eMedicine Specialties > Ophthalmology > Cornea

Corneal Melt, Postoperative: Treatment & Medication

Author: Arun Verma, MD, Senior Consultant, Department of Ophthalmology, Dr Daljit Singh Eye Hospital, India
Contributor Information and Disclosures

Updated: Jun 10, 2008

Treatment

Medical Care

Corneal melting, a condition that may lead to corneal perforation (open injury), is often an indication of a systemic disease, such as rheumatoid arthritis or lupus, and, therefore, requires systemic treatment rather than just topical eye drop application. It is extremely important that patients be treated by an expert physician who specializes and understands the process of eye melt, which can be a presenting sign of serious systemic disorder that can benefit dramatically with systemic treatment. The team of physicians and ophthalmologists should be experts at providing ocular and systemic care to patients with such disorders. Drugs used in the treatment of these eye diseases can have significant adverse effects, including bone marrow suppression, and improper use or dosages can be devastating. However, the corneal melt itself can be equally devastating to one's vision, potentially leading to perforation of the cornea and/or loss of vision. Therefore, the risks and benefits are heavily weighed, and an informed decision is made as to the best course of treatment.

Patients who initially present with punctate corneal staining that becomes an epithelial defect may ultimately develop stromal loss. Most of these patients do not complain of pain.

Yang and Kline reported 5 cases of stromal loss among approximately 600 patients, which is an incidence rate of 0.01%.2 Gelender reported 5 cases of stromal loss, and Insler and colleagues reported 4 cases.3,4 All of the patients described by Yang and Kline as well as by Insler and colleagues had associated collagen vascular disease.2,4 All but one of these patients had rheumatoid arthritis; the other patient had scleroderma. In Gelender's initial report, only one patient had Stevens-Johnson disease; the other patients were apparently healthy.3 The findings from the studies performed to detect collagen vascular diseases after the ulcer was detected were negative. More recently, several cases believed to be secondary to the extended use of topical nonsteroidal anti-inflammatory drugs (NSAIDs) have been reported.

Acute bacterial, viral, or fungal ulcers usually produce a prominent inflammatory reaction, often with a hypopyon, while eyes with corneal melting appear quieter. Postoperatively, if a surgeon discovers a corneal ulcer in a patient, the ulcer should be cultured. Eye drops that are toxic to the epithelium (eg, steroids, NSAIDs, antibiotics, beta-blockers, epinephrine) should be discontinued.

If the eye is relatively quiet and the problem appears to be a corneal melt rather than an infectious corneal ulcer, frequent lubrication with a nonpreserved drop or ointment should be instituted, and the patient should be monitored closely, particularly if a descemetocele seems imminent. Hospitalization may be necessary. Bandage contact lenses may also be of value, but the patient should be monitored closely because a secondary bacterial ulcer may develop.

Corneal cyanoacrylate gluing is recommended if the cornea appears to be progressively thinning. Healing results in approximately 60% of cases. Spontaneous perforation should be treated with either a lamellar keratoplasty or a penetrating keratoplasty. Gelender reported that a conjunctival flap helps stabilize the cornea.3 Tarsorrhaphy and punctal occlusion may also be considered. The proteases produced by PMNs and diseased epithelium may contribute to corneal melting. The eye should be treated with nonpreserved lubricating ointments combined with taping the lid shut or tarsorrhaphy unless the eye is inflamed.

Keratoconjunctivitis sicca always should be ruled out and treated appropriately when corneal disease is associated with rheumatoid arthritis because sterile corneal ulceration and melting may be associated with dry eyes. Corneal involvement in rheumatoid arthritis includes keratitis, sclerosing keratitis, keratolysis, and peripheral corneal melting. The marginal corneal ulceration may involve the entire circumference in the limbal area, or it may be in a localized zone and frequently is accompanied by significant pain. Marginal corneal ulceration may be quiet and asymptomatic in other patients, and it occurs with or without associated scleral or episcleral inflammation.

  • Adequate lubrication with preservative-free tear and ointment supplements is very important.
    • Acetylcysteine (Mucomyst 10-20%), used 4-6 times daily, is a topical collagenase inhibitor that may be beneficial in some patients. Topical high-dose corticosteroids may relieve associated scleritis and prevent progression of ulcerative keratitis. In certain cases, especially in patients with dry eye, topical corticosteroids can enhance melting.
    • Later in the disease process, medroxyprogesterone acetate 1% may be used as a topical anti-inflammatory agent that does not inhibit collagen synthesis.
    • If melting is progressive, a hydrophilic bandage contact lens may be helpful in promoting epithelial resurfacing; in thin corneas with impending perforation, a tissue adhesive may be applied.
    • If the above treatment is ineffective, a 3-5 mm resection of the conjunctiva adjacent to the furrow itself may be performed. Systemic immunosuppression is the definitive therapy.
  • The use of collagenase inhibitors as adjunctive therapy in the treatment of progressive corneal melting has been disappointing. Both disodium edetic acid and acetylcysteine have been used to inhibit collagenase activity, particularly in Pseudomonas corneal infections. Additional enzyme inhibitors, such as the metalloproteinases, are under investigation and may be of clinical value in the future. The rationale for their use is to prevent corneal tissue destruction, but there has been no clear evidence that they have been of clinical benefit.
  • Corticosteroids also can predispose to secondary complications, including microbial superinfection, stromal melting, secondary glaucoma, and cataract formation. Once corticosteroids are begun, it often is difficult to discontinue them, and a marked rebound inflammatory response can ensue with a withdrawal that is too abrupt. Patients should be forewarned of the potential for chronic topical corticosteroid treatment, even at low doses. Steroids should not be used in cases of exposure or neurotrophic keratitis because of the possibility of keratolysis.
  • People have underscored the prophylactic benefit of early, large tarsorrhaphy to prevent initial epithelial erosion with subsequent corneal melting and perforation. Therapeutic soft contact lenses may be a reasonable short-term strategy.
  • Impending or actual corneal perforation, if less than 1.5 mm in diameter, can be treated successfully with 2-butyl-cyanoacrylate (Histoacryl) adhesive and a therapeutic soft contact lens (eg, Bausch & Lomb plano T). Larger perforations should be treated immediately with scleral or corneal patch grafting. These grafts may need to be covered with conjunctiva (or amniotic membrane) to prevent the same melting process from destroying the scleral or corneal patch graft. Topical steroid therapy should be tapered, and cycloplegics should be added in concert with corneal gluing.
  • Clinical and basic research continues to explore how stem cell functions can be modulated by soluble cytokines and how insoluble matrix autologous serum eye drops (frequent preservative-free artificial tears, highly viscous methyl cellulose) probably help promote epithelial healing. A high rate of immune reactions can be expected because of the high immunogenic stimulus of the limbal transplant related to relative abundance of Langerhans cells and human leukocyte antigen DR (HLA-DR) antigens. Effective immunosuppression is considered essential.
  • Oral cyclosporin A and topical cyclosporin A (0.05%) can be used in melting stromal ulcers. It may be a good alternative mode of achieving ocular immunosuppression.

Surgical Care

Single dose application of topical mitomycin can be associated with serious complication (ie, corneal melting leading to perforation). The patient can be treated with lamellar corneal transplant. Epithelial ingrowth may develop in the lamellar interface after LASIK and may be associated with melting of the edge of the flap. This undesirable complication can be treated successfully with early surgical removal of the epithelium and proper reattachment of the flap.

  • Keratoplasty
    • Prompt initiation of therapy directed at the specific cause is required to promote epithelial healing. Conjunctival flaps play a less important role in the treatment of perforations than they do in the prevention of progression of corneal melting. Nonetheless, in some leaking descemetoceles and small perforations, conjunctival flaps may serve as a temporizing measure before keratoplasty. However, with the use of tissue adhesives and patch grafting, the use of conjunctival flaps for perforation has become almost obsolete.
    • Partial-thickness scleral flaps may be dissected with a base at the limbus and then reflected onto the cornea and sutured in place to treat small peripheral corneal perforations. To be most effective, the epithelium and the necrotic material surrounding the leak must be removed, and dissection of a small lamellar bed is helpful in suturing the sclera to the cornea. This technique is cosmetically less acceptable than the use of corneal material but may be of value in emergency situations.
    • Another technique using autologous cornea has been described in which a small trephine (2 mm) was used to dissect a half-thickness peripheral corneal button, which was sutured in place over a perforation in the cornea of the same eye. The donor site healed without complication, and the perforation was repaired. The most frequently used techniques for definitive repair of perforations involve some form of keratoplasty using donor material. The choice between lamellar and full-thickness penetrating keratoplasty depends on a number of factors, including location and size of the perforation, donor tissue availability, and associated ocular findings. It is better to choose lamellar grafting when the perforation is small and peripheral. Also, when marked anterior segment inflammation and a formed chamber are present, lamellar patch grafting may avoid instrumentation of the anterior chamber and the risk of fibrin outpouring, chamber flattening, and formation of synechiae.
    • Lamellar keratoplasty depends on the same principles as the use of tissue adhesive, ie, debridement of necrotic material and removal of surrounding epithelium. Additionally, a clean edge for suture placement is necessary and a dry bed is not necessary.
    • Penetrating keratoplasty for corneal perforation is the most aggressive approach but also may be mandated by the circumstances present. Large perforations, too large to seal with tissue adhesives or lamellar patch grafting, and smaller perforations surrounded by large areas of tissue necrosis may need penetrating grafts. The technique is that of standard penetrating keratoplasty with modifications because of the softness of the eye. With smaller perforations, tissue adhesives may be used to temporarily plug the leak, so that trephination may be performed. Viscoelastics may be used to help form the anterior chamber by injection through the perforation site. Either way, a trephine large enough to surround all the necrotic tissue should be used. A donor cornea that is 0.50 mm larger, then is sutured in place.

Consultations

An internist or rheumatologist may be consulted if a systemic disease is believed to cause the melting.

Medication

The goal of pharmacotherapy is to reduce morbidity and to prevent complications. Tissue adhesives can be used with small perforations or descemetoceles with impending perforation.

Tissue adhesives

These agents may be applied under topical anesthesia at the slit lamp. The glue may induce significant inflammation and may be uncomfortable for the patient. They may adhere inadequately, may serve to harbor organisms once polymerized, and often are effective only in small perforations that can be dried readily. These substances polymerize rapidly when in contact with water. The favored adhesive for ocular surgery appears to be isobutyl-2-cyanoacrylate. Patients with progressive corneal melting secondary to ulcerative disease and patients with frank corneal perforations have been successfully treated with these cyanoacrylate adhesives.

The tissue adhesives most commonly used in the United States are cyanoacrylates, usually isobutyl or higher alkyl compounds. None of these are approved for ophthalmic use by the Food and Drug Administration, but N -butyl cyanoacrylate is under evaluation at this time.


N-butyl cyanoacrylate (Nexacryl)

Sterile, nontoxic, biocompatible, hemostatic, and bacteria static. A monomer, but when it comes in contact with moisture it is converted into a polymer. Inert material that solidifies within less than 5-10 seconds. Solidifies rapidly in alkaline media but slowly in acidic media. Does not get absorbed into the blood stream. Bacteria free and unaffected by many other bacteria.
Iso amyl-2 cyanoacrylate is a thickened monomer. Allows rapid wound closure with minimal scarring, reduced risk of subsequent infection, less traumatic, more efficient, precise, and safe.
The cyanoacrylate adhesive may be useful for covering ulcers and sealing perforations, because it can be applied over an ulcer bed and covered with a therapeutic soft contact lens. If glue displaces spontaneously from cornea in a few weeks, it can be reapplied to achieve continued stromal protection.
Various techniques have been described for the use of tissue adhesives; all require debridement of necrotic tissue and epithelium surrounding perforation, drying of area to which glue is to be applied, and application of least amount of glue that can cover the defect. Drying of defect can be carried out with cellulose sponges, and air or viscoelastic may be placed behind the perforation to separate tissue and reduce fluid present. The glue itself may be applied to a small plastic disk and then placed over the perforation, applied directly from the tip of a fine needle attached to a tuberculin syringe, or applied with a specially made applicator. The glue may come off and need to be reapplied, at times repeatedly. Usually, because of the rough surface of polymerized glue, a bandage soft contact lens is placed on the eye after the glue has polymerized.

Adult

Draw solution from ampule into special applicator; keep corneal tissue as dry as possible and apply solution on the perforation edges; a very thin layer is applied, and the excess removed immediately with a dry swab; may leave glue in place until there is obvious healing of perforation, until glue spontaneously loosens because epithelium has grown beneath it, or until a more definitive procedure such as keratoplasty is carried out

Pediatric

Not established

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Avoid very thick applications because heat on polymerization can cause injury to adjacent tissue and reduce healing because of slow absorption; tissue adhesive is stored below 8-15°C, preferably in a refrigerator and protected from light

Topical collagenase inhibitors

Mucolytic agent acetylcysteine has been advocated by some authors because they have shown to inhibit the lytic effect of collagenase in presence of, as well as in absence of, corticosteroids. Corneal melting, when it occurs, usually does not occur until after the fifth day following corneal surgery. Thus, it is reasonable to use corticosteroids to suppress the inflammatory response and prevent scarring for at least the first 5-7 days. The exact value of anticollagenase agents such as acetylcysteine has not been proven. Cysteine also inhibits collagenase and is more readily available as acetylcysteine, 10-20% concentration (Mucomyst). Another collagenase inhibitor is penicillamine. The use of collagenase inhibitors as adjunctive therapy in the treatment of progressive corneal melting has been disappointing.

Both disodium edetic acid and acetylcysteine have been used to inhibit collagenase activity, particularly in Pseudomonas corneal infections. These agents should be started if postoperative melting is observed.

Disodium ethylenediaminetetraacetic acid (EDTA) (Endrate) and calcium disodium EDTA (Calcium Disodium Versenate) inhibit collagenase through chelation. Evidence of local effective doses is not available, but 0.2 M irritation has been documented.

Among the many synthetic inhibitors of collagenase is Galardin. This agent appears to prevent the corneal ulceration of alkali injury by diminishing the release from PMNs of matrix metalloproteinases (MMPs) that digest capillary walls to allow extravasation of the PMNs. Any decrease in the number of locally extravasated PMNs decreases the potential pool of MMPs at the site of injury. Galardin further reduces inflammation by preventing release of tumor necrosis factor-a (TNF-a), a cytokine that activates PMNs, from producer cells such as macrophages and activated T cells. Galardin also may block MMPs released from inflammatory cells, corneal fibroblasts, and epithelial cells. It has been tried in cases of postoperative corneal melts.

Other synthetic inhibitors of MMPs include mercaptan (thiol)-containing compounds resembling the drug captopril, which inhibits the metalloproteinase angiotensin-converting enzyme in the treatment of heart failure and hypertension. One of the MMP inhibitors derived in this manner, HSCH2 CH[CH2 CH(CH3)2]CO-Phe-Ala-NH2 (SIMP), is effective in inhibiting corneal ulceration.

The alpha2-macroglobulin of serum is a powerful inhibitor of collagenase and the other MMPs. Alpha1-antitrypsin is considerably less effective against collagenase, but it too has been documented to prevent corneal ulceration after ocular chemical injuries. Blood is drawn into dry, sterile containers containing no anticoagulants clots and yields serum that can be separated and refrigerated until needed. If autologous blood is available, its therapeutic use need not be delayed by testing for human immunodeficiency virus or hepatitis. Gentamicin sulfate sufficient to achieve a concentration of 0.003% can be added to the serum before its administration by drops or by continuous perfusion.


N-acetylcysteine (Mucomyst 10-20%),

Topical collagenase inhibitor that may be beneficial in some patients. Formulated from commercially available Mucomyst, diluted to a 5% or 10% solution with artificial tears, and is applied 4-6 times/d. The 10% acetylcysteine drops can be given several times daily. Mucolytic action of this agent sometimes clears the ulcer. Not harmful to the globe or adnexum and obviously should be tried in pediatric age group before subjecting a child to a general anesthetic.
Ask the pharmacist to supply the acetylcysteine in a dark dropper bottle because of its instability in light.
Adequate lubrication with preservative-free tear and ointment supplements is important. Guidelines for solution have been used safely.

Adult

10% acetylcysteine solution and sodium citrate 10% solution may be applied q2h around the clock; 100 mg doxycycline can be taken PO q12h

Pediatric

Not established

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Rule out keratoconjunctivitis sicca because sterile corneal ulceration may be associated with dry eyes

Corticosteroids

Adequate lubrication with preservative-free tear and ointment supplements such as corticosteroids are very important. Corticosteroids modify the body's immune response to diverse stimuli.


Prednisone (Deltasone, Orasone, Sterapred)

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Adult

15-80 mg/d PO

Pediatric

Not established

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

Immunosuppressive agents

Used for unresponsive severe corneal inflammatory disease or to prevent postoperative corneal melting syndromes in susceptible cases. Immunosuppressive medication may be beneficial. A more direct strategy in immuno intervention involves inhibition of various effector cells. Targeting effector cell products such as cytokines or their receptors has been effective.

Systemic and topical administration has been investigated regarding corneal graft rejection, intermediate and posterior uveitis, and noninfectious, immune-related corneal ulcers and postoperative corneal melts.

Topical CsA is of use in corneal graft rejection and prevention of postoperative corneal melts. A marginal corneal ulceration related to autoimmune disease can be improved through the use of topical and systemic CsA.


Cyclosporine (Sandimmune, Neoral)

Specific modulator of T-cell function and an agent that depresses cell-mediated immune responses by inhibiting helper T-cell function. Has been used to treat a variety of forms of uveitis, often with good results. Binds to cyclophilin, an intracellular protein, which in turn prevents formation of interleukin 2 and the subsequent recruitment of activated T cells. Oral CsA and topical CsA (0.05%) can be used in melting stromal ulcers. It may be a good alternative mode of achieving ocular immunosuppression. Topical CsA has been shown to prevent postoperative corneal melts and to reduce the incidence of graft rejections in patients at high risk. A marginal corneal ulceration related to autoimmune disease can be improved through the use of topical and systemic CsA.
Cyclosporine has about 30% bioavailability, but there is marked interindividual variability. Cyclosporine specifically inhibits T-lymphocyte function with minimal activity against B cells. Maximum suppression of T-lymphocyte proliferation requires that the drug be present during the first 24 h of antigenic exposure.
Oral cyclosporine has been used, with apparent efficacy, to treat corneal melting syndromes such as Mooren ulcer and that associated with Wegener granulomatosis.
The use of systemic cyclosporine significantly improves the results of surgery.

Adult

10-50 mg/kg/d PO; monitor blood level of cyclosporine for optimum management of dosage
If perforations are impending immediately at surgery: 15 mg/kg/d IV followed by 7.5 mg/kg/d for 2 d; adjust dose to maintain a level of 250-400 µg/L of whole blood (usually requires 4-4.5 mg/kg/d); maintained treatment for 4 mo
For topical application: Use 2% in olive oil q2h while awake beginning 1-2 d before surgery; after 4 d of treatment, frequency is reduced to qid for 3 mo

Pediatric

Not established

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease cyclosporine concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase cyclosporine toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UVB radiation in psoriasis since it may increase risk of cancer

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin and liver enzymes; may increase risk of infection and lymphoma; a potentially lethal form of lymphoma, associated with Epstein-Barr viral infection, is reversible if the drug is stopped; although immunosuppressive agents, in general, are associated with an increase incidence of lymphomas, there is no evidence that cyclosporine treatment poses a greater risk than the other drugs

Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.


Doxycycline (Vibramycin, Doryx, Bio-Tab, Vibra-Tabs)

Inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

Adult

100 mg PO q12h

Pediatric

Not established

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy

Documented hypersensitivity; severe hepatic dysfunction

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

More on Corneal Melt, Postoperative

Overview: Corneal Melt, Postoperative
Differential Diagnoses & Workup: Corneal Melt, Postoperative
Treatment & Medication: Corneal Melt, Postoperative
Follow-up: Corneal Melt, Postoperative
References
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References

  1. Cottinger, AJ, Berkley, RP, Nordan IT, et al. Bacterial corneal ulcers following keratorefractive surgery. In: A retrospective study of 14163 procedures. Paper presented at: Ocular Microbiology Immunology Group Meeting. San Francisco, CA; September 28, 1985.

  2. Yang HK, Kline OR Jr. Corneal melting with intraocular lenses. Arch Ophthalmol. Aug 1982;100(8):1272-4. [Medline].

  3. Gelender H. Descemetocele after intraocular lens implantation. Arch Ophthalmol. Jan 1982;100(1):72-6. [Medline].

  4. Insler MS, Boutros G, Boulware DW. Corneal ulceration following cataract surgery in patients with rheumatoid arthritis. J Am Intraocul Implant Soc. Nov 1985;11(6):594-7. [Medline].

  5. Barletta JP, Angella G, Balch KC, Dimova HG, Stern GA, Moser MT, et al. Inhibition of pseudomonal ulceration in rabbit corneas by a synthetic matrix metalloproteinase inhibitor. Invest Ophthalmol Vis Sci. Jan 1996;37(1):20-8. [Medline].

  6. Barletta JP, Balch KC, Dimova, et al. Inhibition of Pseudomonas corneal ulcers by a synthetic matrix metalloprotease inhibitor Galardin (GM[6001]). Invest Ophthalmol Vis Sci. 1993;34:1058.

  7. Benson WE, Diamond JG, Tasman W. Intraocular irrigating solutions for pars plana vitrectomy. A prospective, randomized, double-blind study. Arch Ophthalmol. Jun 1981;99(6):1013-5. [Medline].

  8. Bernauer W, Ficker LA, Watson PG, Dart JK. The management of corneal perforations associated with rheumatoid arthritis. An analysis of 32 eyes. Ophthalmology. Sep 1995;102(9):1325-37. [Medline].

  9. Binder PS, Baumgartner SD, Fogle JA. Histopathology of a case of epikeratophakia (aphakic epikeratoplasty). Arch Ophthalmol. Sep 1985;103(9):1357-63. [Medline].

  10. Binder PS, Zavala EY. Why do some epikeratoplasties fail?. Arch Ophthalmol. Jan 1987;105(1):63-9. [Medline].

  11. Cameron ME. Preventable complications of pterygium excision with beta-irradiation. Br J Ophthalmol. Jan 1972;56(1):52-6. [Medline].

  12. Castillo A, Diaz-Valle D, Gutierrez AR, Toledano N, Romero F. Peripheral melt of flap after laser in situ keratomileusis. J Refract Surg. Jan-Feb 1998;14(1):61-3. [Medline].

  13. Chung H, Tolentino FI, Cajita VN, Acosta J, Refojo MF. Reevaluation of corneal complications after closed vitrectomy. Arch Ophthalmol. Jul 1988;106(7):916-9. [Medline].

  14. Clewes AR, Tunn EJ, Kaye S, Bucknall RC. Use of intravenous cyclophosphamide in the prevention of corneal melt: justified or not?. Rheumatology (Oxford). Feb 2005;44(2):257-8. [Medline].

  15. Dougherty PJ, Hardten DR, Lindstrom RL. Corneoscleral melt after pterygium surgery using a single intraoperative application of mitomycin-C. Cornea. Sep 1996;15(5):537-40. [Medline].

  16. Dua HS, Saini JS, Azuara-Blanco A, Gupta P. Limbal stem cell deficiency: concept, aetiology, clinical presentation, diagnosis and management. Indian J Ophthalmol. Jun 2000;48(2):83-92. [Medline].

  17. Edelhauser HF, Hine JE, Pederson H, Van Horn DL, Schultz RO. The effect of phenylephrine on the cornea. Arch Ophthalmol. May 1979;97(5):937-47. [Medline].

  18. Ewing-Chow DA, Romanchuk KG, Gilmour GR, Underhill JH, Climenhaga DB. Corneal melting after pterygium removal followed by topical mitomycin C therapy. Can J Ophthalmol. Jun 1992;27(4):197-9. [Medline].

  19. Farrell PL, Smith RE. Bacterial corneoscleritis complicating pterygium excision. Am J Ophthalmol. May 15 1989;107(5):515-7. [Medline].

  20. Foulks GN, Thoft RA, Perry HD, Tolentino FI. Factors related to corneal epithelial complications after closed vitrectomy in diabetics. Arch Ophthalmol. Jun 1979;97(6):1076-8. [Medline].

  21. Geerling G, Joussen AM, Daniels JT, Mulholland B, Khaw PT, Dart JK. Matrix metalloproteinases in sterile corneal melts. Ann N Y Acad Sci. Jun 30 1999;878:571-4. [Medline].

  22. Gelender H. Corneal melting syndrome. Arch Ophthalmol. Feb 1983;101(2):303. [Medline].

  23. Gilliland GD, Hutton WL, Fuller DG. Retained intravitreal lens fragments after cataract surgery. Ophthalmology. Aug 1992;99(8):1263-7; discussion 1268-9. [Medline].

  24. Grayson, M. Diseases of the Cornea. 2nd ed. St Louis: CV Mosby; 1983.

  25. Gupta S, Basti S. Corneoscleral, ciliary body, and vitreoretinal toxicity after excessive instillation of mitomycin C. Am J Ophthalmol. Oct 15 1992;114(4):503-4. [Medline].

  26. Hoffer KJ, Darin JJ, Pettit TH, Hofbauer JD, Elander R, Levenson JE. Three years experience with radial keratotomy. The UCLA study. Ophthalmology. Jun 1983;90(6):627-36. [Medline].

  27. Hong C, Kitazawa Y, Tanishima T. Influence of argon laser treatment of glaucoma on corneal endothelium. Jpn J Ophthalmol. 1983;27(4):567-74. [Medline].

  28. Lam DS, Leung AT, Wu JT, Fan DS, Cheng AC, Wang Z. Culture-negative ulcerative keratitis after laser in situ keratomileusis. J Cataract Refract Surg. Jul 1999;25(7):1004-8. [Medline].

  29. Latina MA, Melamed S, March WF, Kass MA, Kolker AE. Gonioscopic ab interno laser sclerostomy. A pilot study in glaucoma patients. Ophthalmology. Nov 1992;99(11):1736-44. [Medline].

  30. Leahey AB, Gottsch JD, Stark WJ. Clinical experience with N-butyl cyanoacrylate (Nexacryl) tissue adhesive. Ophthalmology. Feb 1993;100(2):173-80. [Medline].

  31. Lemp MA. Cornea and sclera. Arch Ophthalmol. Aug 1974;92(2):158-70. [Medline].

  32. Liu SM, Su J, Hemady RK. Corneal melting after avulsion of a Molteno shunt plate. J Glaucoma. Dec 1997;6(6):357-8. [Medline].

  33. Mamalis N, Johnson MD, Haines JM, Teske MP, Olson RJ. Corneal-scleral melt in association with cataract surgery and intraocular lenses: a report of four cases. J Cataract Refract Surg. Jan 1990;16(1):108-15. [Medline].

  34. Mandelbaum S, Waring GO 3rd, Forster RK, Culbertson WW, Rowsey JJ, Espinal ME. Late development of ulcerative keratitis in radial keratotomy scars. Arch Ophthalmol. Aug 1986;104(8):1156-60. [Medline].

  35. Margherio RR, Cox MS Jr, Trese MT, Murphy PL, Johnson J, Minor LA. Removal of epimacular membranes. Ophthalmology. Aug 1985;92(8):1075-83. [Medline].

  36. Margo CE, Polack FM, Hood CI. Aspergillus panophthalmitis complicating treatment of pterygium. Cornea. 1988;7(4):285-9. [Medline].

  37. Morgan KS, Asbell PA, McDonald MB, May JG, Loupe DN, Kaufman HE. Preliminary visual results of pediatric epikeratophakia. Arch Ophthalmol. Oct 1983;101(10):1540-4. [Medline].

  38. Nelson JD, Williams P, Lindstrom RL, Doughman DJ. Map-fingerprint-dot changes in the corneal epithelial basement membrane following radial keratotomy. Ophthalmology. Feb 1985;92(2):199-205. [Medline].

  39. Ohashi Y, Matsuda M, Hosotani H, Tano Y, Ishimoto I, Fukuda M, et al. Aldose reductase inhibitor (CT-112) eyedrops for diabetic corneal epitheliopathy. Am J Ophthalmol. Mar 15 1988;105(3):233-8. [Medline].

  40. Pflugfelder SC, Saulson R, Ullman S. Peripheral corneal ulceration in a patient with AIDS-related complex. Am J Ophthalmol. Nov 15 1987;104(5):542-3. [Medline].

  41. Portnoy SL, Insler MS, Kaufman HE. Surgical management of corneal ulceration and perforation. Surv Ophthalmol. Jul-Aug 1989;34(1):47-58. [Medline].

  42. Pérez-Santonja JJ, Bellot J, Claramonte P, Ismail MM, Alió JL. Laser in situ keratomileusis to correct high myopia. J Cataract Refract Surg. Apr 1997;23(3):372-85. [Medline].

  43. Quillen DA, Rosenwasser GO. Aerosol application of cyanoacrylate adhesive. J Refract Corneal Surg. Mar-Apr 1994;10(2):149-50. [Medline].

  44. Refojo MF, Dohlman CH, Ahmad B, Carroll JM, Allen JC. Evaluation of adhesives for corneal surgery. Arch Ophthalmol. Nov 1968;80(5):645-56. [Medline].

  45. Rosenbery S. Corneal dellen following contact-lens wear. Am J Ophthalmol. Jun 1969;67(6):970. [Medline].

  46. Roy FH. Ocular Differential Diagnosis. 4th ed. Philadelphia: Lea and Febiger; 1984.

  47. Rubinfeld RS, Pfister RR, Stein RM, Foster CS, Martin NF, Stoleru S, et al. Serious complications of topical mitomycin-C after pterygium surgery. Ophthalmology. Nov 1992;99(11):1647-54. [Medline].

  48. Schwartz DE. Corneal sensitivity in diabetics. Arch Ophthalmol. Mar 1974;91(3):174-8. [Medline].

  49. Shivitz IA, Arrowsmith PN. Delayed keratitis after radial keratotomy. Arch Ophthalmol. Aug 1986;104(8):1153-5. [Medline].

  50. Smith RE, Schanzlin DJ. Rheumatoid diseases. In: Smolin, Thoft, eds. The Cornea: Scientific Foundations and Clinical Practice. 2nd ed. Boston: Little, Brown & Co; 1997.

  51. Smith SG, Lindstrom RL, Nelson JD, Weiss JL, Doughman DJ. Corneal ulcer-infiltrate associated with soft contact lens use following penetrating keratoplasty. Cornea. 1984;3(2):131-4. [Medline].

  52. Soong HK, Quigley HA. Dellen associated with filtering blebs. Arch Ophthalmol. Mar 1983;101(3):385-7. [Medline].

  53. Stern GA, Weitzenkorn D, Valenti J. Adherence of Pseudomonas aeruginosa to the mouse cornea. Epithelial v stromal adherence. Arch Ophthalmol. Dec 1982;100(12):1956-8. [Medline].

  54. Swinger CA, Villasenor RA. Homoplastic keratomileusis for correction of myopia. J Refr Surg. 1985;1:219-23.

  55. Townsend WM. Corneal melt after cataract surgery. Conjunctival flaps. In: The Cornea. New York: Churchill Livingstone; 1988:669.

  56. Vitrectomy with silicone oil or perfluoropropane gas in eyes with severe proliferative vitreoretinopathy: results of a randomized clinical trial. Silicone Study Report 2. Arch Ophthalmol. Jun 1992;110(6):780-92. [Medline].

  57. Vitrectomy with silicone oil or sulfur hexafluoride gas in eyes with severe proliferative vitreoretinopathy: results of a randomized clinical trial. Silicone Study Report 1. Arch Ophthalmol. Jun 1992;110(6):770-9. [Medline].

  58. Waring GO 3rd, Lynn MJ, Gelender H, Laibson PR, Lindstrom RL, Myers WD, et al. Results of the prospective evaluation of radial keratotomy (PERK) study one year after surgery. Ophthalmology. Feb 1985;92(2):177-98, 307. [Medline].

  59. Weiss JL, Williams P, Lindstrom RL, Doughman DJ. The use of tissue adhesive in corneal perforations. Ophthalmology. Jun 1983;90(6):610-5. [Medline].

  60. Wilhelmus KR. Corneal edema following argon laser iridotomy. Ophthalmic Surg. Aug 1992;23(8):533-7. [Medline].

  61. Wilhelmus KR, Hamburg S. Bacterial keratitis following radial keratotomy. Cornea. 1983;2:143-6.

  62. Zabel RW, MacDonald IM, Mintsioulis G. Corneal endothelial decompensation after argon laser iridotomy. Can J Ophthalmol. Dec 1991;26(7):367-73. [Medline].

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Further Reading

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Keywords

postoperative corneal melt, corneal melting, corneal perforation, corneal scarring, corneal epithelial defect, corneal tissue, corneal ulcer, corneal ulceration, cornea, vision loss

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Contributor Information and Disclosures

Author

Arun Verma, MD, Senior Consultant, Department of Ophthalmology, Dr Daljit Singh Eye Hospital, India
Disclosure: Nothing to disclose.

Medical Editor

Richard W Allinson, MD, Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center, Scott and White Clinic
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Christopher J Rapuano, MD, Professor, Department of Ophthalmology, Jefferson Medical College of Thomas Jefferson University; Co-Chairman of the Cornea Service, Co-Chairman of Refractive Surgery Department, Wills Eye Institute
Christopher J Rapuano, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Eye Bank Association of America, Pennsylvania Medical Society, and Philadelphia County Medical Society
Disclosure: Allergan Honoraria Speaking and teaching; Allergan Consulting fee Consulting; Alcon Honoraria Speaking and teaching; Inspire Honoraria Speaking and teaching; RPS Ownership interest Other

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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