Special Report

Ocular Surface Management

Early diagnosis and more accurate therapies are key to patient comfort.

By James V. Aquavella, MD

For the purposes of this discussion, the ocular surface comprises the total epithelia of the bulbar and tarsal conjunctiva, the corneal epithelium and the overlying tear film as well as the lid margins and orifices of the secretory apparatus. A properly constituted tear film is essential for visual clarity, to protect the underlying ocular structures, and to the maintenance of the homeostasis with the concurrent absence of subjective symptoms.

There are two distinct entities that comprise the majority of ocular surface pathology necessitating intervention by an eyecare physician. While distinct, they can coexist and not infrequently present a differential diagnostic dilemma.

Ocular Allergy

Allergic manifestations of the conjunctiva are often referred to as ocular allergy. Akpek and Hodges^1,2 in reviewing the topic differentiate four distinct conditions: allergic conjunctivitis (seasonal/SAC or perennial/PAC), vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC) and giant papillary conjunctivitis (GPC).

A basic understanding of immunological defense mechanisms is useful. The afferent arm results in recognition by the host of the presence of an antigen, while the efferent arm mediates the response. When antigens attack the conjunctiva, an exquisite immunologically active structure, they bind to macrophages and dendritic Langerhan cells. T-cells then travel along lymphatic channels to the lymph nodes. There is a strong role for the corneal epithelium in T-cell activation on the corneal surface, while in the nodes, both T and B lymphocytes proliferate and travel to the surface as well as to the lacrymal gland. Lymphokines are produced, complement activated and histamine released. This typical histamine reaction chain of events continues with the production of leukotrines, prostaglandins and cytokines.

The subsequent cascade of acute symptoms involves pruritis, tearing and vasodilatation. A typical rhinoconjunctivitis follows. Conjunctival injection, postnasal drip, coughing and sinus congestion are apparent. The more chronic PAC is usually a reaction to household antigens.

Acute allergic conjunctivitis

The more severe vernal conjunctivitis (VKC) can be sight-threatening and predominantly affects peripubescent male children in warmer climates and often involves the cornea. Shield ulceration and secondary anterior uveitis are not uncommon.

Atopic conjunctivitis is chronic, severe, bilateral and affects the lids as well as the entire ocular surface. This sight-threatening inflammation affects an older age group without geographic distribution. Scarring and secondary infection are not uncommon.

Giant papillary conjunctivitis is associated with constant mechanical irritation from sutures, prosthetics and contact lenses. This is a non-IgE mediated inflammation. Characteristic features include the formation of large cobblestone papillae, chemosis and mucous reaction. In contact lens wearers, significant amounts of chronic mucoid reaction are often tolerated. While increasing the rate of lens exchange, topical stabilizers and anti-inflammatory agents can have modest beneficial effects, the most effective therapy is the discontinuation of lens wear.

In all of these allergic conditions, the results of the antigen binding to specific mast cell receptors causes degranulation of the cells with the release of histamine, proteases, proteoglycans, as well as prostaglandins, leukotrines and platelet-activating factor—all mast cell-related contributions to the inflammatory cascade. Repeated eye rubbing may further accelerate mast cell disruption and degranulation. Ocular surface component cells (fibroblasts, epithelial cells, dendritic cells) are essential to the promulgation of the symptoms. The individual symptoms of various specific allergic entities may coexist and the entire immune process is complex,² all compounding the difficulty in accurate diagnosis. Furthermore, dry eye syndrome is much more frequent and easily misdiagnosed.³ The resemblance of many of the symptoms and signs with those of keratitis sicca represents an additional confounding circumstance.

Dry Eye Syndrome

Dry eye syndrome is a multifactorial disease of the ocular surface and tears, resulting in symptoms of discomfort, visual disturbance, and instability of the tear film with potential for ocular surface damage. It is accompanied by increased osmolarity and inflammation of the ocular surface.⁴ It is recognized as one of the most frequent ocular disorders, with symptoms affecting as many as 15 % of the U.S. population and a majority of the population over age 80. Traditional classification into aqueous, evaporative and lipid deficiency has proven to be overly simplistic, perpetuated by the lack of totally objective and non-invasive diagnostic tests.

Also at increased risk are postmenopausal women, contact lenses wearers and patients who have undergone refractive surgery.

Typical symptoms have been described as dryness, irritation, burning, itching, redness, foreign body sensation, blurred vision particularly at near, and on occasion, tearing and photophobia. One of the main difficulties in both diagnosis and treatment of these conditions is the wide variation (disconnect) between the degree of subjective symptoms and objective findings. Dry eye syndrome can cause prolonged and serious disruption with functional incapacity, while the slit lamp examination is within normal limits. In some instances, the reverse is true with significant staining of both cornea and conjunctiva while the patient has little distress and functions normally.

Positive findings can include reduced Schirmer's values of less than 10 mm of wetting, decreased tear breakup time to less than 10 seconds, the presence of filaments on the cornea surface, and associated blepharitis or meibomian gland dysfunction.

Management options include improvement of the lid appearance with a combination of warm compresses, lid hygiene, perhaps systemic doxycycline and omega 3 vitamin supplements. Inflammation may require topical steroids in varying dosages for varying periods of time. Attention to possible secondary elevation in intraocular pressure is mandatory. Frequent application of tear substitutes is one of the first lines of attack with the knowledge that preservatives may be toxic in this population. Anti-evaporative goggles along with modifications of environment and lifestyle are important adjuncts. Punctal occlusion, mucolytic agents and the use of a bandage soft contact lens may be indicated as well.

The goal of every therapeutic regimen must be to improve the quality and quantity of tears, increase the stability of the tear film, reduce evaporation and reduce or eliminate concurrent inflammation.

Shortcomings of our therapy include the inconvenience associated with drop instillation, the lack of a single therapeutic focus and the lack of objective means to determine the relative success of therapy.

In severe disease, we can anticipate a modest increase in comfort with little or no improvement in functional capacity and an unchecked intensity and progression of the disease.

In more moderate disease, we can anticipate improvement in comfort and functional capacity with the necessity for ongoing treatment and the continued dependence on environmental factors. Thus geography, airline travel and working conditions play an important role.

Our research has been focused upon developing purely objective means of assessing dynamic tear film architecture in an attempt to develop biomarkers enabling early diagnosis, more accurate therapy and the means of assessing efficacy of treatment.

We utilize specially designed ocular surface OCT, wave front, sensors, ellipsometry and thermal imaging deployed in a controlled adverse environmental chamber to conduct our analysis. The ultimate aim is to achieve early and more accurate diagnosis, understand the disease process, design improved treatment modalities and enable the objective testing of efficacy of new treatment modalities.

As a result of the frequency of these ocular surface conditions and their disruptive effects on functional capacity, all eyecare practitioners need to become actively involved in their management. For most, we are unable as yet to offer definitive treatment and cure, but the creation of a comprehensive therapeutic regimen, combined with frequent monitoring and modification, can result in significant improvement for our patients.

References

1. Akpek EK, Gottsh JD. Immune defense at the ocular surface. Eye (Lond.) 2003;17(8)949-959.
2. Hodges MG, MD, Keane-Myers AM. Classification of ocular allergy. Curr Opin Allergy Clin Immunol 2007; 7(5):424-428.
3. Aquavella JV. When allergy & ocular surface diseases collide. Review of Cornea & Contact Lens April 2009;30-32.
4. Gipson, IK, Argueso P, Beuerman R.. et al. Research in Dry Eye: Report of the Research Subcommittee.of the International Dry Eye WorkShop (2007). The Ocular Surface. 2007;5(2):179-193.

James V. Aquavella, MD, is Professor of Ophthalmology at the University of Rochester Flaum Eye Institute.