Meibomian gland dysfunction: Current strategies and future directions
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Michael A. Lemp, MD, FACS: According to the American Academy of Ophthalmology, between 30% and 35% of patients present with symptoms consistent with dry eye disease.1 Although ophthalmologists frequently treat patients with meibomian gland dysfunction (MGD), the most prevalent form of dry eye disease,2 there is still much that physicians need to learn about its causes, diagnosis and management to better relieve symptoms and improve quality of life for patients. When Stern and colleagues3 first described the lacrimal functional unit as comprising the meibomian glands, MGD’s principal role in dry eye disease could no longer be disputed.
With MGD being the most common form of dry eye disease,4 do you find that MGD significantly affects your patients?
John A. Hovanesian, MD, FACS: My colleagues and I perform a range of general procedures, LASIK and cataract surgeries. MGD has a profound effect on my patients’ vision, and it must first be controlled to acquire accurate keratometry (K) measurements. Significant MGD alters the stability of the tear film, which is measured by interferometry.5 A stable lipid film is essential for cataract surgery because an error of 1 D in K measurement results in a refractive error of 1 D. This one-to-one ratio indicates the need for consistent measurements at the front of the cornea.
William B. Trattler, MD: I find that, although MGD profoundly affects patients as they age, older patients are less symptomatic than younger patients. My colleagues and I performed a screening study of patients scheduled for cataract surgery and found that 59% had MGD.6 Furthermore, a high percentage of patients with active MGD and rapid tear breakup time were asymptomatic or minimally symptomatic. Although these patients were coming in for routine cataract surgery, we first had to address their MGD to obtain accurate K readings.
I have also found that a poor tear film resulting from MGD could be a reason why younger patients become intolerant to contact lenses.
Stephen S. Lane, MD: In my practice, MGD is the most prevalent diagnosis – 85% of my patients have MGD. When a patient presents with the typical symptoms of dryness, bogginess, lid redness and especially fluctuations in vision, the diagnosis is most likely MGD, even in postoperative refractive and LASIK patients.
J.E. “Jay” McDonald II, MD: The meibomian gland is the sentinel place around which dry eye revolves. My colleagues and I discuss MGD with approximately 30% to 40% of our patients. We examine the meibomian expressions routinely and stain with Fluramene (fluorescein sodium/lissamine green; Noble Vision Group) to evaluate the tear film, corneal surface and lid wiper.
Dry eye disease and MGD: Demographic breakdown
Lemp: Demographic studies suggest that the prevalence of dry eye disease is much higher than previously thought. A Harvard study7,8 suggests that 5.9 million people have moderate to severe dry eye in the United States and that, for every one of those moderate to severe cases, there are probably three or four patients with a less significant form of the disease. In total, an estimated 20% of the population has either chronic dry eye problems or episodic dry eye in response to environmental stress. How has dry eye disease affected your patients?
Hovanesian: My practice has a high incidence of both dry eye disease and MGD because more than half of my patients are age 60 or older.
McDonald: I practice in an area that has four distinct seasons, and in the fall, when humidity drops and people start heating their homes, I see an upswing of patients with asymptomatic dry eye. Patients also present with, as TearScience cofounder and researcher Donald R. Korb, OD describes, non-symptomatic MGD – patients have decreased meibomian gland secretions, yet, have not developed symptoms.
Trattler: About 20% of my patient population has dry eye disease and MGD. I treat a large number of young patients who spend a significant portion of the day using a computer. Selection is a factor as well. Ophthalmologists treat patients who present with vision fluctuations and mild cataracts. However, if the ophthalmologist treats the patient’s dry eye or MGD, then the patient’s vision is corrected sufficiently and surgery may not be necessary.
Parag A. Majmudar, MD: I believe that dry eye in general, and MGD specifically, are under-diagnosed, yet they account for a high percentage of patients’ symptoms. As we know, the majority of patients do not present with a chief complaint of, “I have MGD.” Rather, they may have a constellation of signs and symptoms that the practitioner must analyze to make a connection. The main complaint that patients likely have is poor vision, yet many eye care providers may not correlate a poor quality tear film as having any significant impact on visual acuity.
Lemp: Traditionally, most ophthalmologists do not think dry eye affects vision, except in patients who have advanced dry eye disease. What happens mechanistically that affects patients’ vision?
Trattler: Most commonly, central corneal staining could be the cause for a patient’s declining vision, due to an irregular corneal surface. Using fluorescein, I often will see subtle, more advanced corneal changes in the center, in addition to seeing a rapid tear breakup time. Patients with a rapid tear breakup time who keep their eyes open longer while staring at something will experience fluctuations in vision because of a poor tear film after blinking.
Lemp: One study from Japan by Ridder and colleagues9 has shown that visual acuity declines 3 to 5 seconds after blinking, causing many patients to fail a driver’s test. Until recently, ophthalmologists have not been able to report this phenomenon because few patients present with vision loss due to dry eye. Rather, they complain of tired eyes and excessive blinking. Another study by Sullivan10 confirms that hormonal changes associated with menopause are another factor that increases the risk for dry eye disease.
Several population-based studies show a significant number of patients have MGD. Schaumberg and colleagues11 showed a high distribution of the disease in the elderly Japanese population. Another study by Tong and colleagues12 evaluated a referral practice in Singapore and found a high prevalence of MGD in patients who have severe dry eye, and a more recent study out of Spain by Viso and colleagues13 showed similar results when examining the general population.
It has been suggested that there is a higher prevalence of MGD in Asian populations, but I am not sure that is true. However, my colleagues and I conducted a large study in Europe and the United States evaluating the frequency of aqueous tear deficiency and/or MGD in patients and we found that 86% of patients had MGD (Figure 1).14 Our study outcomes also suggest that the mixed form of the disease is more prevalent as the disease becomes more severe, and that MGD and dry eye disease are interrelated.
Trattler: Upon completing my residency, I believed that patients with MGD would have a rapid tear breakup time while patients with aqueous deficient dry eye would demonstrate a more normal tear breakup. Now we have learned that both aqueous deficient and MGD groups experience the same problems, including rapid tear breakup time, corneal staining and conjunctival staining, which lead to similar effects on the ocular surface.
McDonald: I think of MGD as being at the base of a pyramid. In my opinion, the first sign ophthalmologists should look for in 90% of patients with dry eye is decreased meibomian gland secretions, because it is generally the primary factor in the development of all dry eye disease. Learning to express and grade gland secretions is very helpful.
Figure 1: Evaporative dry eye is a highly prevalent condition, with 86% of patients suffering from meibomian gland dysfunction.
Graphic source: TearScience, Inc.
Adapted from data published in: Lemp MA, Crews LA, Bron AJ, Foulks GN, Sullivan BD. Distribution of aqueous deficient and evaporative dry eye in a clinic-based patient population. Cornea. In press.
Terminology and education
Lemp: What are your recommendations for educating patients and general practitioners about MGD and dry eye?
Majmudar: I believe we have to restructure the way we think about dry eye, perhaps referring to it as ocular surface dysfunction. Some patients have aqueous deficiency, but I think much of the impetus for developing symptoms that we associate with dry eye are unrelated to the fact that the eye is dry. If ophthalmologists start talking in terms of ocular surface or lid dysfunction, then we can fully understand the importance of meibomian glands and the role they play in this dysfunctional state.
Lemp: The terminology that ophthalmologists use has been debated over the last 5 years. For example, dysfunctional tear syndrome is certainly more descriptive of the symptoms, but it is more universally referred to as dry eye. If we examine the causes of dry eye disease and whether it begins with increased evaporation or decreased lipid secretion, I believe most ophthalmologists agree that the tear film is unstable, as reflected in visual problems between blinks and a hyper concentration of the tear film. How can we help practitioners and patients better understand the terminology?
Hovanesian: A general practitioner may have a better understanding of the pathophysiology that ophthalmologists refer to as dry eye if we describe it in a different way and encourage, for example, an examination of the meibomian glands to determine the root cause of the problem.
McDonald: Instead of using the term “dry eye” as a single entity, since it is usually present in most patients, I also include Korb’s description of lid wiper epitheliopathy15 to better explain the problem to my patients. Since this change in terminology, I find that my patients are more compliant to therapy.
Trattler: I educate my patients about evaporative dry eye disease versus aqueous deficient dry eye syndrome. I find that my patients understand that if there is not enough of a lipid layer to lock in the tears, then evaporation results. If the condition is aqueous deficient dry eye, then the physician should increase tear film thickness with a topical treatment such as topical cyclosporine.
Hovanesian: I focus more on treatment than pathogenesis because, although it is worthwhile to explain, I have limited time in the exam room with patients. Instead, in addition to providing patients with a handout with tailored treatment options, I direct patients to a 30-minute YouTube presentation about all forms of dry eye. The video includes details about warm compresses, lid hygiene and treatment options.
Standardized terminology may facilitate improved diagnosisConfusion exists in the ophthalmologic community regarding the various forms of dry eye disease, which commonly leads to misdiagnosis and underdiagnosis. Using consistent terminology, classification and clinical examination methods can help clinicians differentially diagnose dry eye disease and select the most appropriate and effective treatment for their patients. A proper exam for dry eye disease includes gland expression, lid inversion and examination of the tear film. When a patient presents with dry eye disease, ophthalmologists should examine the lids as well as the cornea, and check the consistency of the expressed contents of the glands. Gland expression is performed not only for meibomian gland dysfunction (MGD), but also to prevent patients from progressing to an obstructive form of the disease. Because the average clinician may not be familiar with the gland expression technique, developing a standard, step-by-step examination procedure is necessary. Clinicians must be challenged to become better and more thorough in their diagnosis and treatment. With so many forms of dry eye disease, including mixed dry eye, aqueous tear deficiency and MGD, such a diagnostic spectrum calls for a more specific classification that details symptoms associated with each form. By “speaking the same language,” ophthalmologists can eliminate confusion, increase awareness of dry eye disease and properly educate patients. Edward J. Holland, MD, is director of Cornea Services at Cincinnati Eye Institute and professor of Ophthalmology at the University of Cincinnati. |
Diagnosing MGD
Lemp: How do you evaluate a patient for MGD?
Hovanesian: Because proximity to the eye can cause reflex tearing, I prefer to examine a patient using the overhead lights with the slit lamp light turned off when I examine the tear lake. I look at the overall wetting of the eye. Tear film debris indicates some form of dry eye, but it is fairly nonspecific for MGD versus aqueous deficiency. In addition, a Schirmer tear test is useful for examining aqueous production. Most importantly, I conduct a thorough visual inspection by pressing on the glands to see the secretion consistency and magnitude of the blockage to determine how much MGD is present.
Lane: I perform an external exam first, looking at the overall appearance of the eyelids and the symmetry of the two eyes in terms of swelling and redness. Then, at the slit lamp, I look at telangiectasia of the lid margins, inspissation of the glands, and the tarsal and bulbar conjunctiva for inflammation (Figure 2). At this point, I will also use a cotton swab to attempt to express the meibomian glands to determine the nature and quality of the expressed secretions. I also look for foaminess at the canthi of the eyes, which usually indicates the presence of MGD. I prefer lissamine green over fluorescein to aid in diagnosis, but I do not use a Schirmer tear test unless the patient has severe Sjögren syndrome.
Figure 2: Meibomian gland dysfunction with conjunctival reaction. Lid expression reveals inspissated dysfunctional glands.
Source: McDonald JE.
Lemp: When evaluating the lid margin, what emphasis do you put on vascular changes versus secretory changes?
Lane: Although they most often go hand in hand, I believe that the secretory changes are more important than the vascular changes. In my experience, patients with secretory changes are more symptomatic, whereas vascularization may be an early sign of MGD.
Majmudar: Since MGD is now recognized as one of, if not the, leading cause of dry eye, the first thing a clinician should do when diagnosing MGD is incorporate the signs and symptoms into the thought process prior to any patient encounter. It is also important to take the time to listen to a patient discuss his or her symptoms and let that be the guide during examination and diagnosis.
McDonald: I always use Fluramene and evert the lid to look at the lid wiper. I then perform a lower lid meibomian gland expression.
Trattler: Many physicians may not realize that, when assessing severity with fluorescein, they should wait at least 1 to 3 minutes to observe maximum corneal staining.
Grading MGD severity
Lemp: Do you use a grading scale to develop a treatment plan?
Majmudar: If the patient has no secretion, then conventional therapies will not work. However, I grade patients on the following scale: a secretion of clear liquid is considered grade 1; a secretion that is slightly more turbid is considered grade 2; and a secretion that is thicker, like toothpaste, is grade 3. For MGD grades 2 and 3, advising patients about grade-specific treatments will be more impactful and will lead to better compliance.
McDonald: My colleagues and I quantitate symptoms in two ways and enter these values into our electronic medical records for use practice-wide. First, we changed the algorithm in our medical record so that we grade how many glands are open during expression. The three categories are four or fewer, four to seven, and more than seven. We also grade lid wiper epitheliopathy using Fluramene. The grading is based on the thickness and length of the lid wiper, as well as the absence or presence of furrows.
Hovanesian: In my opinion, the severity of symptoms does not correlate with the objective signs of turbidity or inspissation of the glands. Particularly, there is a loss of correlation in patients who have MGD with minimal to no aqueous secretions because most of those patients are fairly symptomatic.
Majmudar: This lack of correlation indicates a need for patient education because, although patients may not show symptoms of MGD, they have been diagnosed and must start treatment.
Lemp: Blackie and colleagues16 recently wrote about nonobvious MGD (Figure 3). How frequently do you see patients who do not have obvious signs of MGD yet are symptomatic?
Lane: Although a patient may not exhibit symptoms, the meibomian glands may be abnormal. The question becomes whether to intervene and treat this patient who is not symptomatic or wait until the patient returns in 3 to 6 months. In my practice, I would intervene and treat nonobvious MGD. Although patients may be hesitant to treat the problem due to lack of symptoms, there are simple things that I suggest to help prevent them from becoming symptomatic, including lid scrubs or artificial tears. I have found Systane Balance (Alcon Laboratories, Inc.) to be particularly useful in these cases.
Furthermore, I never diagnose a patient with dry eye syndrome. Instead, I will indicate signs of anterior and posterior blepharitis or MGD in my chart notes. A patient who presents with classic dry eye symptoms, such as itching and burning sensation, and who does not have full meibomian gland dysfunction, should be diagnosed with nonobvious MGD, not dry eye syndrome.
Lemp: Traditionally, ophthalmologists have been taught to differentiate between aqueous tear deficiency, MGD and posterior blepharitis by asking patients to describe the time of day they experience the worst symptoms. Although we have been taught to differentiate between dry eye conditions by taking into account the time of day, this may not be a helpful indicator, based on demographic data about the high prevalence of patients with a mixed form of the disease. Do you feel it is a useful tool in diagnosis?
Hovanesian: I am not aware of any data that support using time of day to determine what kind of dry eye is present.
McDonald: Although rare, patients may say that their eyes hurt worse in the morning or upon waking up during the night. For those patients, I recommend nighttime ointments and lubrications, but noting time of day is typically not a useful way to diagnose my patients. Instead, my treatment is based on my findings as well as symptoms.
Figure 3: Patients with obvious (A) and nonobvious (B)
meibomian gland dysfunction. The cross-section (C) shows an occluded meibomian
gland. |
MGD and rosacea
Lemp: One of the most common associations with MGD reported in literature is rosacea.17 How frequently do you see the association with rosacea in patients with MGD?
Hovanesian: In my practice, roughly 20% of patients with MGD also have rosacea.
Trattler: In my practice, a patient with rosacea will typically have a more severe form of MGD, although this represents a small subset of my patients with MGD.
Lane: After seeing several physicians who fail to diagnose their symptoms as rosacea, I find that these patients often present when their MGD is more advanced, showing fairly significant corneal changes with vascularization and irregular or frank scarring. I have treated some children who have severe lid changes and vascularization of the eyelid margins, yet do not show other signs of rosacea, such as flushing and telangiectasia of the face and the nose.
Lemp: In general, I believe rosacea develops with age in people who have a predisposition to develop it. I do not think they have the facial features in childhood.
Do you think that the prevalence of rosacea is higher in certain ethnic groups?
Lane: I find patients of Mediterranean, Irish and English descent to be more prone to rosacea. I believe the incidence of rosacea in patients with MGD may be higher than clinicians think. Rosacea presents with a spectrum of severity, just like MGD, causing physicians to underrecognize it. There are several reasons to believe that rosacea and MGD are part of the same disease spectrum, in that they are both vasodilatory malfunction.
When to treat MGD
Lemp: What is the natural history of MGD if left untreated?
Majmudar: Whether patients present with nonobvious MGD or minimal-to-moderate symptoms, they will become worse as they age. Physicians should start treatment early in an effort to improve symptoms and delay further complications.
Lane: Pediatric ophthalmology partners in my practice sometimes refer to me children who have moderate to severe MGD. If not treated chronically to maintain stability, the patients are at risk for future lid changes and severe corneal problems.
Lemp: When is the proper time to treat MGD? Do you treat asymptomatic and symptomatic patients alike?
Lane: With new treatment options now available, clinicians should always examine a patient’s lids to find a potential problem at an early stage, whether the patient comes in for a routine exam, a LASIK consultation, cataract consultation, or surgical follow-up exam.
Hovanesian: I believe it is important to treat a patient if I suspect that symptoms will become worse at other times of the year, or during the perioperative stage.
Treatment options
Lemp: What is your recommended treatment protocol?
McDonald: I prescribe a nighttime ointment, lubrication such as Soothe eye drops (Bausch + Lomb, Inc.) for daytime administration, and I teach patients how to express the glands. In addition to these three treatments, I prescribe a steroid for the first 4 to 6 weeks. If a patient has active posterior blepharitis or active infection, I prescribe a steroidal antibiotic combination, or more commonly, AzaSite (azithromycin ophthalmic solution 1%; Merck & Co., Inc.).
Trattler: In some of my patients, the MGD pathogenesis begins with the presence of bacteria, which secrete lipases that metabolize good oils into bad oils. I treat these patients with an antibiotic, such as topical azithromycin, for 1 month. Studies show that azithromycin can be effective in treating MGD and blepharitis, from improving signs and symptoms to improving the quantity of the meibomian gland lipids.2 I may also prescribe a steroid, such as Pred Forte (prednisolone acetate 1%; Allergan, Inc.), for 1 to 2 weeks.
Hovanesian: My decision to use steroids depends on the level of discomfort and inflammation the patient experiences. I prescribe antibiotics in more severe cases. However, warm compresses are the mainstay of therapy that I recommend because I find that lid hygiene with soap or baby shampoo is difficult for patients to carry out.
Lane: Lid hygiene is extremely important, however, in my experience, most patients are not compliant or do it improperly. To more thoroughly relieve symptoms, I recommend expression therapy. Regarding antibiotics, I prescribe TobraDex ST (tobramycin/dexamethasone ophthalmic suspension 0.3/0.05%; Alcon Laboratories, Inc.) because it is more viscous than other antibiotic therapies. For patients with moderate MGD symptoms, I will first prescribe a steroid and then azithromycin twice a day. If symptoms are chronic, then I will prescribe the antibiotic every other month to fully benefit from its anti-inflammatory properties.
I also routinely recommend Omega 3 fatty acid supplements, yet many patients already take them for other health reasons.
Majmudar: Patients must understand that there is no cure for MGD, so treatment compliance is imperative. Because MGD is a multifactorial disease, a multifactorial treatment process is necessary, and includes lubrication, tear replacement, and physical measures, such as mechanical expression, thermal application or a combination of both.
Lemp: How should ophthalmologists manage patients whose glands are completely plugged, and who may not respond to standard treatment?
Trattler: I believe adequate therapies for patients with completely clogged meibomian glands are lacking.
McDonald: Until a therapy that restores natural meibomian gland expression is developed, ophthalmologists must turn to traditional therapies.
Majmudar: If a patient presents with physical obstruction of the meibomian glands or damage to the acinar structure, then he or she may have no secretion or abnormal secretion as a consequence. Also, there may be an inhibitory feedback mechanism, or down-regulation, that would potentiate this vicious cycle because further production of abnormal secretions may further damage the acinar structure, and so on.
Lane: For patients with severe complications, I recommend more frequent office visits, perhaps three to four a year. These more frequent visits allow me to perform expression during the appointments and monitor patient compliance and improvements. If inflammation is apparent, then I prescribe TobraDex ST. Until Lotemax (loteprednol etabonate ophthalmic suspension 0.5%, Bausch + Lomb, Inc.) becomes available as an ointment, I prefer TobraDex ST, which features higher viscosity and a long contact time.
McDonald: I prescribe Lotemax for 4 to 6 weeks in patients with severe MGD. Once their symptoms subside, I then prescribe four refills of a mild steroid, such as fluoromethalone, for 1 year.
An alternative to traditional treatment optionsMeibomian gland dysfunction (MGD) associated with dry eye disease is a common diagnosis in my clinical practice. MGD causes significant eye discomfort and blurred vision, often leading to dissatisfaction not only with glasses and contacts, but after refractive and cataract surgery as well. Because of the chronic nature of the disease, treatment is frustrating for patients, consisting of frequent drops, oral medications and mechanical therapy to the lids. Recently, TearScience, Inc. received U.S. Food and Drug Administration clearance for the LipiFlow® Thermal Pulsation System. Our practice took part in the clinical study1 used to support the premarket notification of LipiFlow®. In our experience, patients treated with the device reported positive results. In my opinion, this new technology provides ophthalmologists with an improved treatment modality for patients with MGD and associated dry eye. David R. Hardten, MD, is a founding partner of Minnesota Eye Consultants and director of its Clinical Research Department. Reference:
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Future considerations
Lemp: Although more treatment options are available now than in previous years, ophthalmologists are still looking for better tools to manage obstructive MGD, the most common form. What do you see in the future of MGD care, especially for patients with chronic conditions?
McDonald: Ophthalmologists need a treatment that lasts longer than those currently available and is easier for patients to use.
Lane: It is important to clean out the meibomian glands in an effort to relieve the blockage so that new secretions escape without stagnation. The treatment of MGD in the future, in my opinion, may be to first liquefy the obstructed material, which is complicated by keratinized, desquamated cells, followed by a mechanical means of expressing the glands and relieving the blockages that occur behind the plugs. If ophthalmologists are able to evacuate the glands, I believe patients have a good chance of avoiding severe complications.
McDonald: In my opinion, giving the meibomian glands a chance to reset themselves using a thermal mechanical means of expression, while also administering pharmaceutical agents, would be the best treatment. Since the meibomian glands are obstructed, the first step would be to remove the obstruction without damaging the glands, giving them a chance to up-regulate. Although secretions may not be perfectly normal, the lipids will aid in symptomatic and curative relief.
Lane: This type of mechanical expression has a dual effect, in that it would also prevent corneal changes.
Trattler: With traditional treatments, ophthalmologists continually encounter problems with patient compliance, long-term steroid use and overall patient satisfaction. MGD is a common condition, and I am eager to implement a single thermodynamic treatment, such as the LipiFlow® Thermal Pulsation System (TearScience, Inc.; Figure 4), because I think it will greatly impact our patient outcomes.
Figure 4: Cross-section of an
eye with the LipiFlow® Thermal Pulsation System applied to the eyelid.
Source: TearScience, Inc.
Majmudar: I have treated more than 40 patients with the LipiFlow® system in clinical trials, and many of my patients with dry eye resulting from MGD and/or blepharitis report symptomatic relief.
Lane: Tools that examine osmolarlity in an easy, noninvasive way, will significantly improve diagnostic abilities, as well as the ways of potentially evaluating the success of treatments. As improved tools become available in the near future, frustrated and noncompliant patients will see evidence of success and begin to be proactive in their therapies.
Lemp: Patients may experience expectation fatigue, seeking help from several ophthalmologists without experiencing relief, because physicians do not fully understand dry eye disease. Some diagnostic modalities do not allow physicians to examine the glands; rather, they only provide an opportunity to look at the effects of this condition in terms of the lacrimal functional unit. The promise of not only identifying patients, but also having an objective number from which the ophthalmologist can gather data in response to treatment, is an important component of determining a treatment plan.
McDonald: As occurs with patients who have diabetes and use a meter to test blood sugar levels, compliance in patients who have MGD will improve with the use of a metric. In research, interferometry has been used to provide a quantitative measurement of the lipid layer thickness in the tears. Studies18-20 show a correlation between treatment success or symptom relief and restoration of the ocular lipid layer thickness as measured by the interferometry devices used in research.
Trattler: Interferometry may prove to play a significant role in evaluating patients prior to cataract surgery. An unstable tear film can negatively impact the accuracy of our preoperative corneal measurements.21 In my practice, we were part of a multicenter study and found that 62% of patients scheduled for cataract surgery had an abnormal tear breakup time of 5 seconds or less.22 Patients with a rapid tear breakup time are more likely to have inaccurate K and topography readings, so identifying and treating patients with an abnormal tear film may help improve the accuracy of the preoperative tests and potentially cataract surgery outcomes.
If my practice implements the LipiFlow® system, my colleagues and I could pretreat patients for MGD with the objective of improving surgical planning.
Hovanesian: Patients dislike lid hygiene and warm compresses, and medications prove difficult in terms of tolerability, administration and cost. Patient satisfaction is important, but duration of benefit is essential as well. It is really the area under the curve where ophthalmologists must focus. A treatment that provides prolonged,23,24 significant benefit relative to a warm compress regimen, as data suggests is the case with the LipiFlow® system, is something to which patients will respond.
Conclusion
Lemp: To summarize, MGD is a widespread condition and exists as part of a larger condition called dry eye disease. In response to this phenomenon, ophthalmologists are better understanding the pathogenetic mechanisms that lead to problems, such as fluctuating vision, that were not truly understood just a few years ago. Although better technology is available, there is still room for improvement in relieving symptoms and achieving better surgical results.
I would like to thank the faculty for their time and expertise, as well as TearScience, Inc. for sponsoring this supplement.
References
- AAO Cornea/External Disease PPP Panel. Preferred Practice Pattern: Dry Eye Syndrome. American Academy of Ophthalmology; 2003.
- Nichols KK, Foulks GN, Bron AJ, et al. The international workshop on meibomian gland dysfunction: executive summary. Invest Ophthalmol Vis Sci. 2011;52(4):1922-1929.
- Stern ME, Beuerman RW, Fox RI, Gao J, Mircheff AK, Pflugfelder SC. The pathology of dry eye: the interaction between the ocular surface and lacrimal glands. Cornea. 1998;17(6):584-589.
- Lemp MA, Nichols KK. Blepharitis in the United States 2009: a survey-based perspective on prevalence and treatment. Ocul Surf. 2009;7(2 Suppl):S1-S14.
- King-Smith PE, Fink BA, Fogt N. Three interferometric methods for measuring the thickness of layers of the tear film. Optom Vis Sci. 1999;76(1):19-32.
- Luchs J, Buznego C, Trattler W. Asymptomatic or minimally symptomatic blepharitis in patients having cataract surgery. Poster presented at: American Society of Cataract and Refractive Surgery 2011 Symposium and Congress; March 25-29, 2011; San Diego.
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- Schaumberg DA, Dana R, Buring JE, Sullivan DA. Prevalence of dry eye disease among US men: estimates from the Physicians’ Health Studies. Arch Ophthalmol. 2009;127(6):763-768.
- Ridder WH 3rd, Tomlinson A, Huang JF, Li J. Impaired visual performance in patients with dry eye. Ocul Surf. 2011;9(1):42-55.
- Sullivan DA. Tearful relationships? Sex, hormones, the lacrimal gland, and aqueous-deficient dry eye. Ocul Surf. 2004;2(2):92-123.
- Schaumberg DA, Nichols JJ, Papas EB, Tong L, Uchino M, Nichols KK. The international workshop on meibomian gland dysfunction: report of the subcommittee on the epidemiology of, and associated risk factors for, MGD. Invest Ophthalmol Vis Sci. 2011;52(4):1994-2005.
- Tong L, Chaurasia SS, Mehta JS, Beuerman RW. Screening for meibomian gland disease: its relation to dry eye subtypes and symptoms in a tertiary referral clinic in Singapore. Invest Ophthalmol Vis Sci. 2010;51(7):3449-3454.
- Viso E, Gude F, Rodríguez-Ares MT. The association of meibomian gland dysfunction and other common ocular diseases with dry eye: a population-based study in Spain. Cornea. 2011;30(1):1-6.
- Lemp MA, Crews LA, Bron AJ, Foulks GN, Sullivan BD. Distribution of aqueous deficient and evaporative dry eye in a clinic-based patient population. Cornea. In press.
- Korb DR, Herman JP, Greiner JV, et al. Lid wiper epitheliopathy and dry eye symptoms. Eye Contact Lens. 2005;31(1):2-8.
- Blackie CA, Korb DR, Knop E, Bedi R, Knop N, Holland EJ. Nonobvious obstructive meibomian gland dysfunction. Cornea. 2010;29(12):1333-1345.
- Driver PJ, Lemp MA. Meibomian gland dysfunction. Surv Ophthalmol. 1996;40(5):343-367.
- Blackie CA, Solomon JD, Scaffidi RC, Greiner JV, Lemp MA, Korb DR. The relationship between dry eye symptoms and lipid layer thickness. Cornea. 2009;28(7):789-794.
- Korb DR, Greiner JV. Increase in tear film lipid layer thickness following treatment of meibomian gland dysfunction. Adv Exp Med Biol. 1994;350:293-298.
- Lacrimal gland, tear film, and dry eye syndromes. Basic science and clinical relevance. November 14-17, 1992, Southampton, Bermuda. International conference proceedings. Adv Exp Med Biol. 1994;350:1-710.
- King-Smith PE, Fink BA, Nichols JJ, Nichols KK, Hill RM. Interferometric imaging of the full thickness of the precorneal tear film. J Opt Soc Am A Opt Image Sci Vis. 2006;23(9):2097-2104.
- Trattler W, Reilly C, Goldberg D, et al. Cataract and dry eye: prospective health assessment of cataract patients ocular surface study. Poster presented at: American Society of Cataract and Refractive Surgery 2011 Symposium and Congress; March 25-29, 2011; San Diego.
- Korb DR, Blackie CA. Restoration of meibomian gland functionality with novel thermodynamic treatment device: a case report. Cornea. 2010;29(8):930-933.
- Friedland BR, Fleming CP, Blackie CA, Korb DR. A novel thermodynamic treatment for meibomian gland dysfunction. Curr Eye Res. 2011;36(2):79-87.