Dr. Gupta’s blog is designed to cover the latest innovations in ocular surface and MGD diagnosis and treatment from a practical, clinical perspective. Topics will range from dry eye demographics to treatment pearls and workflow tips and tricks, all focusing on real-world implementation of techniques and technologies.

BLOG: Glaucoma and dry eye, part 2: Preventing irreversible damage to meibomian glands

In glaucoma and dry eye, part 1, I discussed the high prevalence of dry eye symptoms among patients with glaucoma and the effect of chronic topical medications on the ocular surface. In addition to eye drop-related toxicity, several studies have shown that topical glaucoma medications can cause meibomian gland dysfunction and irreversible dropout — findings that encourage monitoring the eyelids and making informed decisions about treatment.

Evidence of meibomian gland damage

Two recent studies illuminate the meibomian gland damage associated with glaucoma medications. The first looked at patients on topical therapy to treat their glaucoma: 71 patients on one glaucoma drop, 61 patients on two drops and 30 patients on three drops to treat their disease. The study revealed evidence of morphological and functional changes in the meibomian glands in all groups — even those using just one medication. Patients using glaucoma drops long term exhibited lid margin abnormalities, superficial punctate keratopathy and higher rates of meibomian gland changes compared with the control group. Subjects also had significantly lower tear breakup time, a sign that the meibomian glands were not producing healthy oils.

Even more interesting is that degradation of meibomian gland health did not occur only with prostaglandin analogs as we might expect, but also with other classes of glaucoma drugs. This points to a need to evaluate the meibomian glands in patients using any type or number of topical therapies. And I have to believe that if we start looking at gland health prior to therapy initiation and along the course of a patient’s treatment, we will be better able to avoid leading patients to an “end-stage” phase in which they suffer severe gland atrophy and irreversible compromise of the ocular surface that is severely symptomatic in terms of vision quality decline and neurotrophism.

Another interesting study of 85 patients with glaucoma found that as the burden of antiglaucoma medications grew, so did tear film instability and meibomian gland dropout. Because we know we cannot reverse meibomian gland dropout, this result may well change the conversation about adding more glaucoma drops to a patient’s treatment regimen vs. initiating drug-sparing treatments, such as selective laser trabeculoplasty, or employing novel drug delivery tools to achieve adequate IOP control without damaging the surface.

Putting the findings into practice

To date, meibomian gland atrophy is thought to be irreversible. Thus, it is very important to identify negative effects of glaucoma medications on the meibomian glands early in the process. To give glaucoma patients the best care, it may be best to integrate meibography into the assessment, starting with baseline images and continuing with regular follow-up.

Although we cannot bring back lost meibomian glands, we can treat MGD and inflammation at the level of the ocular surface to preserve the health of the remaining glands and maintain the integrity of the ocular surface. For example, when I see patients in which chronic ocular surface disease is caused by years of topical antiglaucoma therapy, I often initiate Xiidra (lifitegrast, Novartis) to treat the surface inflammation and repair the punctate erosions. In addition, I offer MGD therapy such as thermal pulsation therapy (LipiFlow, Johnson & Johnson Vision), intense pulsed light therapy, iLux (Alcon) and/or TearCare (Sight Sciences). These therapies are an important part of treating MGD, as is controlling inflammation. They can be effective in returning the meibomian glands to healthy function, and perhaps it then becomes more reasonable to keep the patient on a topical glaucoma medication. If the surface or glands cannot be rehabilitated, serious consideration should be given to other options such as MIGS or implantable medication delivery procedures.

My wish is that all ophthalmologists taking care of patients with glaucoma, be it the glaucoma specialist or comprehensive physician, consider assessing patients for MGD and atrophy and use that information to wisely choose their preferred treatment option. Knowing the status of the patient’s meibomian glands, we can better understand the impacts of current treatment, as well the risks of adding more topical medication. Thankfully, we have an increasing armamentarium of alternatives to topical medication for IOP control. Now is the time to make the shift to thinking about glaucoma as an interventional disease that can be controlled with modern tools that aren’t topical medications.

 

References:

Arita R, et al. Cornea. 2012;doi:10.1097/ICO.0b013e31823f8e7d.

Cho WH, et al. J Glaucoma. 2018;doi:10.1097/IJG.0000000000000841.

 

Disclosure: Gupta reports she is a consultant to Allergan, Alcon, Johnson & Johnson Vision, Kala, NovaBay, Novartis, Oyster Point Pharmaceuticals, Ocular Science, Shire, Sight Sciences, TearLab and Zeiss.