A review of the surface - from disease to co-managing anterior segment surgery.
As our profession moves towards an increased awareness of ocular surface disease, the question is often posed: How do we manage the ocular surface? There are so many ocular surface diseases that it takes book chapters to fully describe the pathophysiology and various treatment strategies that we can use to treat each individual disease. Here I intend to provide a broad overview and a general "recipe" for treating an assortment of ocular surface diseases.
Get to know the surface
Let's first review some characteristics of the ocular surface so we can better understand how to treat these patients. The ocular surface is composed of the cornea, the bulbar and the palpebral conjunctiva. The corneal surface is composed of the cuboidal epithelium with microvilli that secrete glycocalyx, the protein that covers the epithelium. The glycocalyx makes it possible for the remainder of the tear film to rest on the hydrophobic corneal surface. The microvilli have a ciliary function. They move various antigens and waste products that can be trapped in the surface mucin nasally toward the lacrimal drainage system.
The conjunctiva contains goblet cells that secrete mucins 1 and 4. These mucins are absorbed into the ocular surface and blend with the aqueous component of the tear film. The function of these mucins is to protect the ocular surface from contaminates. The tear prism is a delicate balance of mucin, electrolytes, proteins, pro-inflammatory cytokines, immunoglobulins, and outer meibum lipids that functions to prevent desiccation. It also provides nutrition, removes waste products and protects the ocular surface immunologically.
Identify the problem
The daunting task every clinician faces is to treat each person promptly and effectively. The first step: Correctly identify the problem. As we review that process, keep in mind that all diseases fall into one or more of the major categories of disease as listed in Table 1, below.
The key is to develop a systematic plan to examine each segment of the ocular surface individually for the presence of each of these major disease categories. This plan will reduce the likelihood of missing any key components. Ask yourself this series of questions:
1. What level of inflammation in the form of chemosis, hyperemia, or hypoxia is present in each part of the ocular surface?
2. Are the lids involved?
a. Are the changes focal, localized, or geographic?
b. Is there a void or change in the normal architecture?
c. Is one or more of the six types of blepharitis present?
d. Is the lid margin keratinized?
3. Is the palpebral conjunctiva involved?
a. Are there inflammatory cysts, deposits or mechanical changes present?
b. Is there a follicular or papillary reaction, or both?
4. Is the bulbar conjunctiva involved?
a. Is there chemosis or focal thickening?
b. Is there focal epithelial loss?
5. Is the cornea involved and if so, at what level?
a. Is there any specific corneal staining pattern? (See Table 2, "OSD Staining Patterns.")
b. Is there any epithelial cellular infiltration, edema or opacification?
c. Is there any change in normal cellular architecture?
d. Are these changes local or geographic?
6. What is the status of the tear film?
a. Are there mucous strands or filaments present?
b. Is there sufficient tear film?
Manage the patient
The key to success in treating any disease is effective and honest communication. A few points to keep in mind when talking with your patient:
* Explain what they have
* Explain why you are treating
* Explain how you're treating
* Give written instructions
* Have patient repeat instructions
* Make them commit
* Ask if they have questions.
If your patient doesn't understand, then poor compliance is the likely result, so your chance of success diminishes greatly. Have an honest discussion about the patient's condition, prognosis and various treatment options available. Discuss your treatment strategy. Explain what to expect during the treatment process, including potential drug interactions, side effects and anticipated patient symptoms during the recovery process. Advocate that the patient's compliance is critical to the successful treatment. Emphasize that failure to follow the treatment regimen will prolong the disease, the symptoms and also potentially cause an increased threat to vision and health. Lastly, ask if the patient understands your instructions and if she has any questions.
Manage the problem
When it comes to the true medical management of the ocular surface, there are a few basic rules to keep in mind before embarking on any treatment strategy. Treatment options depend on many conditions including:
* Threat to life or vision
* Degree of secondary inflammation, etc.
Here is a step-by-step guide for treating various ocular surface diseases:
1. Stop infection. Treat ocular surface infection quickly and aggressively with the most potent antibiotics, antiviral or antifungal available. Currently the fourth-generation fluoroquinolones, Zymar (gatifloxacin ophthalmic solution 0.3%, Allergan) and Vigamox (moxifloxacin hydrochloride ophthalmic solution 0.5%, Alcon), are the drug(s) of choice (DOC) for bacterial infactions due to their wide range of coverage, high kill rate and low resistance. Viroptic is the DOC for herpetic infections.
2. Stop cicatridal changes, mechanical agents, antigen contact, etc. Remove any mechanical force that is causing damage to the surface, including foreign body in the lid margin, conjunctiva or cornea. In some instances this may even indicate removal of metaplastic or degenerating tissue. Include aggressive lubricant therapy to irrigate the surface and wash away localized antigens, foreign bodies and inflammatory mediators. In allergic disease this may also mean taking aggressive avoidance strategies to decrease or eliminate antigen exposure.
3. Treat associated inflammation. Often overlooked but crucial to a successful outcome, you must treat inflammation deriving from the ocular surface disease. The inflammatory process in ocular surface disease is very complex and often engaged at multiple levels. Effective treatment may call for concomitant use of multiple anti-inflammatory medications along the continuum (see Table 4, "Antiinflammatory Treatments"). The goal is to impede negative inflammatory changes that can lead to patient discomfort or visual loss as well as permanent changes in the cellular architecture of the ocular surface. Being initially aggressive will cause a quicker mediation of the irritating agent and allow for a faster overall recovery.
On the opposite side of the spectrum is a more generalized "shotgun" approach. It may temporarily calm the clinical signs but prolong the actual recovery time while allowing for a chronic sub-clinical inflammatory process to develop on the ocular surface. Chronic inflammation results in degenerative or atrophie morphological changes of the ocular surface cellular structures.
4. Control patient discomfort. Patients want to feel better and often gauge their success by their symptoms. Provide adequate pain management techniques including both oral and topical alternatives when necessary. Use lubricant therapy, cold compresses and topical analgesia in the form of Acular (ketorolac tromethamine ophthalmic solution 0.4%, Allergan) or Voltaren (diclofenac sodium ophthalmic solution 0.1%, Novartis). It's essential to control photophobia so cycloplegia, preferably homatropine 5% ophthalmic solution, should be employed when there is an impending or active intraocular involvement. Be judicious in using oral agents in the form of non-narcotic or narcotic analgesics. Start aggressively and taper as needed.
5. Restore normal anatomy and physiology. Once you have arrested the progression of the ocular surface disease, the secondary challenge is to restore the ocular surface to its original state. Think clinically: Begin at the external surface and work inward.
* Is the eyelid apposition correct? Does it allow the meibum to deposit correctly onto the tear prism, and the tear prism to drain correctly through the punctum?
* Is the lid elasticity normal?
* Are the eyelid margins clear?
* Is the tear film balance normal, or does the patient have issues in either the outer meibum layer or the inner aqueous mucin complex?
* Is the tear prism normal and sufficient to prevent desiccation?
* Is the ocular surface normal including the glycocalyx? Is there epithelial desquamation or metaplasia resulting in non-secretory keratinized epithelium present?
* Are there any basement membrane or epithelial dystrophies present, resulting in an elevation of the overlying epithelium?
Remember these steps
I hope this has provided you with a conceptual idea of how to treat the wide array of OSDs. Identify the etiology of the disease through careful analysis and astute clinical skills. Treat aggressively, stop infection or other mechanical event, treat inflammation, control patient discomfort, and restore normal physiology and anatomy.
BY SCOT MORRIS, O.D., F.A.A.O., Conifer, Colo.
Dr. Morris is the director of Eye Consultants of Colorado, LLC, and Morris Education & Consulting Associates. He is a member of the American Optometric Association and is a Fellow of the American Academy of Optometry.
Copyright Boucher Communications, Inc. Aug 2005
Provided by ProQuest Information and Learning Company. All rights Reserved