Postoperative Corneal Melt Treatment & Management
- Author: Arun Verma, MD; Chief Editor: Hampton Roy, Sr, MD more...
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, andaninformed 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%. Gelender reported 5 cases of stromal loss, and Insler and colleagues reported 4 cases.[7, 8] All of the patients described by Yang and Kline as well as by Insler and colleagues had associated collagen vascular disease.[6, 8] 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. 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. 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.
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.
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.
An internist or rheumatologist may be consulted if a systemic disease is believed to cause the melting.
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