At A Glance

  • Both glaucoma and dry eye disease are chronic conditions that must be managed over a patient’s lifetime.
  • Minimizing the number of topical medications a patient must take daily is one way to improve the ocular surface.
  • Topical glaucoma formulations that omit benzalkonium chloride can reduce corneal toxicity. 

Glaucoma and dry eye disease (DED) are each chronic and multifactorial in nature, and management of each condition can present many challenges, including patients’ adherence to medications, patients’ continued motivation to manage their disease, and health care costs. So what happens when the two exist concurrently?


Studies have found that 60% of patients treated for open-angle glaucoma or ocular hypertension also experience symptoms of DED.1 This comorbidity can complicate the treatment of glaucoma, as damage to the ocular surface from DED has the potential to reduce patients’ adherence to medical treatment for their glaucoma and reduce their quality of life2,3 and vision.

When asked about dry eye symptoms, 59% of patients with glaucoma reported symptoms in at least one eye, and 27% of patients reported severe symptoms.1 That’s one in every three patients with glaucoma reporting severe symptoms of DED—when asked. If we are not asking our glaucoma patients whether they experience dry eye symptoms, we may not be aware if they are affected by DED and, if so, on what level.

When investigators looked at clinical signs of DED in patients with glaucoma, they found conjunctival and corneal staining in 22% and abnormal tear breakup time (TBUT) in 78%, with 65% displaying severe TBUT.1 Schirmer scores were reduced in 61% of patients in at least one eye, with severe deficiency in about 35% of patients.1 Remember, glaucoma patients have 22% lower basal tear turnover compared to normal physiology, increasing their risk for DED even before their glaucoma treatment begins.4 Compounding this with a reduction in Schirmer score in one out of every three patients we treat for glaucoma is a recipe for DED.

Other risk factors for DED include the number of medications a patient uses to treat his or her glaucoma, the duration of treatment, and the preservative system in the medication as well as its active ingredients. The medications considered the first-line therapy for glaucoma management because of their once daily dosing schedule and effectiveness—the prostaglandin analogues—can also increase meibomian gland dysfunction.5 Beta-blockers, another mainstay, can decrease the aqueous layer of the tear film.6

Failure to treat DED in our glaucoma patients can negatively affect these patients’ quality of life and their adherence to their sight-saving glaucoma therapies. Ocular side effects of these medications—stinging, burning, itching, redness, etc.—pose significant barriers to patient adherence.7 Poor adherence increases the risk for glaucoma progression. Further, glaucoma tests such as visual fields have been shown to be unreliable when DED is not properly treated.8


Due to the risk of these negative impacts on patients’ adherence and therefore their quality of life, it is imperative to evaluate glaucoma patients for DED before initiating therapy with topical glaucoma medications. This can be done simply with an in-office questionnaire such as the Standardized Patient Evaluation of Eye Dryness or the Ocular Surface Disease Index and the use of vital dyes looking for corneal and conjunctival staining or rapid TBUT. Tear film osmolarity is also important, if you have access to point-of-care testing in your clinic.

If DED is present, treat it along with the patient’s glaucoma. Starting early with antiinflammatory medications such as cyclosporine ophthalmic emulsion 0.05% (Restasis, Allergan, or generic) and lifitegrast ophthalmic solution 5% (Xiidra, Novartis) can help combat the inflammation associated with DED.

Remember also to examine the lid margins and assess the structure and function of the meibomian glands. Gland-clearing treatments such as the LipiFlow Thermal Pulsation System (Johnson & Johnson Vision), the TearCare System (Sight Sciences), the iLux MGD Treatment Device (Alcon), or intense pulsed light can positively affect tear film stability and patient symptoms.

If the patient does not have DED at the start of glaucoma management, be sure to continue to look for signs and symptoms as you see the patient back over the next several months to years. Commonly used glaucoma medications present known risks to corneal and conjunctival health and meibomian gland function. Studies have shown that increased duration of medication use and exposure to preservatives can lead to DED.9


How can we effectively manage glaucoma and DED simultaneously? Whenever possible, reduce the number of glaucoma medications prescribed for a patient. For those with DED, start them on antiinflammatory medication early to reduce inflammation and the number of artificial tears needed during the day. Consider the benefits of oral omega-3 fish oil supplements for inflammatory control, and offer meibomian gland clearing treatments to aid with tear film stability.

For the management of glaucoma in patients with DED, consider opting for selective laser trabeculoplasty as first-line therapy rather than a topical drop. Research shows that this procedure can be as effective as medication.10 Microinvasive glaucoma surgery is another great option for patients with glaucoma who are undergoing cataract surgery, as these procedures can help to reduce the number of medications used per day. Note, however, that most of these devices are restricted to use in patients undergoing cataract surgery.

If possible, start pharmaceutical treatment with a benzalkonium chloride (BAK)-free medication (See Do Preservatives Matter?). If you like the IOP-lowering ability of the prostaglandin analogues, then consider one of the BAK-free formulations, such as latanoprost ophthalmic emulsion 0.005% (Xelpros, Sun Ophthalmics), which has a fixed cost to patients. Preservative-free alternatives have been shown to be as effective as their BAK-preserved counterparts.9,11


Managing a patient with both DED and glaucoma is a marathon, not a sprint. Be diligent in your care of patients with concomitant diseases. Remember that less can be more, and be mindful of how many topical medications your patient needs to manage each disease on a daily basis. Don’t forget to consider alternative treatments, such as in-office procedures for MGD and surgical options. Finally, monitor your glaucoma patients for DED over their lifetimes, and employ management strategies that can help improve their quality of life and vision

  • 1. Leung EW, Medeiros FA, Weinreb RN. Prevelence of ocular surface disease in glaucoma patients. J. Glaucoma. 2008;17:350-355.
  • 2. Skalicky SE, Goldberg I, McCluskey P. Ocular surface disease and quality of life in patients with glaucoma. Am J Ophthalmol. 2012;153(1):1-9 e2.
  • 3. Paletta Guedes RA, Paletta Guedes VM, Freitas SM, Chaoubah A. Quality of life of medically versus surgically treated glaucoma patients. J Glaucoma. 2012;22:369-373.
  • 4. Kuppens EV, van Best JA, Sterk CC, et al. Decreased basal tear turnover in patients with untreated primary open-angle glaucoma. Am J Ophthalmol 1995;120:41-46.
  • 5. Mocan MC, Uzunosmanoglu E, Kocabeyoglu S, Karakaya J, Irkec M. The association of chronic topical prostaglandin analog use with Meibomian gland dysfunction. Eur J Ophthalmol. 2015;25:38-39.
  • 6. Petounis AD, Akritopoulos P. Influence of topical and systemic beta-blockers on tear production. Int Ophthalmol. 1989;13:75-80
  • 7. Zimmerman TJ, Hahn SR, Gelb L, et al. The impact of hyperemia on open-angle glaucoma (OAG) treatment. Invest Ophthalmol Vis Sci. 2007;48(13):4345.
  • 8. Yenice Ö, Temel A, Örüm Ö. The effect of artificial tear administration on visual field testing in patients with glaucoma and dry eye. Eye. 2007;21, 214-217.
  • 9. Uusitalo H, Egorov E, Kaarniranta K, Astakhov Y, Ropo A. Benefits of switching from latanoprost to preservative-free tafluprost eye drops: a meta-analysis of two Phase IIIb clinical trials. Clin Ophthalmol. 2016;10:445-454.
  • 10. Waisbourd M, Katz LJ. Selective laser trabeculoplasty as a first-line therapy: A review. Can J Ophthalmol. 2014;49(6):519-522.
  • 11. Katz G, Springs CL, Craven ER, Montecchi-Palmer M. Ocular surface disease in patients with glaucoma or ocular hypertension treated with either BAK-preserved latanoprost or BAK-free travoprost. Clin Ophthalmol. 2010;4:1253-1261.
  • 12. Whitson JT, Cavanagh HD, Lakshman N, Petroll WM. Assessment of corneal epithelial integrity after acute exposure to ocular hypotensive agents preserved with and without benzalkonium chloride. Adv Ther. 2006;23(5):663-671.
  • 13. Kamath AP, Satyanarayana S, Rodrigues F. Ocular surface changes in primary open angle glaucoma with long term topical anti glaucoma medication. Med J Armed Forces India. 2007;63(4):341-345.
  • 14. Lavin MJ, Wormald RPL, Migdal CS, Hitchings RA. The influence of prior therapy on the success of trabeculectomy. Arch Ophthalmol. 1990;108(11):1543-1548.
  • 15. Panchapakesan J, Mitchell P, Tumuluri K, Rochtchina E, Foran S, Cumming RG. Five year incidence of cataract surgery: the Blue Mountains Eye Study. Br J Ophthalmol. 2003;87(2):168-172.
  • 16. Bron A, Chiambaretta F, Pouliquen P, Rigal D, Rouland JF. Efficacy and safety of substituting a twice-daily regimen of timolol with a single daily instillation of nonpreserved beta-blocker in patients with chronic glaucoma or ocular hypertension. J Fr Ophtalmol. 2003;26(7):668-674.