Dry Eye

Find dry eye clues in patient medications

After identifying exacerbating medications, dry eye therapies and treatments have greater impact on preventing progression.

BY LAURA M. PERIMAN, MD

Systemic medications, including prescription and OTC drugs, have the potential to limit lacrimal or meibomian gland output and may contribute to dry eye disease (DED).

Here, I describe how I approach a dry eye patient and why I carefully examine each patient’s medications list.

DED and medications

DED is an inflammatory disease that results when the chronic inflammatory cycle begins and self-perpetuates. Desiccating stress and hyperosmolarity are keys to underlying mechanisms of DED and can result from a wide variety of causes, including age, hormone status, lifestyle, and environmental exposures.^1-3

Another cause, patient’s medications, has become an increasingly important component of my assessment and recommendations for the DED patient. In each of my exam rooms, I placed a laminated copy of a table that summarizes the medications that most exacerbate DED, which I still refer to when necessary.⁴ (For a list of common systemic medications that may cause dry eye, see the online version of this article at www.ophthalmicprofessional.com.)

Our staff also plays a role in the dry eye diagnosis. They ask patients about all medications they take, including prescriptions, OTC drugs and herbs/supplements. In my experience, patients often erroneously assume that OTC medications, as well as herbs and supplements, are inherently safe. However, many OTC medications have unwanted side effects, especially for the eyes.

The following case report summary illustrate the interesting and various presentations of the effect of systemic medications on the ocular surface.

Case report

A 73-year-old Asian female referred to us with a 15-year history of chronic DED with frequent exacerbations. Her short medication list included metoprolol (Lopressor, Novartis) for 12 years for mild essential hypertension. She reported bothersome DED symptoms with overlying exacerbations three to four times per year. The patient’s symptoms and clinical signs indicated ITF level 3 DED as well as marked meibomian gland loss (grade 3+). (See “ITF level severity and treatment recommendations,” page 33.)

External examination revealed a grossly incomplete blink and incomplete lid seal.⁴ Her moderate incomplete lid closure and significant MGD prompted questions regarding past oculoplastic surgery and concurrent use of neuromuscular junction blocking injectables [e.g., botulinum toxin (Botox)] around the eyes. The patient reported a bilateral upper eyelid blepharoplasty (excellent result) 20 years prior and received neuromuscular junction blocking injectables in the forehead, glabellum and orbicularis muscles three to four times per year for the past 10 years.

In pointing this out, the patient realized that her symptoms were significantly exacerbated two months after starting Lopressor and one to two weeks after each administration of neuromuscular junction blocking injectables. We identified these drugs as the patient’s identifiable and modifiable desiccating stresses. Systemic beta blockers directly limit lacrimal gland output and may effect the sympathetic innervation of the meibomian glands.⁵ Neuromuscular junction blockade injectables to the temporal orbicularis muscle likely weaken blink forces and lid wiper function.⁶ We asked her PCP to switch to a less exacerbating anti-hypertensive and the patient to stop receiving cosmetic botulinum toxin injections in the “crow’s feet” area.

At her most recent visit, DED symptoms significantly improved just three months after changing her systemic medications and four months after discontinuing Botox injections. Ongoing success will depend upon keeping inflammation under control with the ITF level 3 interventions as well as addressing the comorbid meibomian gland dysfunction.

Discussion and summary

Prescription and OTC medications affect the whole body more than our patients routinely consider. Common systemic medications impact the ocular surface, so ask yourself whether any of the patient’s medications limit normal physiologic function (such as decreased tear, mucin or meibum production) and/or limit normal mechanical function (such as reduced blink force or blink frequency).

DED is a chronic, self-perpetuating inflammatory cycle, so you must initiate treatment to prevent DED progression and improve each patient’s OSD. After identifying the suspected desiccating stress-inducing medications, they can often be discontinued, decreased or switched to a less offending class.

Look closely at your DED patients’ complete systemic medication list — rewarding clues await discovery. OP

REFERENCES

Laura M. Periman, MD, is a cornea and refractive surgery trained ophthalmologist in Redmond, WA. Her interests in immunopathophysiology started as a researcher and development associate at Immunex Corp. in the early 1990s. She can be reached at lauram perimanmd@gmail.com.