Recurrent Corneal Erosion

Updated: Mar 20, 2023
Author: Arun Verma, MD; Chief Editor: Hampton Roy, Sr, MD 



Recurrent corneal erosion (RCE) syndrome is a condition that is characterized by a disturbance at the level of the corneal epithelial basement membrane, resulting in defective adhesions and recurrent breakdowns of the epithelium.

Recurrent corneal erosion. Recurrent corneal erosion.

RCE syndrome may occur secondary to corneal injury or spontaneously. In the latter case, some predisposing factor, such as diabetes or a corneal dystrophy, may be the underlying cause. Management of RCE syndrome is usually aimed at regenerating or repairing the epithelial basement membrane to restore the adhesion between the epithelium and the anterior stroma.

Corneal erosions are perhaps one of the most common and neglected ocular disorders. Some of these cases occur after ocular trauma, but most of them occur spontaneously. Painful RCE syndrome, whether due to trauma or to anterior basement membrane dystrophy (Cogan dystrophy or map-dot-fingerprint dystrophy), results from abnormalities in the epithelial basement membrane.

Map-dot-fingerprint dystrophy. Map-dot-fingerprint dystrophy.


Recurrent corneal erosions and epithelial basement membrane dystrophy are usually bilateral and are characterized by various patterns of dots, parallel lines that mimic fingerprints, and patterns that resemble maps, which appear in the epithelium. Individual microcysts may be oval, oblong, or comma-shaped and rarely appear alone but usually are associated with map and fingerprint patterns. On the other hand, the map and fingerprint patterns appear without dots or individual microcysts.

Map and fingerprint alterations of the corneal epithelium are not rare and can be found in asymptomatic individuals without prior history of trauma or ocular disease. Literature suggests that these epithelial changes are more common than previously recognized. They frequently are seen in conditions involving corneal edema, such as near a healing cataract surgery incision, or in the center of the cornea associated with Fuchs corneal dystrophy.

Clinical manifestations of Fuchs dystrophy

Three stages of Fuchs endothelial dystrophy are recognized. The 3 stages usually evolve gradually over a period of 25 years, and, like other corneal dystrophies, they usually are bilateral but asymmetric.

The first stage is the onset of cornea guttata, usually in the fourth decade of life. Subjective symptoms rarely occur until the fifth or sixth decade. During the asymptomatic phase, endothelial guttata and pigment dusting can be seen by slit lamp examination of the central corneal endothelium and by specular reflection. The guttate excrescences can become more numerous and confluent so that individual guttata are lost completely in the beaten-metal appearance of the endothelial surface. The central cornea is involved first, and, as the disease progresses, it spreads toward the periphery.

In the second phase of the disease, blurred vision, glare, and halos around lights develop because of incipient corneal edema in the stroma and epithelium. Epithelial edema can be seen as small droplets (bedewing) on retroillumination with the slit lamp. Epithelial microcysts coalesce to form bullae, which produce varying amounts of pain when they burst; hence, the name bullous keratopathy. Striae form in the Descemet membrane as the cornea thickens posteriorly due to stromal swelling. The arc of the Descemet membrane from limbus to limbus is shortened, causing wrinkles in the Descemet membrane called striae. The microcystic epithelial vesicles may break, causing foreign body sensations and severe pain with more extensive corneal epithelial disruption.

In the third stage, recurrent corneal erosions, microbial ulceration, and persistent pain may occur. Corneal sensitivity usually is reduced.


The 2 categories of corneal abrasions are as follows: superficial (those not involving the Bowman layer) and deep (those that penetrate the Bowman layer but do not rupture the Descemet membrane). Corneal abrasions may result from foreign bodies, contact lenses, chemicals, fingernails, hair brushes, tree branches, and dust.

Corneal abrasion. Corneal abrasion.

The cornea has remarkable healing properties. The epithelium adjacent to any insult expands in size to fill in the defect, usually within 24-48 hours. Lesions that are purely epithelial often heal quickly and completely without scarring. Lesions that extend below the Bowman layer are more likely to leave a permanent scar.

The epithelial healing process begins when basal epithelial cells undergo mitosis, producing new cells that occupy fresh wounds. Basal cells adhere the epithelium to the stroma in 2 ways: they secrete the basement membrane, and they contain hemidesmosomes, which are essentially linchpins that protrude through the posterior surface of basal cells and into the stroma; each is held in place by an anchoring fibril. Any disruption to basal cell production makes the eye more prone to recurrent erosion.

Recurrent corneal erosions occur because there is a defect in the epithelial basement membrane and in hemidesmosomes formation, resulting in epithelial loss, microcysts, and bullae.

Recurrent corneal erosions occurring after injury or any corneal insult result because of improper or inadequate healing of the basement membrane, either because the basal epithelial cells fail to produce proper basement membrane complexes to attach to the Bowman layer and stroma or because of faulty basement membrane adherence.

A traumatic cause has a better eventual prognosis for full recovery than does the spontaneous form. In the case of spontaneous corneal erosions, the underlying disease process may be an epithelial basement membrane corneal dystrophy. Studies with the electron microscope have shown that during recurrent corneal erosion episodes, there is 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 leucocytes (PMNs) were found within and between the epithelial cells and within the anchoring layer. The degenerate PMNs may secrete metalloproteinases that cleave the Bowman layer below the anchoring system.



United States

Recurrent corneal erosions are quite frequent in developing countries where lack of proper nutrition plays a significant role in the health of the cornea. Moreover, they are more frequent in patients with the predisposing factors and in those patients that have associated skin problems (see Causes).


The tendency for epithelial basement membrane dystrophy, recurrent erosion, or both is probably hereditary, with variable penetrance. If corneal erosions are inherited, the pattern is dominant; however, most corneal erosions are acquired. In a study by Laibson, it has been found that 6% of the patients treated for a variety of other ocular conditions and diseases also demonstrated map, dot, and fingerprint changes in the epithelium.[1]

A recurrent corneal erosion is most likely to develop in a person who has had a previous corneal abrasion that was very sharp, clean, and linear, like that from a paper cut. Because the cut is so sharp, without ragged edges, it is less likely to stick down tightly to the underlying basement membrane. Those who have an abnormal structure to the corneal epithelium (called map-dot-fingerprint dystrophy) are at a much greater risk for poor healing following a corneal abrasion and, thus, can develop a recurrent corneal erosion.

Just as it is nearly impossible to see a corneal abrasion with the naked eye, the same is true for a recurrent corneal erosion. The time course is most important. In a recurrent corneal erosion, the patient can remember having had a corneal abrasion relatively recently (usually within the past 3–10 d) and then most often when first opening the eye in the morning.


Recurrent corneal erosions usually are seen as a bilateral problem occurring somewhat more frequently in females than in males. The epithelium may show a slipped-rug appearance; filaments are often seen. The recurrent erosions may occur over multiple sites on the cornea, a situation different from traumatic erosions.


Recurrent corneal erosions and epithelial basement membrane dystrophy occur in adults, usually after the fourth decade of life. However, there are studies that have associated recurrent corneal erosions with juvenile Alport syndrome, which is an X-linked condition that also presents with anterior lenticonus and retinal flecks, as well as renal complications. Certain anterior corneal dystrophies, such as Reis-Bücklers, and lattice dystrophies can cause painful recurrent erosions in children.


Overall, the prognosis is very good to excellent with proper attention. Unless there is an ongoing underlying corneal disease, most patients will ultimately heal completely and not have any more episodes; however, the healing process may take years.

While most patients respond to medical treatment, surgical treatment in the form of anterior stromal puncture (especially in localized posttraumatic erosions), epithelial debridement, diamond burr polishing of the Bowman layer, or excimer laser phototherapeutic keratectomy have excellent success rates, and they should not be used as last resort but rather a next step in the treatment regimen.

Patient Education

Patients should be instructed to take very good care of their eyes. Once corneal erosion develops, although it can be treated, there is no guarantee that it will not recur. Therefore, patients should always wear protective sunglasses when the sun is out and always use lubricating eye drops.

Precautionary measures for patients with recurrent corneal erosion associated with epithelial basement membrane dystrophy include the following:

  • Avoidance of rubbing the eyes through the eyelids

  • Liberal use of ointment medications at bedtime during an erosion episode

  • Sometimes these measures must be performed for several months after resolution of the episode.

Educate patients on how to open the eyes upon awakening (see Deterrence/Prevention).




For all patients who present with signs and symptoms of RCE syndrome, a careful history and examination of the cornea should be undertaken to ensure that no underlying factors have predisposed these patients to this condition.[2] This applies even in those cases where a history of injury to the cornea is present because a defect in the epithelial basement membrane complex may have been present before the initial trauma.[3]

Of patients with anterior basement membrane dystrophy, 80-90% are asymptomatic. The primary symptom of recurrent erosion syndrome is mild to severe eye pain. Symptoms, when they occur, consist of 1 or more of the following:

  • Slightly blurred vision (when the epithelial and basement changes are in the visual axis)

  • Visual acuity loss

  • Astigmatism

  • Epithelial blebs

  • Foreign body sensation with recurrent erosion, when the epithelium loosens

Foreign body sensation with recurrent erosion, when the epithelium loosens, is commonly the first symptom of recurrent erosion, and, in some cases, patients who have previously experienced this pain on awakening are so fearful of the pain that they are unable to sleep well.

The pain is fleeting in most cases, lasting only for a few seconds, but it may last from minutes to 1-2 hours and is a warning that the epithelium has not healed.

Attacks of pain and ocular irritation occurring in the early morning hours or upon awakening are understandable because corneal hydration from lid closure may be a factor affecting epithelial adhesion. An abnormal adherence between lid and cornea may be a factor in setting the stage for an attack of epithelial erosion.

Sudden sharp pain often is felt in the early morning during sleep or on awakening when a frank epithelial defect occurs because of the eyelid movement across the loosened epithelium.

Recurrences affect the area of the cornea that was previously injured.


Depending on the severity of the erosion, corneal examination findings may be totally normal, or they may reveal telltale signs of RCE syndrome. A classic history of recurrent pain upon awakening is often more important than seeing classic signs of corneal irregularity in making the correct diagnosis of RCE syndrome.

During an acute attack, one may see epithelial loss, epithelial microcysts, bullae, lack of adherence of sheets of epithelium, and epithelial filament formation. In these instances, the visual acuity may be impaired severely if the pathogenic condition occurs in the pupillary area. The examination findings may be totally normal, or there may be barely visible epithelial irregularities (may have negative staining) where the erosion has almost completely resolved.

An external eye examination generally shows a corneal abrasion, often centrally located, that stains brightly with fluorescein. The abraded area tends to create loose edges with moderate-to-large epithelial flaps, which commonly form. A brownish granular edema (brawny edema) may occupy the underlying anterior stroma. The tendency toward a central location and dense secondary edema can cause a significant deterioration in vision.

Recurrent corneal erosions can be classified as either microform or macroform. With the latter, severe pain persists from hours to days as a result of a large area of the epithelium being separated from the cornea. In posttraumatic cases, the microform type of erosion always occurs at the site of the original abrasion. Microform recurrent erosions are characterized by intraepithelial microcysts with a minor break in the epithelium. These erosions usually are associated with brief episodes of pain, lasting from seconds to minutes.

Laibson et al have stated that in the interval between attacks, one can detect epithelial cysts, surface irregularity, and some subepithelial scarring on slit lamp examination.[1] The healed epithelial area may even resemble a dendritic figure, a pseudodendrite. This fact should be kept in mind to avoid prescribing unnecessary medication.


The corneal epithelial basement membrane complex is responsible for the tight adhesion of the epithelial basal cell layer to the underlying stroma. The primary abnormality with RCE syndrome is poor adhesion of the epithelium to the Bowman layer due to a failure to establish or maintain normal adhesion complexes. Multiple recurrences are common because the basal epithelial cells require at least 8-12 weeks to regenerate or repair the epithelial basement membrane.

Most cases of recurrent erosions are related to anterior basement membrane dystrophy or are caused by corneal injuries from fingernails and paper. Acquired recurrent erosions also are observed after the following:

  • Alkali burns

  • Foreign bodies

  • Post infectious ulcers from herpes simplex

  • Exposure

  • Cockayne syndrome

  • Reis-Bücklers dystrophy

  • Vitrectomy

  • Photocoagulation

  • Secondary to other corneal dystrophies (eg, lattice, Fuchs, other anterior membrane dystrophies)

  • Contact lenses

Contact lenses

Soft contact lenses have many uses and are made from a variety of materials. The most common pitfall in the matter of lens care is the inability to keep lenses clean of deposits. These deposits can consist of protein, lipid, or calcium. They can cause discomfort, pseudomyopia, loss of vision, displacement of lenses (usually in an upward direction), and corneal erosions.

Unfortunately, thimerosal (sodium ethylmercurithiosalicylate) is the major offender in producing a delayed hypersensitivity response. It causes recurrent corneal erosions, conjunctival hyperemia, or corneal deposits. Many thimerosal-free solutions are now being prepared.

Drying of the lenses can result in a change in lens curvature, which alters the fit and can cause conjunctival irritation and swelling or corneal epithelial erosions. Conjunctival swelling results in tightening of the lens, which can cause pain, corneal edema, and epithelial erosions.

A flat-fitting contact lens moves too much and is uncomfortable to wear. Such a lens can give rise to central corneal epithelial edema and erosions. If the lens is too tight, the eye becomes uncomfortable, there is circumcorneal injection, and there may be epithelial erosions.

Postoperative management of corneal transplants for severely alkali-burned corneas includes the protection of the epithelium with well-fitted bandage contact lenses. But if the lenses are not of proper fit, they can lead to recurrent corneal erosions.

Recurrent corneal erosion is an indication for the use of a therapeutic lens. However, with the advent of anterior stromal puncture and related procedures, many clinicians choose to definitively treat typical posttraumatic recurrent corneal erosions, thereby minimizing the number of such patients requiring therapeutic lenses. Bandage lens treatment, if used for this indication, must be continued for up to 8-26 weeks to facilitate repair of the corneal epithelial basement membrane.

Junctional epidermolysis bullosa

Patients with junctional epidermolysis bullosa, one of the rarest types, have more corneal problems (eg, recurrent corneal erosions) but relatively little conjunctival involvement.

In the acquired autoimmune form, the immune response is believed to be directed against the basement membrane proteins uncein and collagen VII. It may be associated with small subepithelial vesicles in the cornea, symblepharon, and scarring of the lacrimal puncta.

Topical neomycin produces contact hypersensitivity in 5-10% of patients. Eyelid edema, conjunctivitis, and punctate corneal erosions may be due to allergic and toxic effects of topical neomycin.

While the corneal epithelium is affected minimally by a low dose of topical neomycin, cytotoxicity occurs at concentrations greater than 5 mg/mL. Corneal sensation can be altered with very high levels of neomycin eye drops.

Topical paromomycin

The effects of topical paromomycin on the ocular surface have not been studied adequately. Frequent dosing and prolonged administration presumably can slow wound healing and may contribute to conjunctival hyperemia and punctate corneal erosions.

Topical diamidines

Topical diamidines can produce stinging and burning immediately after application. Conjunctival hyperemia and punctate corneal erosions have been attributed to its use.


Mast cell degranulation with histamine release is produced by propamidine. Contact hypersensitivity has been described.

Topical anesthetics

While some corneal epithelial damage occurs with all topical anesthetics, it is most exaggerated when cocaine is used, with epithelial loosening and corneal erosions. This may be an advantage when removing epithelium in the treatment of a dendritic ulcer.

Toxic effects on epithelial cell metabolism and ultrastructure include depressed cellular respiration and glycolysis with lactic acid accumulation; alterations in desmosomes, intracellular mitochondria, rough endoplasmic reticulum, and tonofibrils; and inhibition of cell mitosis and migration.

Epithelial microvilli loss results in instability and rapid breakup of the tear film. Thus, local anesthetics may retard healing of corneal erosions as epithelial cells round up and accumulate at the wound margin. The epithelium may totally lift off the basement membrane proteins and cell membrane permeability; destruction of mitochondria, rough endoplasmic reticulum, and tonofibrils; and inhibition of cell mitosis and migration.


Complications include corneal haze, corneal scarring, infectious keratitis, and permanently decreased vision.



Diagnostic Considerations

Punctate epithelial erosions are associated with the following: viral keratitis, especially molluscum contagiosum; inclusion conjunctivitis; herpetic keratitis/postinfectious herpetic keratitis; rubeola and rubella; keratitis sicca; exposure keratitis; vernal conjunctivitis; topical steroids; and vaccinia.

Other conditions associated with recurrent corneal erosions include the following: Thygeson superficial punctate keratitis, herpes zoster, adenovirus infections, prolonged eye patching, corneal edema, keratoconus, neuropathic keratopathy, degenerative condition of the cornea (eg, advanced glaucoma), aerosol keratitis, ectodermal dysplasia, acne rosacea, postcataract surgery, and trauma (eg, wounds, abrasions, exposure to short-wave diathermy).

Epithelial basement membrane dystrophy (map-dot-fingerprint dystrophy): Epithelial basement membrane dystrophy is the most common corneal dystrophy, affecting approximately 2% of the population. Although most patients remain asymptomatic, about 10% experience recurrent corneal erosions as a consequence of faulty attachment complexes. These attachment complexes consist of hemidesmosomes of the basal epithelial cells, the underlying basement membrane, and the subadjacent anchoring fibrils of the Bowman layer.

Diabetes mellitus: Corneal opacities, dry eyes, and changes in the Descemet membrane have rarely been observed in patients with diabetes. It has become apparent that patients with diabetes have a problem related to epithelial adherence to the Bowman layer. Significant recurrent corneal erosions have been reported after intraocular surgery and specifically after vitrectomy on such patients.

In the nondiabetic cornea, corneal epithelial scraping results in rupture of the basal cells with maintenance of the basement membrane attachment to the Bowman layer. However, in the diabetic cornea, the entire epithelium separates as an intact sheet with the entire basement membrane remaining adherent to the basal cells. Use of prolonged semipressure patching and bandage soft contact lenses is recommended in the event that such corneal changes occur after intraocular surgery.

Cystinosis: The clinical feature common to the 3 types of cystinosis is the pathognomonic deposition of cystine crystals in the cornea and conjunctiva. Severe photophobia is often the only presenting visual symptom. The symptoms result from the diffraction of light by the corneal crystals. The fusiform crystals initially involve the anterior portion of the central cornea but occupy the full thickness of the peripheral cornea by age 1 year. No visual impairment occurs in the early stages.

By age 7 years, most patients have crystals either within or on the endothelial surface of the cornea, with markedly decreased corneal sensitivity. Decreased tearing and painful corneal erosions occur. Corneal thickness is increased. The conjunctiva has a ground-glass appearance. Birefringent, hexagonal, polychromatic, polymorphic, rectangular, or rhomboidal crystals can be seen with the biomicroscope.

Toxic epidermal necrolysis/Stevens-Johnson syndrome/erythema multiforme: Toxic epidermal necrolysis (Lyell disease, Ritter disease, scalded skin syndrome) is an acute systemic illness associated with a bullous eruption of the skin and mucous membranes that, in many respects, is similar to Stevens-Johnson syndrome.

Ocular involvement in toxic epidermal necrolysis is limited to the conjunctiva; it is usually less severe than is the ocular involvement in Stevens-Johnson syndrome. A mucopurulent conjunctivitis is the most common early manifestation, and, unlike the involvement in erythema multiforme, this does not usually result in ulceration, scarring, symblepharon, or corneal pannus formation. However, it may do so, with recurrent corneal erosions and all the other consequences described for Stevens-Johnson syndrome.

Trachoma: The constant corneal abrasion by the lashes and inadequate tears can produce corneal erosions, ulceration, and opacity, which constitute the major pathway to blindness in trachoma. In this case, there is notching of the upper lid due to previous lid surgery; this can produce corneal exposure and further corneal damage.

Corneal epithelium changes eventually occur in all patients with aniridia. A superficial, slightly elevated, faint gray pannus with fine radially oriented blood vessels that stain positive with fluorescein is characteristic. Defects appear in the corneal periphery and progress to the center with age.

In some cases, corneal erosions and frank ulceration occur whether or not glaucoma is present. These lesions may progress to end-stage corneal scarring involving all layers. Others have described avascular opacities present at birth, involving the Descemet membrane and the deep stroma. Technically, these corneal opacifications cannot be considered dystrophies. Microcornea is a frequent finding.

Mucolipidosis IV: Mucolipidosis IV, also referred to as Berman syndrome, is a rare storage disease characterized by severe psychomotor retardation and early corneal clouding. It differs from mucolipidosis I, II, and III in its lack of skeletal abnormalities. Patients show developmental delay and progressive psychomotor deterioration. Survival is variable. Corneal clouding may be present at birth, or it may develop later. The clouding is primarily due to epithelial involvement. Marked corneal surface irregularities may be present. Some patients experience bouts of pain, tearing, photophobia, and conjunctival injection, possibly related to recurrent corneal erosions. Lubrication may be helpful.

Lattice dystrophy type II (Meretoja syndrome): Lattice dystrophy type II is found in familial systemic amyloidosis (Meretoja syndrome, type IV familial neuropathic syndrome). This also is an autosomal dominant disease, usually found in patients of Finnish, Dutch, or Scotch-Irish ancestry. Systemic involvement consists of progressive cranial and peripheral neuropathies, skin changes, and multisystemic involvement secondary to eventual deposition of amyloid throughout the body. The corneal changes usually are quite mild, presenting in the third decade or later. Recurrent corneal erosions and poor vision can occur. In contrast to lattice dystrophy type I, the refractile lines are located peripherally, are fewer in number, and are larger.

Filamentary keratitis: Combination of punctate epithelial keratitis and increased mucus are the necessary ingredients for filamentary keratitis. In filamentary keratitis, important differentiating features for the numerous causes include the location of filaments, tear film status, and the presence of associated ocular disease.

Filamentary keratitis occurs with numerous disorders other than keratoconjunctivitis sicca (KCS) and superior limbic keratoconjunctivitis (SLK). Recurrent erosion, postcataract extraction, postpenetrating keratoplasty, neurotrophic keratitis, herpetic keratitis, bullous keratopathy, prolonged patching (padding), and hereditary hemorrhagic telangiectasia are among these disorders.

Whatever the cause, filament formation results from a derangement in the corneal epithelium and a relative excess of mucus. The excess mucus usually is secondary to chronic irritation, and the location of the filaments depends on the type of underlying corneal pathology. Herpes zoster ophthalmicus produces changes in the corneal epithelium, probably as a consequence of denervation and alteration in tear secretion.

Differential Diagnoses



Other Tests

Lesions, such as corneal erosions, are stained mainly by fluorescein, whereas devitalized but intact epithelium is stained exclusively by rose bengal. One drop of 1% rose bengal placed on the upper bulbar conjunctiva, while the patient looks down, is generally sufficient.

Recurrent erosion with fluorescein in an area of s Recurrent erosion with fluorescein in an area of staining.
Stromal puncture seen with fluorescein. Stromal puncture seen with fluorescein.

A careful slit lamp examination often reveals corneal erosions. Many times, there may be associated generalized or localized patches of corneal edema. In some cases, there may be associated microbial keratitis, which can be diagnosed with bacterial cultures of these corneas.

Direct view with a slit lamp. Direct view with a slit lamp.

Corneal topographic analysis (using computerized videokeratography) often reveals focal areas of corneal flattening (called corneal topographic lagoons) in eyes with RCE syndrome. This finding is important, as the identification of areas of focal abnormality in RCE syndrome remains a significant clinical problem in those patients with frank symptoms but no evident epithelial abnormalities.

Histologic Findings

Fingerprint lines and maplike 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 (nontraumatic) recurrent erosions, there may be an inherent structural weakness of the corneal basement membrane with respect to the synthesis and deposition of type 4 collagen.

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 microdepressions, indicative of microscopic folding and redundancies in the basement membrane, especially in posttraumatic recurrent erosions.



Approach Considerations

The treatment approach for recurrent corneal lesions at the authors’ center is as follows:

  • Mechanical debridement, with or without chemical cautery, depending on the size of the defect and the amount of ocular irritation
  • Application of local cycloplegic agents such as atropine or homatropine
  • “Polishing” of the Bowman layer with a diamond burr after mechanical debridement
  • Delamination of the corneal epithelium using alcohol or silver nitrate, which can improve the symptoms of recurrent corneal erosions in eyes that do not respond to topical lubrication or bandage contact lenses

For the delamination procedure, a 20% alcohol solution is dripped into a circular well placed over the defect and applied for 30-40 seconds.

The treated area of the corneal epithelium is then completely debrided using a sponge, and the corneal surface is irrigated with saline before a bandage contact lens is placed.

The authors apply cotton bud dipped in silver nitrate on the affected area.

The authors have recently started using plasma energy in the form of Fugo blade. Scratches are made to the affected with the Fugo plasma knife. The tissues ablate away, leaving a smooth surface without scarring.

In a study by Hykin et al, 117 patients with a history of recurrent corneal erosion were recruited at initial hospital presentation.[4]

Seventy-five cases had a history of shallow corneal injury, 23 cases had epithelial basement membrane dystrophy (EBMD), 8 cases had both, and 11 cases had neither. Mean age at presentation was 38 years and follow-up ranged from 6-16 months (mean, 10.6 mo).

Sixty-one patients presented first with acute corneal erosion, 21 patients presented with subsequent acute corneal erosion, and 35 patients presented with chronic symptoms. Patients with EBMD or a trauma-related focal epithelial basement membrane abnormality were more likely to present with chronic recurrent symptoms than trauma-related cases with no abnormality on examination. Both EBMD and trauma-related cases typically recurred in the lower half of the cornea, frequently in the midline (z=7.3, P=0.0001), suggesting an intrinsic or acquired abnormality of the epithelial basement membrane at this site.

Only 4 of 82 acute episodes did not resolve by 5 days with simple patching, cycloplegia, and topical antibiotic ointment. In most patients presenting with acute erosion, only simple management measures were required. Of 117 cases started on prophylactic ointment at night, further therapy due to prophylaxis failure was required in only 5 patients.

Medical Care

Management of RCE syndrome is usually aimed at regenerating or repairing the epithelial basement membrane to restore the adhesion between the epithelium and the anterior stroma.

In mild cases, the condition may resolve spontaneously within a few hours. However, more often, treatment is required to promote healing and to relieve the symptoms. The healing rate for an abrasion due to RCE syndrome is generally slower than the healing rate for a similar abrasion due to other factors.

Most patients with recurrent corneal erosions respond to topical lubrication therapy, bandage soft contact lenses, debridement of the epithelium and basement membrane, or anterior stromal micropuncture. An occasional patient will continue to have painful recurrent erosions despite all of these measures.

Pain relief

Of first importance for the patient with epithelial basement membrane dystrophy is minimization of the pain associated with recurrent corneal erosion. If the erosion is small, it usually heals spontaneously or with the aid of the following:

A pressure patch placed on the eye for 1-2 days

An antibiotic ointment, which can be used beneath the patch

Sometimes these measures must be followed for several months after resolution of the episode. The literature suggests that patching for longer than 2 days can introduce hypoxia, a lacrimal hyposecretion coefficient, or both that may actually inhibit healing. Use lubricating ointments alone, especially at bedtime, for several weeks to months to control symptoms.

Treatment of dry eye

In a study by Lopez et al, it was found that in severe dry eye syndromes, the corneal epithelium is compromised with development of punctate erosions and increased permeability.[5]

In their study, the ability of artificial tear solutions to promote recovery of the corneal epithelial barrier was determined by measurement of corneal uptake of 5,6-carboxyfluorescein (CF).

Corneas of anesthetized rabbits were exposed to 0.01% benzalkonium for 5 minutes to increase epithelial permeability. Then, the cornea was exposed to an artificial tear solution for 1.5 hours, followed by measurement of CF uptake.

During exposure to 3 commercial isotonic nonpreserved solutions and a solution preserved with polyquaternium-1, CF uptake decreased significantly but did not return to control. No recovery of the epithelial barrier occurred during exposure of corneas to nonpreserved hypotonic solutions. During exposure to an experimental tear solution with an electrolyte composition similar to human tears, buffered with bicarbonate, CF uptake returned to control levels.

Bicarbonate is an essential component of this solution because the same formula buffered with borate or without buffer was ineffective in promoting recovery of the damaged corneal epithelium.

Lens treatment

In some cases of multiple recurrent erosions, soft contact lenses can be helpful. Bandage lens treatment, if used for this indication, must be continued for up to 8-26 weeks to facilitate repair of the corneal epithelial basement membrane. However, persistent use of soft contact lens increases the risk of infectious corneal disease. 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.[6]

Prevention of mild corneal erosion

In some cases, the recurrence of very mild corneal erosion may be prevented with the following: sodium chloride drops 2% or 5% several times during the day and sodium chloride ointment 5% at bedtime. Many surgeons believe that sodium chloride ointment is no more effective than a lubricant ointment or an ointment without preservatives. Each patient must be established on a regimen of medication that seems to control the symptoms more 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.

Treatment of resistant cases

Resistant cases may require the following:

  • 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" the Bowman layer after mechanical debridement (proven to be effective in preventing recurrences)

Delaminatiion of the corneal epithelium

Delaminating the corneal epithelium using alcohol can improve the symptoms of recurrent corneal erosions in eyes that do not respond to topical lubrication or bandage contact lenses.[7]

For the delamination procedure, a 20% alcohol solution is used that is dripped into a circular well placed over the defect and applied for 30-40 seconds.

The treated area of the corneal epithelium is then completely debrided using a sponge, and the corneal surface is irrigated with saline before placing a bandage contact lens.

Surgical Care

Simple superficial debridement for removal of the abnormal epithelium and basement membrane, thereby leaving a smooth substrate of the Bowman layer, can be performed at the slit lamp. The adjacent normal epithelium can resurface in this area, allowing formation of competent attachment complexes and resulting in prompt cessation of erosive symptoms with a reduced frequency of recurrences. This procedure can be used if more conservative measures (eg, lubricants, patching, bandage contact lenses) fail in halting the erosions.

Debriding of the epithelium. Poorly adherent epith Debriding of the epithelium. Poorly adherent epithelium with a second layer of basement membrane.

A small group of patients with epithelial basement membrane dystrophy experience reduction of vision and/or recurrent erosions from the extreme deposition of an abnormal basement membrane and fibrillar collagenous material between the epithelium and the Bowman layer. This material may lead to irregular astigmatism and abnormal tear breakup. Patients complain of monocular visual distortion, diplopia, or ghost images. By performing superficial keratectomy, this abnormal material can be removed readily, leaving behind a smooth substrate of an intact Bowman layer. After reepithelialization, a smooth surface is reestablished with the elimination of irregular astigmatism.

Anterior stromal puncture

More severe cases of recurrent corneal lesions are treated with anterior stromal puncture. Marechal et al described anterior stromal puncture in recurrent corneal erosion with a curved needle, which minimizes scarring and prevents corneal perforation. An insertion depth of 0.1 mm was sufficient to result in the production of new basement membrane attached to the anterior stroma.[8]

In more severe cases of recurrent corneal erosion do not seem to respond to any of the above therapies, the use of anterior stromal puncture has been advocated. This procedure involves making 75-150 small punctures with a Rubenfeld needle with a Fugo blade. The authors of this article perform numerous punctures on the affected sites through the epithelium and the Bowman layer into anterior stroma. The Fugo tip is inserted through the loosened epithelium or an epithelial defect, making momentary micropunctures to affect only the anterior stroma.

Anterior stromal puncture with a Fugo blade has resulted in significant improvement among patients who have had multiple recurrent erosions that are unresponsive to debridement alone or debridement with cautery. This is effective in more than 95% of cases of recalcitrant recurrent erosions.

With the advent of anterior stromal puncture and related procedures, many clinicians prefer to treat posttraumatic recurrent corneal erosions with these methods, thereby minimizing the number of such patients requiring therapeutic lenses.

Excimer laser phototherapeutic keratectomy

Excimer laser phototherapeutic keratectomy (PTK) has generated considerable interest in treating recurrent corneal erosions. With the MEL 50 Aesculap-Meditec 193-nanometer argon-fluoride excimer laser, surgeons have treated individuals, who experienced posttraumatic, therapy-resistant, recurrent corneal epithelial erosions. They used the excimer laser in spot-mode under manual guidance. Only in those eyes where the erosion was covered with loose bullous epithelium did they remove the epithelium mechanically prior to surgery.

Gyldenkerne et al in Denmark have observed that recurrent corneal erosions are a troublesome clinical problem.[9] Many patients with erosions do not respond satisfactorily to the standard treatment. In a paper, they presented a study of treatment of 24 patients with recurrent corneal erosions with the excimer laser, where 75% of the patients reported the treatment as a success.[9]

In a study by John et al, after PTK, no patient had a recurrence after 18 months follow-up care.[10] Subjectively, all the patients believed that the treated area healed faster than previous abrasions. Vision, refraction, keratometry, and corneal thickness measurements appeared unaffected by the treatment.

Nd:YAG laser treatment

Katz et al retrospectively studied 8 patients with recurrent corneal erosions treated with the Nd:YAG laser using 0.4- to 0.5-mJ pulses applied to the region of the Bowman layer through an intact epithelium.[11] All 8 patients had resolution of their symptoms after treatment. Mean follow-up time was 21.2 months (range, 12.6-36.6 mo).

A patient who was scheduled for diagnostic enucleation for a posterior choroidal mass consented to undergo this laser treatment with varied energy settings 6 days before his enucleation. The patient’s cornea was studied with specular microscopy, light microscopy, and transmission electron microscopy. Light microscopy of the cornea disclosed rare 100-µm defects in the Bowman layer with subjacent compaction of the anterior stromal layer.

Superficial phototherapeutic keratectomy

Superficial PTK can be curative in some cases of painful recurrent erosions despite conventional treatment, including aggressive anterior stromal micropuncture. The ablated anterior corneal stromal surface appears to be highly supportive of stable reepithelialization.

Although completely normal reformation of the basal lamina complex, including normal density of hemidesmosomes and anchoring fibrils, may take months to years, most investigators of photorefractive keratoplasty (PRK) have been impressed with the rapid and stable reepithelialization that occurs after ablation, with absence of punctate keratitis, staining defects, or symptoms of recurrent erosion. In this condition, the objective of PTK is simply to remove enough of the superficial Bowman layer to permit formation of a new basement membrane with adhesion structures. The current technique is to debride the epithelium in the involved area, and, with the use of a large spot size, such as 5 mm, apply 16 pulses. Usually, this maneuver will remove no more than 4 mm of the Bowman layer.

Because no optical effect is seen with such a superficial ablation, the treatment may be applied centrally or eccentrically. Because these cases are rare, caution should be exercised in the aggressive application of this technique until adequate experience is gained with the long-term success rate.

Superficial keratectomy and penetrating and lamellar keratoplasty all have been advocated when intervention in Reis-Bücklers corneal dystrophy is necessary because of diminished visual acuity. In a study by Rogers et al, 11 eyes were treated by PTK with an excimer laser.[12] Two eyes had been treated previously by penetrating keratoplasty. The visual acuity improved in all eyes, from an average of 6/60 (20/200) to 6/9 (20/30) with complete cessation of recurrent erosions.

Soong et el used diamond burr superficial keratectomy in the treatment of recurrent corneal erosions.[13] They concluded that diamond burr superficial keratectomy appeared to be a safe and effective method of treating recurrent erosions and a good alternative therapy to needle stromal micropuncture, Nd:YAG laser induced epithelial adhesion, and excimer laser surface ablation.

Treatment of spontaneous recurrent erosions and erosions due to corneal dystrophies

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, the following procedures have been used with success:

  • Excimer laser photoablation (PTK) through the basement membrane, just into the Bowman layer, has been performed with some success, although it is more expensive than mechanical debridement.
  • Success has been reported in combining PRK with PTK to treat intractable recurrent erosions in myopic patients; even patients who had frequent recurrent erosions for years were symptom free after this combined photoablative procedures in follow-up periods of 26-42 months.

Collagen punctal plugs

Collagen punctal plugs may help identify individuals who might benefit from punctal occlusion or punctal cautery. 

Granular dystrophy before phototherapeutic keratec Granular dystrophy before phototherapeutic keratectomy.
Granular dystrophy after photorefractive keratecto Granular dystrophy after photorefractive keratectomy.


Patients should avoid rubbing the eyes and splashing water on open eyes.

Patients should use protective glasses.


Preventive measures for patients with recurrent corneal erosion are discussed below.

Avoid dry or irritating environments (eg, cigarette smoke).

Drink plenty of fluids to help prevent drying of the eyes. This may also involve limiting alcohol intake in the evenings. Drinking heavily may cause an erosion episode the following morning, sometimes referred to as "drinker's eye."

Avoid sleeping in late, as corneal hydration from lid closure may be a factor affecting epithelial adhesion.

Apply long-lasting eye ointments (eg, Lacri-Lube) at bedtime. Many patients use a lubricating ointment at night for months or even years to prevent a recurrence.

Control the air quality and the humidity of the room while sleeping. Avoid having an overventilated room. Air flowing over the face, even with the eyes closed, can increase eye dryness. Cool, moist, still air is the best environment to prevent unnecessary evaporation of eye moisture.

Limit exposure to viruses (eg, annual flu shot). Viruses, such as the flu (and associated gastrointestinal symptoms like diarrhea), seem to cause the eyes to dry out and can help cause an erosion episode.

Wear protective glasses (eg, sunglasses, prescription glasses, even "fake" glasses), especially when engaging in activities like gardening or playing with children.

Learn to wake with the eyes closed and still.

Keep high-quality artificial tears within reach of the bed; if the eyes feel “stuck shut” upon awakening, insert the bottle tip slightly into the inner corner of the eye and gently squirt in the artificial tears. The artificial tears will seep under the eyelid, often allowing the opening of the eyes without an erosion episode. Several repeated applications of artificial tears may be necessary, but with patience, the eyes will likely become “unstuck” and allow the pain-free opening of the eyes and erosion avoidance.

Another method, after waking with the eyes closed and still, is to use the fingers to gently rub the closed eyelids in a circular motion before attempting to open them.

The friction of the eyelid against the cornea may be enough to rip off a piece of the corneal epithelium. If a recurrent corneal erosion is suspected, the affected eye should be kept firmly closed, and only the unaffected eye should be opened. Looking around will help lubricate the affected eye so that, when it is opened, there is no friction and, thus, no repeat of the abrasion.

Long-Term Monitoring

Regular follow-up care for many months to even years is required for proper evaluation of the condition.