Dry eye is one of the most common reasons for ophthalmic consultation. It becomes increasingly prevalent with age, affecting approximately 10% of individuals 30–60 years of age and 15% of adults older than 65 years. Most epidemiologic studies have demonstrated a higher prevalence among women; dry eye seems to affect all racial and ethnic groups equally.
The psychological problems associated with a highly symptomatic, incurable, chronic disease can require considerable support. Results of quality-of-life studies have shown that the impact of moderate to severe dry eye on affected patients is similar to that of moderate to severe angina. Organizations such as the Sjögren’s Syndrome Foundation (www.sjogrens.org) can provide valuable resources for these patients. For certain patients, consultation with physicians who specialize in pain management can be very helpful.
The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):75–92.
Mechanisms of Dry Eye
Dry eye results from a combination of factors. Tear hyperosmolarity stresses the surface epithelium and leads to the release of inflammatory mediators, which disrupt the junctions between the superficial epithelial cells. T cells can then infiltrate the epithelium and in turn produce cytokines such as tumor necrosis factor-α and interleukin-1. These cytokines promote accelerated detachment of the epithelial cells and apoptosis (programmed cell death). This results in further disruption of junctions and influx of inflammatory cells, creating a vicious cycle. The cycle of events is shown in Figure 3-9.
One diagnostic classification scheme divides dry eye patients into those with aqueous tear deficiency and those with evaporative dry eye (Fig 3-10). An individual patient may have elements of both conditions, however. In aqueous tear deficiency, T-cell–mediated inflammation of the lacrimal gland occurs, leading to diminished tear production and the propagation of inflammatory mediators on the ocular surface. In evaporative dry eye, the primary abnormality is meibomian gland dysfunction, in which altered lipid metabolism of the meibum causes a transition from unsaturated to saturated fats, resulting in obstruction of the glands. This leads to tear film instability as well as tear evaporation and hyperosmolarity, initiating the inflammatory cycle.
Tear film instability can also be initiated by other conditions, including xerophthalmia, ocular allergy, contact lens wear, a high ratio of dietary n-6 to n-3 essential fatty acids, diabetes mellitus, cigarette smoking, prolonged use of video displays, and long-term use of medications with topical preservatives such as benzalkonium chloride.
Epithelial injury stimulates corneal nerve endings, leading to symptoms such as ocular discomfort, increased blinking, and, potentially, compensatory reflex lacrimal tear secretion. Loss of normal mucins at the ocular surface contributes to symptoms by increasing frictional resistance between the eyelids and globe. During this period of corneal nerve stimulation, the high reflex input may cause neurogenic inflammation within the lacrimal gland.
Tear delivery may be obstructed by cicatricial conjunctival scarring or reduced by a loss of sensory reflex drive to the lacrimal gland from the ocular surface. The etiology of dry eye may include refractive surgery (eg, LASIK), contact lens wear, and chronic topical anesthetic abuse. The pathogenesis of dry eye may involve several interacting mechanisms.
American Academy of Ophthalmology Cornea/External Disease Panel. Preferred Practice Pattern Guidelines. Dry Eye Syndrome. San Francisco: American Academy of Ophthalmology; 2013. Available at www.aao.org/ppp.
The definition and classification of dry eye disease: report of the Definition and Classification Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):75–92.
Bohm KJ, Djalilian AR, Pflugfelder SC, Starr CE. Dry eye. In: Mannis MJ, Holland EJ, eds. Cornea. Vol 1. 4th ed. Philadelphia: Elsevier; 2017:377–396.
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.
Pflugfelder SC. Tear dysfunction and the cornea: LXVIII Edward Jackson Memorial Lecture. Am J Ophthalmol. 2011;152(6):900–909.
Stevenson W, Chauhan SK, Dana R. Dry eye disease: an immune-mediated ocular surface disorder. Arch Ophthalmol. 2012;130(1):90–100.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.