TREATMENT

●When elevated, intraocular pressure should be controlled.

●When inflammation is the source of the edema, it should be controlled.

●Corneal dehydration should be sought for patients with early or mild edema with hypertonic saline drops or ointments (usually drops as frequently as needed during the day and ointment at bedtime). A hairdryer held at arm’s length for stimulation of tear evaporation on awakening in the morning may be helpful.

●Soft contact lenses should be used for painful recurrent bullae or for early mild irregular astigmatism.

Surgical

●Palliative anterior stromal puncture, corneal cautery, conjunctival flap placement, amniotic membrane transplantation, or phototherapeutic keratectomy (PTK) may be sufficient to provide comfort to patients with recurrent painful bullae in eyes with limited or no visual potential.

●Optical penetrating keratoplasty (PKP) may be combined with lens extraction in the face of cataract. Intraocular lens exchange and, if necessary, anterior vitrectomy may be indicated for corneal edema associated with intraocular lenses.

●Posterior lamellar keratoplasty (PLK) is an evolving procedure that involves surgical replacement of the endothelial cell layer with donor tissue, with minimal manipulation of the recipient corneal surface. Deep lamellar endothelial keratoplasty (DLEK) was initially described with instrument and procedural refinements over simple PLK and demonstrated successful results. However lamellar dissection of the recipient cornea still proved to be difficult for many surgeons. The current technique, Descemet’s stripping endothelial keratoplasty (DSEK) or Desecmet’s stripping automated endothelial keratoplasty (DSAEK) is a further technical advancement and involves scraping Descemet’s membrane and endothelium from the recipient cornea. The advantage over a traditional PKP is that these variants of PLK can result in smoother surface topography with minimal astigmatism and decreased risk of wound dehiscence. Also the post-operative corneal power can be more stable and predictable, which allows for accurate calculations of intraocular lens power. Because of the lack of issues regarding sutures, wound stability, and topography, these techniques may result in more rapid visual rehabilitation.

●For patients who have undergone multiple PKPs or have a high risk of graft failure, keratoprosthesis can be offered as a treatment modality.

●Recent studies have shown that the corneal endothelium is arrested in the G1-phase of the cell cycle and retains the capacity to proliferate in vivo, but is inhibited by factors such as TGF-B and p27kip1. In the future, this information may help us to induce endothelial cell proliferation in vivo and create better procedures for repopulation of endothelial cells.

COMPLICATIONS

In addition to decreased vision and pain, patients may develop significant anterior segment inflammation when bullae rupture. This can lead to hypopyon formation in the absence of infection. Treatment with cycloplegic agents is very beneficial, in addition to the mentioned treatments. Secondary infection may also occur in the face of loss of epithelium due to the rupture

of bullae and has been reported at a rate of 4.7% in bullous keratopathy patients.

REFERENCES

Adamis AP, Filatov V, Tripathi BJ, et al: Fuchs’ endothelial dystrophy of the cornea. Surv Ophthalmol 38:149–168, 1993.

Akhtar S, Bron AJ, Hawksworth NR, et al: Ultrastructural morphology and expression of proteoglycans, βig-h3, tenascin-C, fibrillin-1, and fibronectin in bullous keratopathy. Br J Ophthalmol 85:720–731, 2001.

Cormier G, Brunette I, Boisjoly HM, et al: Anterior stromal punctures for bullous keratopathy. Arch Ophthalmol 114:654–658, 1996.

Flowers CW, Chang KY, McLeod SD, et al: Changing indications for penetrating keratoplasty, 1989–1993. Cornea 14:583–588, 1995.

Hatton MP, Perez VL, Dohlman CH: Corneal oedema in ocular hypotony. Experimental Eye Research 78:549–552, 2004.

Hicks CR, Crawford GJ, Lou X, et al. Corneal replacement using a synthetic hydrogel cornea, AlphaCorTM: device, preliminary outcomes and complications. Eye 17:385–392, 2003.

Ishino Y, Sano Y, Nakamura T, et al: Amniotic membrane as a carrier for cultivated human corneal endothelial cell transplantation. Invest Ophthalmol Vis Sci 45:800–806, 2004.

Joyce NC: Proliferative capacity of the corneal endothelium Progress in Retinal and Eye Research 22:359–389, 2003.

Kangas TA, Edelhauser HF, Twining SS, et al: Loss of stromal glycosaminoglycans during corneal edema. Invest Ophthalmol Vis Sci 31:1994– 2002, 1990.

Levenson JE: Corneal Edema: Cause and treatment. Surv Ophthalmol 20:190–204, 1975.

Luchs JI, Cohen EJ, Rapuano CJ, et al: Ulcerative keratitis in bullous keratopathy. Ophthalmology 104:816–822, 1997.

Maini R, Sullivan L, Snibson GR, et al: A comparison of different depth ablations in the treatment of painful bullous keratopathy with phototherapeutic keratectomy. Br J Ophthalmol 85:912–915, 2001.

McMahon TT, Polse KA, McNamara N, et al: Recovery from induced corneal edema and endothelial morphology after long-term PMMA contact lens wear. Optometry Vision Sci 73:184–188, 1996.

Mohay J, Lange DM, Soltau JB, et al: Transplantation of corneal endothelial cells using a cell carrier device. Cornea 13:173–182, 1994.

Pires RTF, Tseng SCG, Prabhasawat P, et al: Amniotic membrane transplantation for symptomatic bullous keratopathy. Arch Ophthalmol 117:1291–1297, 1999.

Terry MA, Ousley PJ: Replacing the endothelium without corneal surface incisions or sutures: The first United States clinical series using the deep lamellar endothelial keratoplasty procedure. Ophthalmology 110:755–764, 2003.

Waring GO, 3rd, Bourne WM, Edelhauser HF, et al: The corneal endothelium: normal and pathologic structure and function. Ophthalmology 89:531–590, 1982.

Melles GR. Posterior lamellar keratoplasty: DLEK to DSEK to DMEK. Cornea 25:879–881, 2006.

190 CORNEAL MUCOUS PLAQUES

371.44

Ramesh C. Tripathi, MD, PhD, FACS, FRCOphth

Columbia, South Carolina

Brenda J. Tripathi, PhD

Columbia, South Carolina

Richard M. Davis, MD

Columbia, South Carolina

Corneal mucous plaques are abnormal collections of a mixture of mucus, epithelial cells, and proteinaceous and lipoidal material that adhere firmly to the corneal surface. The plaques may

190laquesTERCHAP Mucous Corneal •

Cornea • 19 SECTION

a

b

FIGURE 190.1. Corneal mucous plaques. a) Clinical photograph of multiple corneal mucous plaques of varying sizes and shapes in a patient with keratoconjunctivitis sicca. Fluorescein staining reveals breakup of the tear film over the plaques, which are slightly elevated from the corneal surface. b) Photomicrograph of 1 μm thick, toluidine blue stained section of a debrided mucous plaque that consists of desquamated degenerating epithelial cells (arrows), lipid globules (L), mucin (M) and foreign bodies. Original magnification × 160.

also enmesh calcareous granules and bacteria, as well as dust particles and other foreign bodies. The mucous plaques are translucent to opaque and may vary in size and shape from multiple small islands to bizarre patterns that may involve more than half the corneal surface (Figure 190.1).

ETIOLOGY/INCIDENCE

●An abnormality of the exposed surface of the superficial corneal epithelial cells and of tears with excessive mucus formation and the presence of epithelial receptor sites for the plaque elements predispose to this condition.

●The normal desquamation of epithelial cells beneath the plaque is retarded, and exfoliating surface cells become incorporated in the plaque. The plaque is formed when highviscosity mucus and proteinaceous material adhere to the deeper squamous cells of the cornea or even to Bowman’s layer through the intercellular spaces, as well as through abnormally formed transcellular aperture and epithelial

defects; because of its physicochemical property, the mucous plaque enmeshes the desquamated epithelial cells.

●The viscosity of the mucus may increase due to dehydration or an increase in its sialomucin component, or secondarily because of infection with staphylococci, which liberate enzymes that can lyse the mucoprotein and glycosaminoglycan components of mucus produced normally by the conjunctival goblet cells.

●Corneal mucous plaques occur primarily in patients with keratoconjunctivitis sicca but may also occur with herpes zoster, vernal keratoconjunctivitis, and other forms of keratitis, especially in patients with neuroparalytic or neurotrophic keratitis or after local radiation exposure in whom corneal sensation is defective.

●Corneal mucous plaques and filamentary keratitis may coexist in the above conditions and also after Lasik, Lasek and, more frequently, penetrating keratoplasty at the donorrecipient interface.

●In filamentary keratitis, the corneal epithelial cells use the mucin strand as a substrate to grow along the filament, whereas, the cells are enmeshed in the corneal mucous plaque and the plaque remains flat and only slightly elevated from the corneal surface.

●Delayed plaques and pseudodendrites associated with herpes zoster may also be infectious, as they are positive for zoster DNA by polymerase chain reaction.

●Ciliary or conjunctival injection, mild iritis, with or without keratic precipitates, and epithelial and stromal edema are associated findings.

DIAGNOSIS

Clinical signs and symptoms

●Symptoms associated with the plaques vary from blurring of vision to foreign body sensation and marked pain; except when severe, they are often indistinguishable from the symptoms of keratoconjunctivitis sicca with or without Sjögren syndrome.

●These symptoms may also occur with herpes zoster keratitis and in patients using extended-wear soft contact lenses and in recurrent erosion syndrome.

●This entity is also associated with systemic disease, primarily rheumatoid arthritis or other collagen diseases.

TREATMENT

●Topically applied 10% to 20% acetylcysteine drops qd to q.i.d. can rapidly loosen the adherent plaque and dissolve its mucoid component and may prevent reformation.

●Mucous plaques causing severe symptoms may be removed surgically by debridment, scraping or pulled out with forceps or by rolling up with cotton swabs or Weck-cel sponge. A bandage gas permeable soft contact lens may be applied to the cornea. In some patients, a soft contact lens is also of therapeutic or preventive value. However, because of associated dry eye problems and deposit formation, the contact lenses may need frequent replacement or cleaning.

●Staphylococcal blepharitis may occur in association with corneal mucous plaques and may predispose patients to this condition. Treatment should also include the control of associated local microbial infections.

191NeovascularizationCHAPTER Corneal •

Cornea • 19 SECTION

COURSE

Three potential mechanisms for the pathogenesis of corneal neovascularization have been proposed:

●A corneal injury inactivates a restraint that the normal cornea exerts on cell division and migration of the vascular cells of the pericorneal plexus.

●Corneal edema loosens corneal stromal tissue and therefore permits the ingrowth of vessels normally restrained by its composition.

●Corneal neovascularization is related to the production of locally generated angiogenic factors. The most noted of these angiogenic factors are epidermal growth factor, fibroblast growth factor, urokinase-like plasminogen activator, interleukin I, interleukin II, and many other angiogenic factors and cascades yet to be discovered. Increasing basic science research has been aimed at the identification of these angiogenic factors and the cells producing these substances in attempts to improve the prognosis of corneal neovascularization.

ANGIOGENESIS

Angiogenesis as a multistep process involving:

●Extravasation of plasma proteins;

●Degradation of extracellular matrix;

●Endothelial cell migration and proliferation;

●Capillary tube formation.

This angiogenic process is mediated by a wide array of cytokines and growth factors to which both the extracellular matrix and endothelial cells (and in inflammation, infiltrating inflammatory cells) contribute. Accumulating evidence suggests significant codependence between angiogenesis and inflammation in many models of neovascularization. Proinflammatory molecules can stimulate the production of collagenases and lead to degradation of basement membrane, as well as being directly mitogenic for endothelial cells. Furthermore, the chemotactic activity of proinflammatory cytokines can enhance migration (and activation) of inflammatory cells (e.g. neutrophils and macrophages), which can in turn stimulate more angiogenesis and the recruitment of yet more inflammatory cells to the site of inflammation. Corneal neovascularization leads to the loss of immune privilege in the anterior segment manifested as the inability to sustain anterior chamber-associated immune deviation. Moreover, topical angiostatic strategies can lead to the restoration of immune privilege when instituted sufficiently early in the course of the neovascular response.

DIAGNOSIS

Neovascularization can be as simple as a micropannus, which is a superficial fibrovascular proliferation that extends 1 to 2 mm beyond the normal vascular arcade. In contrast, a superficial vascular pannus that extends more than 2 mm beyond the normal vascular arcade is considered a gross pannus. New vessels can be made based on the phases of action. Initially, there is a stimulus. Then, there is localized fragmentation of the basal membrane and the extracellular matrix around the vessel involved. Endothelial cell migration occurs through the vessel wall, and lysis of the extracellular matrix continues, promoting new vessel growth. Multiple enzymes and blood

products perpetuate the cycle and subsequent progression of corneal neovascularization.

Differential diagnosis

●Pterygium.

●Keratoconjunctivitis sicca (inflammatory).

●Vernal conjunctivitis (inflammatory).

●Pellagra (inflammatory).

●Vitamin B deficiency (inflammatory).

●Aphakic/pseudophakic bullous keratopathy (inflammatory).

●Fuchs’ dystrophy (degenerative/inflammatory).

●Glaucoma (degenerative).

●Infectious keratoconjunctivitis (infectious/inflammatory).

●Contact lens use (infectious/inflammatory).

●Rosacea (infectious/inflammatory).

●Phlyctenular keratoconjunctivitis (infectious/inflammatory).

●Molluscum contagiosum (infectious).

●Lymphopathia venereum (infectious).

●Leishmaniasis (infectious).

●Onchocerciasis (infectious).

●Trachoma (infectious).

●Leprosy (infectious).

●Herpes simplex keratitis (infectious).

●Herpes zoster keratitis (infectious).

●Alkali burns (toxic).

●Acid burns (toxic).

TREATMENT

Supportive

Particularly in patients with a micropannus, observation rather than treatment of the underlying condition is indicated. When the micropannus proceeds to gross corneal neovascularization, treatments may be instituted other than simply treating the underlying disease process.

Ocular

The primary treatment of NV is eliminating the underlying cause. Various regimens have been proposed for the treatment of active, corneal vascularization. Sometimes just elimination of the inciting insult will lead to resolution, as is typically seen with contact lens wearers.

The mainstay of the ocular treatment is corticosteroid therapy. Topically applied prednisolone acetate may be administered liberally, except when used in cases with infectious causes. Its judicious use is indicated in infectious cases to prevent collagenase activation and the associated melting of the cornea. In severe cases, subconjunctival injections of corticosteroids may be considered, but their benefit beyond that of topical administration is limited, and complications associated with subconjunctival injections may be potentiated by this therapy. Vascularization that has been present for a long time, particularly when located in the deeper layers of the cornea, is usually resistant to any form of treatment.

Surgical

Various surgical procedures have been recommended in the treatment of corneal neovascularization. Initially, diathermy of large feeding vessels into the cornea has been advised by some clinicians. More recently, corneal laser photocoagulation for the treatment of neovascularization has included the use of the

argon and the yellow dye laser. Both of these methods depend primarily on energy absorption by hemoglobin and oxyhemoglobin. Results from these studies show that many subsets of patients with corneal neovascularization can be treated effectively with laser photocoagulation; however, recurrence of the neovascularization has been an associated problem. Penetrating keratoplasty in vascularized corneas can be very difficult. Some authors have advised pretreatment of the recipient bed with diathermy of large feeder vessels into the cornea. In addition, diathermy of the inside graft edge must be done with extreme caution to prevent induced postoperative astigmatism. Early suture removal has been advocated because sutures have been implicated as a source of irritation and increased neovascularization with associated corneal graft rejection. In the past, the use of ß-irradiation was advocated; but this practice has been abandoned because the use of corticosteroids and immunosuppressive agents achieves better results. The suppression of corneal neovascularization with topical cyclosporin A has also been demonstrated. Investigators have treated corneal NV with argon laser obliteration of the vessel lumen. This can be achieved in the corneal part of the vessels (accessible to be lasered) but usually has a short-term effect, as the vessel lumen invariably reopens. Argon laser pannus obliteration is mainly a temporizing measure. Hyperbaric oxygen treatment has been used with limited success. This treatment modality aims to suppress angiogenesis by supplying the corneal tissue with redundant oxygen supply.

PRECAUTIONS

It is important to keep in mind that prolonged topical ophthalmic treatment with corticosteroids can increase intraocular pressure and cataract formation. It is essential to follow these patients closely. As mentioned, the treatment of certain infectious states with corticosteroids alone can potentiate collagenase activity and exacerbate corneal melting. Radiation, diathermy, and cryotherapy have all been used in an attempt to treat corneal neovascularization, but none of these methods has been found to be any more effective than corticosteroids. For deep, long-standing corneal neovascularization, most of these methods are unsuccessful.

COMPLICATIONS

●Tissue scarring.

●Opacification.

●Lipid keratopathy.

●Persistent inflammation.

●Immune corneal melting.

●Cicatrization.

●Edema.

●Exudates.

●Infiltration.

●Visual loss.

●Blindness.

COMMENTS

As knowledge of the biochemical pathogenesis of corneal neovascularization improves, so will treatment. Current research in arachidonic acid metabolism has shown that corticosteroids and cyclo-oxygenase inhibitors applied topically can significantly decrease the neovascular response to various insults.

Attempts to use lipoxygenase and lipoxygenase inhibitors have not proved to be successful in decreasing the neovascular response in an animal model of corneal neovascularization. An understanding of interleukin and T cell associations has led to the use of cyclosporin A to suppress corneal neovascularization. Also, evaluation of collagenase inhibitors in alkali burns has shown that reducing the initial injury and the associated response of the body can limit the associated disruption of normal corneal architecture. The use of tissue-matched corneas in corneal transplantation has been successful in ABO-matched tissue but not with the HLA-associated markers. Finally, extended contact lens use, either the disposable or nondisposable form, will continue to cause corneal neovascularization via the mechanisms of hypoxia and lactic acid accumulation. Identification of these problems early can be rewarding when closer follow-up of the patients is implemented. In addition, contact lens technology continues to change rapidly, thereby reducing the problems.

The response of the cornea to injury or inflammation and the associated corneal neovascularization that may follow have plagued the ophthalmic surgeon and diagnostician for years. Continued research and the development of new topically applied agents and preventive mechanisms should reduce the prevalence of this potentially devastating ocular pathologic process.

REFERENCES

Baer JC, Foster S: Corneal laser photocoagulation for treatment of neovascularization: efficacy of 577 NM yellow dye laser. Ophthalmology 99:173–179, 1992.

Boyd BD, ed: Highlights of ophthalmology. New York, Arcata Book Group, 1998.

Collaborative Corneal Transplantation Studies: Effectiveness of histocompatibility matching in high risk corneal transplantation. Arch Ophthalmol 110:1392–1403, 1992.

Dana MR, Streilein JW: Loss and restoration of immune privilege in eyes with corneal neovascularization. Invest Ophthalmol Vis Sci 37:2485– 2494, 1996.

Dana MR, Zhu SN, Yamada J: Topical modulation of interleukin-1 activity in corneal neovascularization. Cornea 17:403–409, 1998.

Folkman J, Shing Y: Angiogenesis. J Biol Chem 267:10931–10934, 1992.

Jackson JR, Seed MP, Kircher CH, et al: The codependence of angiogenesis and chronic inflammation. FASEB J 11:457–465, 1997.

Klintworth GK: Corneal angiogenesis: a comprehensive critical review. New York, Springer-Verlag, 1991.

Lipman RM, Epstein RJ, Hendricks RL: Suppression of corneal neovascularization with cyclosporine. Arch Ophthalmol 110:405–407, 1992.

192 DETACHMENT OF DESCEMET’S

MEMBRANE 371.33

Alexandre S. Marcon, MD

Porto Alegre, Brazil

Italo M. Marcon, MD, PhD

Porto Alegre, Brazil

Christopher J. Rapuano, MD

Philadelphia, Pennsylvania

Descemet’s membrane (DM), which is approximately 10 μm thick in adults, is the basement membrane of the corneal endo-

Membrane 192Descemet’sCHAPTERof Detachment •

Cornea • 19 SECTION

analysis of adhesion mechanisms of the corneal epithelium during recurrent erosion episodes have shown separation of the anchoring system at the level of the epithelial cell membrane or below the level of the anchoring plaques. Normal and degenerate polymorphonuclear leukocytes (PMNs) were found within and between the epithelial cells and within the anchoring layer. The degenerate PMNs may secrete metalloproteinases that cleave Bowman’s membrane below the anchoring system.

Epithelial basement membrane dystrophy and recurrent corneal erosions occur:

●In adults of each sex, although slightly more often in women;

●Usually after the fourth decade of life, although literature has associated recurrent corneal erosion with;

●Juvenile Alport’s syndrome, an X-linked condition that also presents with anterior lenticonus and retinal flecks, as well as renal complications.

Epithelial basement membrane dystrophy is usually bilateral and characterized by:

●Various patterns of dots, parallel lines that mimic fingerprints, and random linear pattern that resemble maps, which usually appear in the epithelium of the central twothirds of the cornea.

These intraepithelial cyst patterns are composed of opaque, putty-gray cysts, termed:

●Cogan’s cysts, which are made up of cytoplasmic and nuclear debris and range in size from pinpoints to as much as 2 mm across.

Individual microcysts may be oval, oblong, or comma-shaped and rarely appear along but are usually associated with map and less often fingerprint patterns. The map and fingerprint patterns, on the other hand, frequently appear without ‘dots,’ or individual microcysts.

Map and fingerprint alterations in corneal epithelium are not rare and can be found in asymptomatic individuals without a prior history of trauma or ocular disease; in face, the literature suggests that these epithelial changes are more diffuse than previously recognized. They are frequently seen in conditions involving:

●Corneal edema. This localized edema may occur near a healing cataract surgical incision or in the central cornea associated with Fuchs’ corneal dystrophy.

Epithelial basement membrane dystrophy, and recurrent erosion, are:

●Probably hereditary, with variable penetrance.

In a large study population, 6% of patient treated for a variety of other ocular non corneal conditions and diseases also demonstrated map, dot, and fingerprint changes in the epithelium.

Even when frank epithelial defects or opaque microcysts are absent or undetectable with biomicroscopy, computed videokeratography may reveal the presence of corneal epithelial ‘lagoons,’ or micro depressions, indicative of microscopic folding and redundancies in basement membrane, especially in posttraumatic recurrent erosion syndrome.

Fingerprint lines and map-like patterns are histologically similar, both have:

●An aberrant or a multilaminar basement membrane produced by the basal epithelial cells of the corneal epithelium. The literature suggests that especially in spontaneous (non

traumatic) recurrent erosions, there may be an inherent structural weakness of the corneal basement membrane with respect to the synthesis and deposition of type IV collagen.

DIAGNOSIS

Clinical signs and symptoms

At least 80% to 90% of patients who have epithelial basement membrane dystrophy are asymptomatic. Symptoms, when they occur, consist of one or more of the following:

●Slightly blurred vision (when epithelial and basement membrane changes are in the visual axis);

●Visual acuity loss due to irregular astigmatism;

●Epithelial blebs;

●Foreign body sensation with recurrent erosion, when the epithelium loosens and detaches;

●Sudden sharp pain, often in the early morning during sleep or on awakening, when a frank epithelial defect occurs prompted by eyelid movement across loosened epithelium.

This commonly is the first symptom of a recurrent erosion, and in rare cases, a patient who has previously experienced this pain on awakening is so fearful of the pain that he or she is unable to sleep well. The pain is fleeting in most cases, lasting only seconds, but it may last for some minutes to 1 or 2 hours and is a warning that the epithelium is not healed.

Laboratory findings

In one study, patients with a history of recurrent corneal erosion (12 eyes) presented with signs suggestive of microbial keratitis. They had developed:

●An acute corneal stromal infiltrate beneath the epithelial defect and this was associated with, an intense anterior uveitis; and

●Hypopyon in three eyes.

Bacterial cultures of these corneas, however, revealed a positive isolate in just two eyes; treatment with topical antibiotics and topical corticosteroid rapidly resolved these episodes with good visual outcomes, frequently with a complete resolution of the recurrent erosion as well.

PROPHYLAXIS

Precautionary measure for patients with recurrent corneal erosion associated with epithelial basement membrane dystrophy include:

●Avoidance of rubbing the eyes through the eyelids, especially upon awakening;

●Liberal use of ointment medications at bedtime during an erosion episode.

Some times these measures must be followed for several months after resolution of the episode.

TREATMENT

Ocular

Of first importance for the patient with epithelial basement membrane dystrophy is minimization of the pain associated

Dystrophy Membrane193 CHAPTERBasement Epithelial •

Cornea • 19 SECTION

with recurrent corneal erosion. If the erosion is small, it will heal spontaneously or with the aid of:

●A pressure patch, placed on the eye for 1 or 2 days;

●An antibiotic ointment, such as bacitracin or erythromycin, which can be used beneath the patch.

The literature suggests that patching for longer than 2 days can introduce hypoxia or a lacrimal hyposecretion, or both, that may actually inhibit healing.

Minor corneal erosions can be treated with:

●Lubricating ointment alone, for several weeks to months, to control symptoms;

●Bandage soft contact lenses, which have been helpful in some cases of multiple recurrent erosion; however, concerns persist about overnight use of extended-wear soft contact lenses due to the risk of infectious keratitis.

In some cases, the recurrence of very mild corneal erosion may be prevented with:

●Sodium chloride drops 2% or 5% several times during the day; and

●Sodium chloride ointment 5% at bedtime.

Many patients believe that sodium chloride ointment is no more effective than a lubricant ointment or an ointment without preservatives. Each patient must establish a regimen of medication that seems to control his or her symptoms most effectively. This might involve using a medication only when symptoms recur, or in some instances, daily application for many months after the resolution of an erosion episode to prevent further recurrences.

Resistant case may require:

●Mechanical debridement, with or without chemical cautery, depending on the size of the defect and the amount of ocular irritation;

●Local cycloplegic agents;

●A diamond burr, which is used to ‘polish’ Bowman’s membrane after mechanical debridement (has proved to be very effective in preventing recurrence).

With the more severe cases of recurrent corneal erosion that do not seem to respond to any of the above therapies, the use of:

●Anterior stromal puncture has been advocated. The procedure involves making 75 to 150 small punctures with a bent 23 needle through the epithelium and Bowman’s membrane into the anterior stroma. The needle tip is inserted through the loosened epithelium, making momentary micro depressions in the cornea to enter the stroma; the bent tip limits the excursion of the needle tip and permits the micropunctures to affect only the anterior stroma.

Patients who have had multiple recurrent erosion episodes, unresponsive to debridement alone or debridement with cautery, have shown significant improvements with anterior stromal puncture. Used correctly, the technique is effective in 90% of cases with recalcitrant recurrent erosion with the first application; a few patients may require a second application of anterior stromal puncture.

Surgical

For spontaneous recurrent erosions and erosions secondary to corneal dystrophies such as Reis-Bücklers’ dystrophy, lattice dystrophy, and the superficial variant of granular dystrophy, as well as epithelial basement membrane dystrophy.

●Excimer laser photoablation (phototherapeutic keratectomy, or PTK) of the epithelium, the basement membrane, and just into Bowman’s membrane has been performed with some success, although it is more expensive that mechanical debridement.

PRECAUTIONS

Treatment should be as simple as possible with the use of as few drugs as necessary. Some drugs, such as local anesthetic agents, have been shown to delay epithelial wound healing. For this reason, it is imperative to never prescribe a topical anesthetic agent for the patient’s own use, even when symptoms are severe; ointments, bandage soft contact lenses, or patching should suffice to manage pain while initiating healing.

Indications for chemical cautery or lamellar keratectomy for resistant erosions have become almost non existent with the advent of therapeutic soft contact lenses, anterior stromal puncture, and PTK. In fact, due to the cost of bandage contact lenses and the frequent follow-up visits required, as well as the potential for corneal infections with long-term use, contact lens therapy should be postponed until milder forms of treatment prove to be ineffective. Anterior stromal puncture or PTK is preferred for treatment of the most severe cases of recurrent corneal erosion that do not resolve with ointments and patching.

COMMENTS

Systemic disease does not seem to play a role in epithelial basement membrane dystrophy or recurrent corneal erosion.

REFERENCES

Baum JL: Prolonged eyelid closure is a risk to the cornea. The Castroviejo Lecture, 1997. Cornea 16:602–611, 1997.

Brunette I, Boisjoly HM: Should we patch corneal erosions?[letter] Arch Ophthalmology 115(12):1607, 1997.

Heyworth P, Morlet N, Rayner S, et al: Natural history of recurrent erosion syndrome-A 4-year review of 117 patients. Br J Ophthalmol. 82:537– 540, 1998.

Ionides AC, Tuft SJ, Ferguson VM, et al: Corneal infiltration after recurrent corneal erosion. Br J Ophthalmol 81:537–540, 1997.

Laibson PR: Microcystic corneal dystrophy. Trans Am Ophthalmol Soc 74:488–531, 1976.

Liu C, Buckley R: The role of the therapeutic contact lens in the management of recurrent corneal erosions: a review of treatment strategies. CLAO 22:79–82, 1996.

Maine R, Loughman MS: Phototherapeutic keratectomy re-treatment for recurrent corneal erosion syndrome [letter]. BJ Ophthalmology 86(3):270–272, 2002.

McDonnell PJ, Seiler T: Phototherapeutic keratectomy with excimer laser for Reis-Buckler corneal dystrophy. Refract Corneal Surg 8:306–310, 1992.

McGhee CN, Bryce IG, Anastas CN: Corneal topographic lagoons: a potential new marker for post-traumatic recurrent corneal erosion syndrome. Aust NZ J Ophthalmol 24:27–31, 1996.

McLean EN, MacRae SM, Rich LP: Recurrent erosion: treatment by anterior stromal puncture. Ophthalmology 93:784–788, 1986.

Park AJ, Rapuano CJ: Diamond burr treatment of recurrent erosions. Techniques in Ophthalmology 2(3):114–117, 2004.

Rapuano CJ: Excimer laser phototherapeutic keratectomy: long-term results and practical considerations. Cornea 16:151–157, 1997.

194 CHAPTERKeratitis Filamentary •