Dry eye disease (DED) has undergone a dramatic metamorphosis over the last 20 years. Once exclusively defined as either a tear deficiency or excessive evaporation, according to the NEI, DED is now defined more specifically:
“Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage and neurosensory abnormalities play etiological roles,” according to the Tear Film and Ocular Surface Society’s (TFOS) Dry Eye Workshop (DEWS )II.
This broadened definition includes the patient’s symptoms and clinical signs, such as hyperosmolarity, ocular surface inflammation and resulting ocular surface damage. Notably, neurosensory abnormalities were included, lending some potential explanation for the often encountered discordance between signs and symptoms.
This definition gives license and urgency to O.D.s to serve our patients, and throughout this “Practicing Medical Optometry” section, we will provide you with a blueprint for how to do so. Here, we begin with a look at the condition’s etiology, the key to identifying DED patients and why you should act to find these patients.
The etiology of DED is complex, and much remains to be fully elucidated. The multifactorial nature of the disease is both the origin and the result of its complexity. Some practitioners may exclusively attribute DED to inflammation, and others to meibomian gland dysfunction (MGD), but the truth likely lies somewhere in between with overlapping elements. Other factors, such as patient demographics (women, aging), inadequate blink mechanism, contributory ophthalmic/systemic conditions (post-surgical, autoimmune disease, rosacea), medications (antihistamines, for example, are known to cause ocular surface drying) and poor lid hygiene, also may play significant roles. It’s our jobs as O.D.s to identify those causes. Drs. Vin Dang and Walt Whitley pick this up in “Be the DED Detective.”
Because the condition is rarely vision threatening, but often quality-of-life compromising, the motivation to be aggressive in its treatment lies within the physician.
Two basic types of motivation are intrinsic and extrinsic. An intrinsic motivation is gratifying to the doctor, such as treating the patient with an ophthalmic medication because she believes the patient will have a happier, more productive work day after initiating treatment. An extrinsic motivation is powered by a reward. For example, a doctor recommends an advanced treatment, such as thermal pulsation or intense pulsed light, for which the practice will reap a financial reward in providing symptomatic relief and sign improvement in DED patients, according to Current Eye Research and Advances in Pediatrics. Both treatments are reasonable and, thus, responsible recommendations. (See Dr. Jade Coats’ “Defy Dry Eye.”)
Regardless of a doctor’s motivation, initiating treatment on patients who have DED would tackle one of the largest unmet needs in all of medicine. Patients and practices both stand to benefit. (See Dr. Scott Schachter’s “Practical Steps to DED Care.”)
In addition to the multifactorial nature of DED, presented in DEWS II, the condition affects more than 16 million Americans, reports the American Journal of Ophthalmology. My colleagues and I hope the following pages provide you with actionable steps to better serve these patients. OM