Blackie CA, Korb DR, et al. Nonobvious obstructive meibomian gland dysfunction. Cornea. 2010 Dec;29(12):1333-45.
  10. Leske MC, Heijl A, et al. Early Manifest Glaucoma Trial: design and baseline data. Ophthalmology. 1999 Nov;106(11):2144-53.
  11. Musch DC, Lichter PR, et al. The Collaborative Initial Glaucoma Treatment Study: study design, methods, and baseline characteristics of enrolled patients. Ophthalmology. 1999 Apr;106(4):653-62.
  12. Kass MA, Heuer DK, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002 Jun;120(6):701-13.
  13. Rosenthal P, Borsook D. The corneal pain system. Part I: the missing piece of the dry eye puzzle. Ocul Surf. 2012 Jan;10(1):2-14.
  14. Korb DR, Blackie CA. Debridement-scaling: a new procedure that increases Meibomian gland function and reduces dry eye symptoms. Cornea. 2013 Dec;32(12):1554-7.
  15. Lane SS1, DuBiner HB, et al. A new system, the LipiFlow, for the treatment of meibomian gland dysfunction. Cornea. 2012 Apr;31(4):396-404.
  16. Greiner JV. A single LipiFlow Thermal Pulsation System treatment improves meibomian gland function and reduces dry eye symptoms for 9 months. Curr Eye Res. 2012 Apr;37(4):272-8.
  17. Greiner JV. Long-term (12-month) improvement in meibomian gland function and reduced dry eye symptoms with a single thermal pulsation treatment. Clin Experiment Ophthalmol. 2013 Aug;41(6):524-30.
  18. Cate H, Bhattacharya D, et al. Improving adherence to glaucoma medication: a randomised controlled trial of a patient-centred intervention (The Norwich Adherence Glaucoma Study). BMC Ophthalmol. 2014 Mar 24;14:32.

aoc-1214_coverA dry eye disease (DED) epidemic is upon us. You can choose to recognize this and actively seek out patients to treat or you can miss an opportunity for practice growth by ignoring it. If you look, you will find that the majority of your patients have some stage and type of dry eye disease. Ocular surface disease (OSD) is a complicated process involving adequate quantity and quality of tears to maintain a healthy ocular surface. There have been many advances over the years in defining this disease, in the diagnostic tests available, and in treatment options to help our patients who experience what are often life-altering symptoms. There is still much to learn, but maybe we do not have to reinvent the wheel…

Read full article by Dr. Leslie O’Dell at eyetubeOD